器官血流压力自动调节的异质性和可变性：100 多年来的经验教训

Heterogeneity and Variability in Pressure Autoregulation of Organ Blood Flow: Lessons Learned Over 100+ Years

Meng L, Wang Y, Zhang L, McDonagh DL. Heterogeneity and Variability in Pressure Autoregulation of Organ Blood Flow: Lessons Learned Over 100+ Years. Crit Care Med. 2019;47(3):436-448. doi:10.1097/CCM.0000000000003569

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摘要

Abstract

Objectives: Pressure autoregulation is an organ's intrinsic ability to maintain blood flow despite changes in perfusion pressure. The purpose of this review is to discuss autoregulation's heterogeneity among different organs and variability under different conditions, a very clinically relevant topic.

Data Sources: Systematic search of Ovid MEDLINE; nonsystematic search of PubMed, Google Scholar, and reference lists.

Study Selection: Animal or human studies investigating the potency or variation of pressure autoregulation of any organs or the association between autoregulation and outcomes.

Data Extraction: Two authors screened the identified studies independently then collectively agreed upon articles to be used as the basis for this review.

Data Synthesis: Study details, including subjects, organ investigated, methods of blood pressure intervention and blood flow measurement, and values of the lower limit, upper limit, and plateau were examined. Comparative canine studies were used to demonstrate the heterogeneity of pressure autoregulation among different organs and validate the proposed scale for organ categorization by autoregulatory capacity. Autoregulatory variability is discussed per organ. The association between cerebral autoregulation and outcome is summarized.

目的： 压力自动调节是一个器官的内在能力，它可以在灌注压力变化的情况下保持血流。本综述的目的是讨论自动调节在不同器官之间的异质性和在不同条件下的变异性，这是一个非常具有临床意义的话题。

数据来源： 系统性搜索 Ovid MEDLINE；非系统性搜索 PubMed、Google Scholar 和参考文献列表。

研究选择： 调查任何器官的压力自动调节的效能或变异或调查自动调节与预后关系的动物或人类研究。

数据提取： 两位作者独立筛选搜索入选的研究，然后共同商定了用于本综述的文章。

数据整合： 研究细节，包括受试者、被调查的器官、血压干预和血流测量的方法，以及下限、上限和平台的值都被检查。犬类的比较研究被用来证明不同器官间压力自动调节的异质性，并验证了所提出的按自动调节能力进行器官分类的标准。对每个器官的自动调节变异性进行了讨论。总结了脑部自动调节和预后之间的联系。

Conclusions: The organs with robust autoregulation are the brain, spinal cord, heart, and kidney. Skeletal muscle has moderate autoregulation. Nearly all splanchnic organs including the stomach, small intestine, colon, liver, and pancreas possess weak autoregulation. Autoregulation can be readily affected by a variety of clinically relevant factors. Organs with weak or weakened autoregulation are at a greater risk of suboptimal perfusion when blood pressure fluctuates. Cerebral autoregulation and outcomes are closely related. These lessons learned over 100+ years are instructive in clinical care.

结论： 具有强大自动调节能力的器官是大脑、脊髓、心脏和肾脏。骨骼肌有适度的自动调节功能。几乎所有的内脏器官，包括胃、小肠、结肠、肝脏和胰腺都具有微弱的自动调节功能。自动调节可以很容易地受到各种临床相关因素的影响。当血压波动时，自动调节功能较弱或被削弱的器官发生灌注不足的风险更大。大脑血流自动调节和预后是密切相关的。这些 100 多年来的经验教训对临床救治具有指导意义。

序言

Blood pressure (BP), one of the most volatile physiologic variables that is routinely measured in acute care, drives blood flow for organ perfusion. Pressure autoregulation (PA), the intrinsic tendency of an organ to maintain stable blood flow despite fluctuations in BP or perfusion pressure, is the linkage between organ perfusion pressure and blood flow (1, 2). Defects in PA increase the risk of tissue hypoperfusion during hypotension, hyperperfusion during hypertension, and unstable flow with fluctuating BP.

血压（BP）是急救中常规测量的最不稳定的生理变量之一，它驱动着器官灌注的血流。压力自动调节（pressure autoregulation，PA） 是器官在血压或灌注压波动的情况下保持稳定血流的内在趋势，是器官灌注压和血流之间的联系（1，2）。PA 的缺陷增加了低血压时组织灌注不足的风险，高血压时灌注过度，以及血压波动时血流不稳定的风险。

PA is important physiologically as well as clinically, since BP is "both" measurable and modifiable by the clinician. Although not the "only" determinant of organ perfusion, as discussed later in this review, PA must be understood in order to optimally manage the critically ill patient and patients undergoing anesthesia and surgery.

PA 在生理上和临床上都很重要，因为 BP 既可测量，又可由临床医生调控改变。尽管不是器官灌注的 "唯一" 决定因素，但正如本综述后面所讨论的那样，必须了解 PA，以便对危重病人和接受麻醉和手术的病人进行最佳管理。

PA exists in most organs, including the brain (3), spinal cord (4), heart (5), kidney (6), skeletal muscle (7), and visceral organs (8-12). However, different organs have different autoregulatory capacities (i.e., heterogeneity) (Fig. 1). Furthermore, the PA of specific organs is affected by multiple yet clinically relevant factors (i.e., variability) such as age (3, 13), sex (14), chronic hypertension (15, 16), diabetes mellitus (17, 18), metabolic rate (5, 19), cardiac output (20), hemodilution (21), CO₂ (22), drugs (23, 24), anesthesia (25-28), and sympathetic tone (29). PA's heterogeneity and variability are clinically relevant because organs with a weak or weakened PA are at increased risk of injury when BP is adversely changed.

PA 存在于大多数器官中，包括大脑（3）、脊髓（4）、心脏（5）、肾脏（6）、骨骼肌（7）和内脏器官（8-12）。然而，不同的器官有不同的自动调节能力（即异质性）（图 1）。此外，特定器官的 PA 受多种与临床相关的因素影响（即变异性），如年龄（3, 13）、性别（14）、慢性高血压（15, 16）、糖尿病（17, 18）、新陈代谢率（5, 19）、心输出量（20）、血液稀释（21）、二氧化碳（22）、药物（23, 24）、麻醉（25-28）、交感神经张力（29）。PA 的异质性和变异性是有临床相关性的，因为当血压发生不利变化时，较弱的或被削弱的 PA 的器官受损的风险增加。

Figure 1. Illustration of pressure autoregulation’s heterogeneity among different organs based on previous studies. The abscissa is the perfusion pressure and the ordinate organ blood flow. Coronary autoregulation in a dog with left ventricular hypertrophy is shown (A), with the middle curve derived during rest, the upper curve with dobutamine treatment, and the lower cure with propranolol treatment [5]. The plateau of each pressure-flow plot is also indicated (A). Autoregulation of an isolated and denervated gracilis muscle preparation from a dog is shown by the solid curve with open circles (B) [7]. Gastric autoregulation in dogs is shown (C) [8]. The slope of the plateau and the identifiability of the lower and upper limits of autoregulation differ among different organs. (Reproduced with permission from the various publishers.)

图 1. 根据以前的研究，压力自动调节在不同器官中的异质性的示例。横轴是灌注压力，纵轴是器官血流。图中显示了一只左心室肥大的狗的冠状动脉自动调节（A），中间的曲线是在休息时得出的，上面的曲线是在多巴胺治疗时得出的，下面的是在普萘洛尔治疗时得出的 [5]。每个压力 - 流量图的高点也被标出（A）。带有空心圆的实心曲线显示狗的分离和去神经化的股薄肌制备模型的自动调节（B） [7]。狗的胃自动调节（C）[8]。平台的斜率和自动调节的下限和上限的可识别性在不同的器官中有所不同。(经各出版商许可转载）。

To the best of our knowledge, PA's heterogeneity among different organs and PA's variability for specific organs have not been specifically reviewed. The reactive change in vasomotor tone to changes in BP was first reported by Bayliss (30) in 1902, an event that marked the beginning of PA research. In this narrative review, we present a focused discussion on PA's heterogeneity and variability based on the vast body of literature produced over 100+ years.

据我们所知，PA 在不同器官间的异质性和 PA 对特定器官的变异性还没有专门的综述。Bayliss（30）于 1902 年首次报道了血管运动张力对血压变化的反应性变化，这一事件标志着 PA 研究的开始。在这篇叙述性综述中，我们根据 100 多年来产生的大量文献，对 PA 的异质性和可变性进行了重点讨论。

PA 的研究方法

METHODS INVESTIGATING PA

PA can be quantified using different methods, including a linear regression slope between steady-state changes in pressure and flow (static autoregulation) (3, 22, 31), time-domain rate and latency of changes in blood flow in response to transient changes in pressure (dynamic autoregulation) (32, 33), and a frequency-domain transfer function analysis between transient changes in pressure and flow (dynamic autoregulation) (34, 35). The methods of dynamic autoregulation have been primarily used in the assessment of "cerebral" autoregulation; for the majority of noncerebral organs, PA is normally assessed by the method of "static" autoregulation. Therefore, for consistency and the availability of evidence, we base this review on static autoregulation. Furthermore, static autoregulation is more frequently referenced in clinical practice than dynamic autoregulation, perhaps because of its intuitiveness. The three key components in a typical pressure-flow plot of static autoregulation are the lower limit, the upper limit, and the plateau between these two limits.

量化 PA 有多种方法，包括压力和流量稳态变化之间的线性回归斜率（静态自动调节）（3，22，31）。响应压力瞬时变化的血流变化的时域速率和延迟（动态自动调节）（32，33），以及压力和血流瞬时变化之间的频域传递函数分析（动态自动调节）（34，35）。动态自动调节的方法主要用于评估 "脑" 的自动调节；对于大多数脑外器官，PA 通常是通过 "静态" 自动调节的方法来评估。因此，为了一致性和证据的可得性，我们以静态自动调节为基础进行综述。此外，在临床实践中，静态自动调节比动态自动调节更经常被提及，也许是因为它的直观性。静态自动调节的典型压力 - 流量图中的三个关键部分是下限、上限和这两个极限之间的平台。

不同器官间 PA 的异质性

HETEROGENEITY OF PA AMONG DIFFERENT ORGANS

We propose a three-point scale: robust, moderate, and weak, to categorize organs with different PA capacities. This scale is based on "static" autoregulation and assesses the following aspects: 1) the slope of the plateau, 2) the identifiability of the lower and upper limits, and 3) the reproducibility among different studies (Table 1). We validated this scale using comparative animal studies (Supplemental Table 1, Supplemental Digital Content 1, http://links.lww.com/CCM/E212 (opens new window)). In order to improve comparability, we tried to only include studies that used similar methodologies including the species of animal, type of anesthesia, organ preparation, BP intervention, and flow measurement. We chose to not use human studies because, in humans, the PA of most "noncerebral" organs has not been adequately studied. Based on this scale, the organs with robust PA are the brain, spinal cord, heart, and kidney. Skeletal muscle has moderate PA. Nearly all splanchnic organs including the stomach, small intestine, colon, liver, and pancreas possess weak PA (Fig. 2). Please note, that for the purposes of this review, we refer to muscle tissue as an organ.

我们提出了一个三分法：强壮的、适度的和弱的，对具有不同 PA 能力的器官进行分类。这个等级是基于 "静态" 自动调节，并评估了以下几个方面。1）平台的斜率，2）下限和上限的可识别性，以及 3）不同研究之间的可重复性（表 1）。我们使用比较动物研究来验证这个量表（补充表 1，补充数字内容 1，http://links.lww.com/CCM/E212 (opens new window)）。为了提高可比性，我们试图只包括采用类似方法的研究，包括动物种类、麻醉类型、器官准备、血压干预和流量测量。我们选择不使用人类研究，因为在人类中，大多数 "非脑" 器官的 PA 还没有得到充分的研究。根据这个标准，具有强大的 PA 的器官是大脑、脊髓、心脏和肾脏。骨骼肌有适度的 PA。几乎所有的内脏器官，包括胃、小肠、结肠、肝脏和胰腺都具有微弱的 PA（图 2）。请注意，在本评论中，我们把肌肉组织称为器官。

TABLE 1. The Three-Point Scale for the Categorization of Organs With Different Autoregulatory Capacities Based on Assessments of Static Autoregulation

Category	Definition
Robust	Flat plateau (zero to minimally sloped), prominent lower and upper limits, consistently reproducible
Moderate	Moderately sloped plateau, identifiable lower and upper limits, reproducible
Weak	Significantly sloped plateau, poorly identifiable lower and upper limits, inconsistently reproducible

表 1. 根据对静态自动调节的评估，对具有不同自动调节能力的器官进行分类的三点量表

分类	定义
强	平坦平台（零到最小的倾斜度），突出的下限和上限，持续的可重复性
中	适度倾斜的平台，可识别的下限和上限，可重复的
弱	显著倾斜的平台，难以识别的下限和上限，不一致的可重复性

Figure 2. Classification of organs with different autoregulatory capacities. The abscissa is organ perfusion pressure (PP) and the ordinate organ blood flow. The green bar indicates the PP range that is optimal for the perfusion of most organs.

图 2. 具有不同自动调节能力的器官的分类。横轴为器官灌注压（PP），纵轴为器官血流。绿色条表示大多数器官灌注的最佳 PP 范围。

PA 较强的器官

ORGANS WITH ROBUST PA

The brain (3, 20, 22, 31, 36), spinal cord (4, 37-45), heart (46-48), and kidney (6, 49-58) have robust PA, with conspicuous lower and upper limits, a flat or minimally sloped plateau, and reproducible autoregulatory plots by different studies.

大脑（3, 20, 22, 31, 36），脊髓（4, 37-45），心脏（46-48 ），和肾脏（6。49-58) 有强大的 PA，有明显的下限和上限，有平坦或最小倾斜的平台，以及不同研究的可重复的自动调节图。

脑血流的 PA

PA of Cerebral Blood Flow

In 1928, Forbes and Wolff (59) described the constriction of pial arteries in response to increases in BP, one of the earliest reports documenting a cerebral autoregulatory response. It was not until 1959, when Lassen (31) published the first BP-cerebral blood flow (CBF) plot based on data from 11 groups of patients reported in seven studies, that static cerebral autoregulation was formally introduced. Dynamic cerebral autoregulation was first reported by Aaslid et al (32) using transcranial Doppler sonography in 1989.

1928 年，Forbes 和 Wolff（59）描述了软脑膜动脉对血压升高的收缩反应，这是最早的记录脑血流自动调节反应的报告之一。直到 1959 年，Lassen（31）根据 7 项研究中 11 组患者的数据发表了第一份血压 - 脑血流（CBF）图，才正式提出静态脑血流自动调节。1989 年，Aaslid 等人（32）利用经颅多普勒超声检查首次报道了动态脑自主调节。

Cerebral autoregulation is not unchangeable. Its plateau, lower and upper limits can be affected by the following factors:

大脑血流自动调节不是不可改变的。它的平台、下限和上限会受到以下因素的影响。

1. Age: In extremely low birth weight infants, the lower limit of cerebral autoregulation is at a cerebral perfusion pressure of approximately 30 mm Hg (13), whereas in adults, the most-quoted lower limit is 60 mm Hg (but can be much higher) (22, 60). For children 3-10 years old, the cerebral autoregulation plateau resides at a CBF level of ~100 mL/min/100g (61); approximately twice the value observed in adults (~50 mL/min/100g) (62).

1）年龄：在极低出生体重的婴儿中，脑血流自动调节的下限是在脑灌注压约 30 mmHg 时（13），而在成人中，引用最多的下限是 60 mmHg （但可以更高）（22，60）。对 3-10 岁的儿童来说，脑血流自动调节平台维持在 CBF 约 100 mL/min/100g 的水平（61）；大约是成人观察值（约 50 mL/min/100g ）的两倍（62）。

2. Sex differences: In children, girls have greater cerebral autoregulation in the basilar artery, whereas boys have greater cerebral autoregulation in the middle cerebral artery (14). Elderly women have better dynamic cerebral autoregulation compared with elderly men (63).

2）性别差异。在儿童中，女孩在基底动脉有更强的脑血流自动调节，而男孩在大脑中动脉有更强的脑血流自动调节（14）。与老年男性相比，老年女性的动态脑血流自动调节更好（63）。

3. Diseases: In baboons with renovascular hypertension, the lower (64) and upper (65) limits of cerebral autoregulation shift rightward. Cerebral autoregulation is impaired in patients with long-term diabetes mellitus (3, 17, 18), ischemic stroke (66), traumatic brain injury (TBI) (67-69), aneurysmal subarachnoid hemorrhage (70-73), sepsis (74-76), out of hospital cardiac arrest (77, 78), acute bacterial meningitis (79), and fulminant hepatic failure (80).

3）疾病。在患有血管性高血压的狒狒中，大脑血流自动调节的下限（64）和上限（65）向右移动。大脑血流自动调节功能受损的有：长期糖尿病患者（3, 17, 18）、缺血性中风（66）、脑外伤（TBI）（67-69）、动脉瘤性蛛网膜下腔出血（70-73）、脓毒症（74-76）、院外心脏骤停（77, 78）、急性细菌性脑膜炎（79）和暴发性肝衰竭（80）。

4. Metabolic rate: Moderate hypothermia shifts the plateau of cerebral autoregulation downward and also reduces its slope in dogs undergoing cardiopulmonary bypass (81). In baboons, escalating doses of propofol lead to downward shifts of the plateau of cerebral autoregulation (25). Both changes are presumably related to reduced cerebral metabolic rates.

4. 代谢率。在接受体外循环的狗中，适度的低温使脑血流自动调节的平台向下移动，也降低了其斜率（81）。在狒狒身上，不断增加的异丙酚剂量导致脑血流自动调节的平台向下移动（25）。这两种变化都可能与脑代谢率降低有关。

5. Vasoactive drugs: In healthy and awake humans, CBF velocity follows changes in BP induced by nitroprusside or phenylephrine (82). One early study suggested a direct cerebral vasodilatory effect of nitroprusside (83), which, however, was refuted by multiple later studies (84, 85). Most vasopressors, including phenylephrine, do not exert direct cerebral vasoconstriction (86-88). Therefore, the impacts of vasoactive drugs on cerebral circulation are most likely "indirect" and primarily related to their effects on systemic BP. However, vasoactive drugs affect cardiac output (89), an effect that may confound PA research (20).

5. 血管活性药物。在健康和清醒的人类中，CBF 速度跟随硝普钠或苯肾上腺素引起的血压变化（82。一项早期研究认为硝普钠有直接的脑血管扩张作用（83），但被后来的多项研究驳斥（84, 85）。大多数升压药，包括苯肾上腺素，并不直接施加脑血管收缩（86-88）。因此，血管活性药物对脑循环的影响很可能是 "间接的"，主要与它们对全身血压的影响有关。然而，血管活性药物会影响心输出量（89），这种影响可能会混淆 PA 研究（20）。

6. Anesthesia: In humans, cerebral autoregulation is adversely affected by high doses of volatile anesthetics such as isoflurane (26, 33), desflurane (26), and sevoflurane (90), but not IV anesthetics such as propofol (26, 90). The minimal effect of propofol on cerebral autoregulation is corroborated by animal studies in pigs (91) and baboons (25). Among the volatile anesthetics, sevoflurane has the least adverse effect on cerebral autoregulation (28, 92).

6）麻醉：在人类中，大剂量的挥发性麻醉剂如异氟烷（26, 33）、地氟烷（26）和七氟烷（90）对大脑血流自动调节有不利影响，但静脉麻醉剂如丙泊酚（26, 90）对大脑血流自动调节没有影响。在猪（91）和狒狒（25）的动物研究中证实了丙泊酚对大脑血流自动调节的影响很小。在挥发性麻醉剂中，七氟醚对脑自主调节的不利影响最小（28, 92）。

7. Sympathetic tone: In lambs, increases in BP lead to increases in sympathetic nervous activity in the superior cervical ganglia (93). In baboons, sympathetic stimulation reduces CBF (94). Also in baboons, acute but not chronic cervical sympathectomy leads to a significant leftward shift of the lower limit of cerebral autoregulation (29). In humans, ganglion blockade alters dynamic cerebral autoregulation (95). This collective evidence corroborates that sympathetic tone is an important determinant of CBF (96, 97) and modulates cerebral autoregulation (20).

7）交感神经。在羔羊中，血压升高导致颈上神经节的交感神经活动增加（93）。在狒狒中，交感神经的刺激会降低 CBF（94）。同样在狒狒中，急性而非慢性颈交感神经切断术导致大脑血流自动调节的下限明显左移（29）。在人类中，神经节阻断会改变动态脑自主调节（95）。这些证据共同证实，交感神经张力是 CBF 的重要决定因素（96, 97），并能调节大脑血流自动调节（20）。

8. Hemoglobin and oxygen content: In human subjects, both arterial blood hemoglobin concentration (98, 99) and oxygen content (100, 101) affect CBF, implying that the plateau of cerebral autoregulation can be repositioned by changes in these factors. In dogs, the plateau of cerebral autoregulation is shifted upward and becomes more sloped by hemodilution (21).

8）血红蛋白和氧含量。在人类受试者中，动脉血血红蛋白浓度（98, 99）和氧含量（100, 101）都影响 CBF，这意味着脑自主调节的平台可以通过这些因素的变化而重新定位。在狗身上，脑血流自动调节的平台向上移动，并通过血液稀释变得更加倾斜（21）。

9. CO₂: The plateau of cerebral autoregulation is gradually shifted upward and shortened by increasing hypercapnia (22). Cerebral autoregulation is abolished when the carbon dioxide tension is 60 mm Hg or greater (102). In contrast, hypocapnia leads to a downward shift of the plateau, although its impact on the width of plateau is unclear (22).

9）二氧化碳。高碳酸血症使得大脑血流自动调节的平台逐渐上移，并因高碳酸血症的增加而缩短（22）。当二氧化碳分压为 60 mmHg 或更高时，大脑血流自动调节功能失效（102）。相反，低碳酸血症会导致平台的下移，尽管它对平台宽度的影响还不清楚（22）。

脊髓血流的 PA

PA of Spinal Cord Blood Flow

In 1951, Field et al (103) first reported that spinal cord blood flow is largely independent of BP changes in fresh rabbit preparations. The robust PA of spinal cord blood flow was formally and independently reported by Kindt (38) in 1971 in monkeys and Griffiths (4) in 1973 in dogs and has been substantiated thereafter by multiple studies (37, 39-45).

1951 年，Field 等人（103）首次报道，在新鲜兔子的制备中，脊髓血流在很大程度上与血压变化无关。1971 年 Kindt（38）在猴子身上正式独立报告了脊髓血流的强大 PA，1973 年 Griffiths（4）在狗身上正式独立报告了脊髓血流的强大 PA，此后的多项研究（37, 39-45）证实了这一点。

Spinal cord autoregulation is severely impaired or absent under conditions of hypoxia or hypercapnia in dogs (4, 37). In rats, the lower limit is shifted rightward after mild spinal cord injury (104) and lost after severe injury (104-106). In contrast, spinal cord autoregulation remains intact after high cervical spinal cord complete section (C1-2) in monkeys (39).

在狗的缺氧或高碳酸血症条件下，脊髓自动调节功能严重受损或消失（4，37）。在大鼠中，轻度脊髓损伤后，下限向右偏移（104），严重损伤后则消失（104-106）。相反，猴子高位颈脊髓完全断裂（C1-2）后，脊髓自动调节功能仍保持完整（39）。

Although propofol can reduce spinal cord blood flow by up to 20%, it does not adversely affect rat spinal cord autoregulation (107). Alpha-adrenergic blockade (108), but not beta-adrenergic blockade (109), can adversely affect spinal cord autoregulation in monkeys.

虽然丙泊酚可使脊髓血流减少达 20%，但它不会对大鼠脊髓自动调节功能产生不利影响（107）。α- 肾上腺素能阻断（108），而非 β- 肾上腺素能阻断（109），可以对猴子的脊髓自动调节功能产生不利影响。

冠状动脉血流的 PA

PA of Coronary Blood Flow

In 1959, Berne (47) illustrated for the first time the PA of coronary blood flow using an in situ canine heart model. Although the vigorous PA of the coronary circulation has been substantiated by different studies (46, 48), there have also been numerous reports demonstrating the variability of coronary autoregulation (110-117).

1959 年，Berne (47) 利用原位犬心脏模型首次说明了冠状动脉血流的 PA。尽管不同的研究都证实了冠状动脉循环的强劲 PA（46, 48），但也有许多报告证明了冠状动脉自动调节的变异性（110-117）。

One study showed that right coronary autoregulation is significantly less potent than left coronary autoregulation in dogs (118). However, another study in dogs showed that right coronary autoregulation is more potent than left coronary autoregulation (119). Although the cause of this discrepancy remains to be determined, it does highlight the asymmetry between right and left coronary autoregulation.

一项研究表明，狗的右冠状动脉自动调节的效力明显低于左冠状动脉自动调节（118）。然而，另一项对狗的研究表明，右冠状动脉自动调节比左冠状动脉自动调节更有效（119）。虽然这种差异的原因尚待确定，但它确实突出了左右冠状动脉自动调节的不对称性。

Even for territories perfused by the same coronary artery, different regions may have different autoregulatory potency. In a swine model, it was found that the lower limits of autoregulation in the right ventricle, a portion of the interventricular septum, and right atrium were 20-30 mm Hg, 40 mm Hg, and not recognizable, respectively, despite the fact that these regions are all perfused by the right coronary artery (120).

即使是由同一冠状动脉灌注的区域，不同区域也可能有不同的自动调节能力。在猪的模型中，发现右心室、部分室间隔和右心房的自动调节下限分别为 20-30mmHg、40mmHg 和无法识别，尽管这些区域都是由右冠状动脉灌注的（120）。

PA is not homogeneous across the left ventricular wall. The plateau is higher, and the lower limit more rightward, in the subendocardium than in the subepicardium in dogs (110, 115, 121-123). In contrast, PA is homogeneous across the right ventricular wall at perfusion pressures less than 100 mm Hg, and only becomes more potent in the subepicardium than in the subendocardium at perfusion pressures greater than 100 mm Hg in dogs (124).

整个左心室壁的 PA 并不均匀。与心外膜相比，狗的心内膜下的平台更高，下限更向右（110, 115, 121-123）。相反，当灌注压力小于 100 mmHg 时，右心室壁上的 PA 是均匀的，只有当灌注压力大于 100 mmHg 时，心外膜下的 PA 才会比心内膜下的 PA 更强（124）。

Chronic hypertension with left ventricular hypertrophy is associated with a profound impairment in the lower pressure range (40-75 mm Hg) of autoregulation in the subendocardium of dogs (15). Renovascular hypertension with left ventricular hypertrophy shifts both the lower and upper limits of coronary autoregulation rightward in dogs (5). In patients, hypertension complicated by left ventricular hypertrophy leads to an upward shift of the plateau and a rightward shift of the lower limit of coronary autoregulation (125).

慢性高血压伴左心室肥厚与狗心内膜下的低压范围（40-75mmHg）的自动调节功能严重受损有关（15）。肾血管性高血压伴左心室肥厚使狗的冠状动脉自动调节的下限和上限都向右移动（5）。在患者中，高血压并发左心室肥厚导致平台上移，冠状动脉自动调节下限右移（125）。

Myocardial metabolic rate affects coronary autoregulation. In dogs, increased myocardial oxygen demand, induced via dobutamine, shifts the lower limit rightward, the upper limit leftward, and the plateau upward (and shortened); in contrast, decreased myocardial oxygen demand, induced via propranolol, shifts the lower limit leftward, the upper limit rightward, and the plateau downward (and widened) (5). A two-fold increase in heart rate causes a rightward shift of the lower limit of canine subendocardial autoregulation (126). Exercise leads to an upward shift of the plateau and a rightward shift of the lower limit, with a greater impact in the subendocardium than in the subepicardium (110).

心肌代谢率会影响冠状动脉自动调节功能。在狗身上，通过多巴胺诱导的心肌需氧量增加，下限向右移，上限向左移，平台向上（并缩短）；相反，通过普萘洛尔诱导的心肌需氧量减少，下限向左移，上限向右移，平台向下（并扩大）（5）。心率增加 2 倍会使犬心内膜下自动调节的下限向右移动（126）。运动会导致平台的上移和下限的右移，对心内膜下的影响大于心外膜下的影响（110）。

Barbiturates affect canine subendocardial autoregulation, leading to a rightward shift of the lower limit (113, 127) and a more sloped plateau (113). Enflurane, halothane, and isoflurane at one minimum alveolar concentration mildly disrupt canine coronary autoregulation, leading to increased coronary blood flow out of proportion to myocardial demand (128).

巴比妥类药物影响犬心内膜下的自动调节，导致下限右移（113, 127）和更倾斜的平台（113）。安氟醚、氟烷和异氟醚在一个最低肺泡浓度下会轻度破坏犬的冠状动脉自动调节功能，导致冠状动脉血流增加，与心肌需求不成比例（128）。

肾血流的 PA

PA of Renal Blood Flow

In 1902, Bayliss (30) reported changes in kidney volume, as a surrogate for changes in renal blood flow, in response to changes in BP in dogs. The robust renal autoregulation was formally reported by Waugh and Shanks (50) in 1960 using isolated canine kidneys and has been substantiated thereafter by a large body of evidence and critical reviews (6, 49, 51-58).

1902 年，Bayliss（30）报告了肾脏体积的变化，作为肾脏血流变化的替代物，对狗血压变化的反应。1960 年，Waugh 和 Shanks (50) 使用分离的犬肾正式报告了强大的肾脏自动调节功能，此后大量的证据和评论证实了这一点（6, 49, 51-58）。

Various diseases affect renal autoregulation. Hypertension leads to a rightward shift of the lower limit in rats (129-131). Poorly controlled diabetes affects rat renal autoregulation (132-135), shifting the lower limit leftward (136, 137). Renal autoregulation is defective in patients with long-standing insulin-dependent diabetes complicated by diabetic nephropathy (138). In contrast, renal autoregulation remains normal in normotensive patients with newly diagnosed noninsulin-dependent diabetes mellitus (139).

各种疾病都会影响肾脏的自动调节功能。高血压会导致大鼠的下限右移（129-131）。糖尿病控制不佳会影响大鼠的肾脏自动调节功能（132-135），使下限向左移动（136, 137）。长期胰岛素依赖型糖尿病并发糖尿病肾病的患者，其肾脏自动调节功能有缺陷（138）。相反，新诊断的非胰岛素依赖型糖尿病的正常血压患者的肾脏自动调节功能保持正常（139）。

Nifedipine impairs renal autoregulation in animals (130, 140). Isradipine impairs the autoregulation of glomerular filtration rate in hypertensive patients with type 2 diabetes (141). In dogs, papaverine but not bradykinin leads to a dramatic rightward shift of the lower limit of renal autoregulation, although both drugs are able to shift the plateau upward (142).

硝苯地平会损害动物的肾脏自动调节功能（130, 140）。伊拉地平会损害 2 型糖尿病高血压患者的肾小球滤过率的自动调节（141）。在狗身上，罂粟碱而非缓激肽会导致肾脏自动调节的下限急剧右移，尽管两种药物都能使平台向上移动（142）。

Renal autoregulation was impaired during halothane-induced (via escalating halothane concentration from 0.9% to 1.76%), but not nitroprusside-induced, hypotension in halothane-anesthetized dogs (143). In contrast, renal autoregulation remained intact during gravity-induced changes in BP in dogs anesthetized with 0.9% halothane (144). This seemingly conflicting evidence suggests that deep, but not light, halothane anesthesia impairs renal autoregulation.

在氟烷引起的（通过将氟烷浓度从 0.9% 升级到 1.76%），而非硝普钠引起的氟烷麻醉狗的低血压期间，肾脏自动调节功能受损（143）。相反，在用 0.9% 氟烷麻醉的狗的重力诱导的血压变化期间，肾脏自动调节功能保持不变（144）。这种看似矛盾的证据表明，氟烷深麻醉，而非氟烷浅麻醉会损害肾脏的自动调节功能。

PA 程度中等或较弱的器官

ORGANS WITH MODERATE OR WEAK PA

In 1902, Bayliss (30) reported the use of volumetric changes in the hindlimbs of dogs and cats as surrogates of changes in blood flow. The blood flow in hindlimbs was later directly measured (145-148). In 1961, Stainsby and Renkin (7) first described skeletal muscle autoregulation using isolated canine preparations. The overall evidence suggests that skeletal muscle has moderate PA capacity (7, 19), with identifiable lower and upper limits; but with an autoregulatory plateau that is much more sloped compared with the brain, heart, or kidney. Skeletal muscle autoregulation is defective in patients with long-standing insulin-dependent diabetes with nephropathy and retinopathy (149, 150), and may also be defective in patients with septic shock based on near-infrared spectroscopy measurements (151).

1902 年，Bayliss（30）报道了用狗和猫的后肢的体积变化作为血流变化的替代指标。后来，后肢的血流量被直接测量（145-148）。1961 年，Stainsby 和 Renkin（7）首次使用分离的犬类制备模型描述了骨骼肌的自动调节功能。总体证据表明，骨骼肌具有适度的 PA 能力（7, 19），有可识别的下限和上限；但与大脑、心脏或肾脏相比，其自动调节平台的坡度更大。长期胰岛素依赖型糖尿病伴肾病和视网膜病变患者的骨骼肌自动调节功能有缺陷（149, 150），根据近红外光谱测量，脓毒性休克患者的骨骼肌自动调节功能也可能有缺陷（151）。

It was Bayliss (30) again who pioneered the research of visceral organs' autoregulation 100+ years ago. The collective evidence shows that the blood flow of visceral organs including the stomach (8, 152-155), small intestine (12, 156-160), colon (11, 161, 162), liver (163), and pancreas (10) is weakly autoregulated, with the lower and upper limits poorly identifiable, the plateau remarkably sloped, and the pressure-flow plots varying across different studies. Various factors affect visceral organs' autoregulation. In dogs, the lower limit is poorly identifiable in innervated stomach. However, after denervation, it becomes identifiable, and the regression slope becomes smaller, suggesting improved autoregulation (154). Gastric autoregulation can be consistently demonstrated in dogs when the oxygen uptake by the stomach is greater than 4.0 mL/min/100g, but not less (155). Histamine enhances gastric autoregulation (155). Intestinal autoregulation is more potent in fed than in fasted dogs, suggesting a close link between the intestinal metabolic rate and autoregulatory potency (164).

100 多年前，又是贝利斯（30）率先研究了内脏器官的自动调节功能。证据共同显示，内脏器官的血流包括胃（8, 152-155）、小肠（12, 156-160）、结肠（11, 161, 162 ）、肝脏（163）和胰腺（10）的自动调节较弱，下限和上限不好确定，平台明显倾斜，不同研究的压力 - 流量图也不同。各种因素影响内脏器官的自动调节。在狗身上，神经支配的胃的下限很难辨认。然而，在去神经支配后，它变得可识别，而且回归斜率变小，表明自动调节得到改善（154）。当胃的摄氧量大于而非小于 4.0 mL/min/100g，可以持续证明狗的胃自动调节（155）。组胺会增强胃的自动调节功能（155）。肠道自动调节在喂养的狗中比在禁食的狗中更有效，表明肠道代谢率和自动调节效力之间有密切联系（164）。

个体间与个体自身 PA 的变异性

INTERINDIVIDUAL VERSUS INTRAINDIVIDUAL VARIABILITY IN PA

Interindividual variability refers to the difference in a specific organ's PA among different individuals within a population (165, 166). For example, the difference in the lower limit of cerebral autoregulation can be as large as 60 mm Hg (from 53 to 113 mm Hg, mean = 79 mm Hg) in healthy volunteers (167). This implies that an individual patient's autoregulation can be easily underestimated or overestimated when using the population mean in clinical decision-making (22, 165). In contrast, intraindividual variability refers to the variation in PA for an individual patient. Factors that can lead to PA's interindividual or intraindividual variabilities are summarized in Figure 3.

个体间变异性是指一个群体中不同个体之间特定器官的 PA 的差异（165, 166）。例如，在健康志愿者中，大脑血流自动调节的下限差异可高达 60 mmHg （从 53 到 113 mmHg ，平均 = 79 mmHg ）（167）。这意味着在临床决策中使用群体平均值时，个体患者的自动调节功能容易被低估或高估（22, 165）。相比之下，个体自身变异性是指单个病人的 PA 变化。可导致 PA 的个体间或个体自身变异的因素在图 3 中进行了总结。

Figure 3. Clinical implications related to pressure autoregulation’s variability. The abscissa is organ perfusion pressure and the ordinate organ blood flow. The implications related to the left and right shifts of the lower (blue fonts) and upper (red fonts) limits are explained. A sloped or shortened plateau is associated with a poor tolerance of perfusion pressure fluctuations. The factors related to pressure autoregulation’s variability are summarized on the top.

图 3. 与压力自动调节变异性有关的临床意义。横轴为器官灌注压，纵轴为器官血流。解释了与下限（蓝色字体）和上限（红色字体）的左移和右移有关的含义。倾斜或缩短的平台与对灌注压波动的耐受性差有关。与压力自动调节的变异性有关的因素在上面进行了总结。

BP 的稳定性、病人预后和动态自动调节

BP LABILITY, PATIENT OUTCOME, AND DYNAMIC AUTOREGULATION

An exceedingly volatile BP may give rise to abrupt changes in organ blood flow that may be detrimental. Some studies have examined the association between intraoperative BP lability or fluctuation and postoperative outcomes. Two studies performed by the same research group showed that the BP lability during cardiac surgery is associated with postoperative 30-day mortality (168, 169). A different study found that increased BP lability, rather than absolute or relative hypotension, is predictive of postoperative delirium after major noncardiac surgeries (170). In contrast, a study performed in noncardiac surgical patients showed that lower ("rather than higher") intraoperative BP lability is weakly associated with a higher 30-day mortality (171). This finding is corroborated by a separate study that also found an association between decreased BP lability and increased 30-day mortality in noncardiac surgical patients (172). The contradictory findings among these studies remain to be reconciled and may be in part attributable to the different methods used by different studies for BP lability calculation (i.e., BP value dependent (168, 169) vs independent (171) approaches). Therefore, the relation between BP lability and patient outcome remains to be elucidated. The dynamic response, that is, the speed and strength of the response, of the vasomotor tone to a rapid change in BP is typically investigated using the method of dynamic autoregulation. Similar to static autoregulation, there may exist heterogeneity among different organs and variability for specific organs in dynamic autoregulation. How the heterogeneity and variability of dynamic autoregulation, in the face of an exceedingly labile BP, are associated with patient outcomes and the details of these speculated traits of dynamic autoregulation remain to be elucidated.

过度波动的血压可能引起器官血流的突然变化，可能是有害的。一些研究考察了术中血压不稳定或波动与术后结果之间的关系。由同一研究小组进行的两项研究显示，心脏手术期间的血压不稳定与术后 30 天的死亡率有关（168, 169）。一项不同的研究发现，血压不稳定性的增加，而不是绝对或相对低血压，是重大非心脏手术后谵妄的预测因素（170）。相反，在非心脏手术患者中进行的一项研究表明，较低（"而不是较高"）的术中血压稳定性与较高的 30 天死亡率有微弱的关系（171）。另一项研究也证实了这一发现，该研究还发现非心脏手术患者的血压稳定性降低与 30 天死亡率增加有关（172）。这些研究中的矛盾结果仍有待调和，部分原因可能是不同研究在计算血压稳定性时采用的方法不同（即血压值依赖（168, 169）与独立（171）方法）。因此，血压稳定性与患者结果之间的关系仍有待阐明。通常使用动态自动调节的方法研究血管运动张力对血压快速变化的动态反应，即反应的速度和强度。与静态自动调节类似，在动态自动调节中，不同器官之间可能存在异质性，特定器官也存在变异性。在血压极不稳定的情况下，动态自动调节的异质性和变异性如何与病人的预后相关，以及动态自动调节的这些推测特征的细节还有待阐明。

100 多年来的经验教训

LESSONS LEARNED OVER 100+ YEARS

The heterogeneity of PA among different organs implies that, for the same change in BP (from BP-1 to BP-2), the changes in blood flow in different organs are different or organ-dependent assuming that BP is the only flow-relevant factor that has changed (Fig. 2). It can be inferred from the preceding discussion that organs that are functionally essential, vulnerable to suboptimal perfusion, and have poor regenerative or self-repair potential, such as the brain, spinal cord, heart, and kidney, are equipped with more robust PA than other organs. The origin of PA's heterogeneity remains elusive. It could have been the result of Darwinian's "survival of the fittest" principle and relates to the distinctive aspects of the mechanisms responsible for achieving and regulating PA in different organs (2). A future-focused review on this topic is warranted.

不同器官间 PA 的异质性意味着，对于相同的 BP 变化（从 BP-1 到 BP-2），假设 BP 是唯一发生变化的流量相关因素，不同器官的血流变化是不同的或器官依赖的（图 2）。从前面的讨论中可以推断出，那些功能重要、易受到灌注不良影响、再生或自我修复潜力差的器官，如大脑、脊髓、心脏和肾脏，比其他器官具备更强大的 PA。PA 的异质性的起源仍然难以捉摸。它可能是达尔文的 "适者生存" 原则的结果，与负责完成和调节不同器官的 PA 的机制的独特面有关（2）。未来需要对这一主题进行重点综述。

Although heterogeneous, there may be an internal link among different organs' PA, which can be inferred from studies showing a close relationship between "cerebral" autoregulation and "noncerebral" outcomes such as acute kidney injury (173) and mortality (174-180). At this time, the brain is the only organ whose PA can be assessed at the bedside based on advanced software solutions (181, 182). It is interesting to consider whether or not the brain might be an index organ, such that management guided by cerebral autoregulation monitoring would improve both "cerebral" and "noncerebral" outcomes. This is inadequately studied. Alternately, the impact on outcomes from clinical care guided by the PA monitoring of a noncerebral organ with a weak or moderate autoregulatory capacity remains to be determined.

虽然是异质性的，但不同器官的 PA 之间可能存在着内在联系，这可以从研究中推断出，"脑" 自动调节与 "其他器官" 的预后如急性肾损伤（173）和死亡率（174-180）之间有密切关系。目前，大脑是唯一可以在床边根据先进的软件解决方案评估 PA 的器官（181, 182）。值得考虑的是，大脑是否可能是一个指数器官，这样由大脑血流自动调节监测指导的管理将改善 "脑" 和 "其他器官" 的预后。这方面的研究还不够充分。另外，由自动调节能力较弱或中等的脑以外的其他器官的 PA 监测指导的临床救治对预后的影响也有待确定。

Variability refers to the changeability of the PA of any organ by patient age, sex, deranged physiology, acute conditions, or chronic diseases (Fig. 3). A wider and less-sloped plateau indicates a better autoregulatory range and potency; otherwise, a poor tolerance of perfusion pressure fluctuations in an organ. A leftward-shifted lower limit and a rightward-shifted upper limit indicate improved tolerance of hypotension and hypertension, respectively. In contrast, a rightward-shifted lower limit and a leftward-shifted upper limit indicate worsening tolerance of hypotension and hypertension, respectively (Table 2). PA can be improved in certain conditions (5, 29, 81, 154, 185); however, in most scenarios, variability results in worsening.

变异性是指任何器官的 PA 因患者年龄、性别、生理机能紊乱、急性病症或慢性疾病而发生变化（图 3）。较宽且斜度较小的平台表明有较好的自动调节范围和效力；否则，对一个器官的灌注压波动的耐受性较差。下限向左偏移和上限向右偏移分别表示对低血压和高血压的耐受性提高。相反，下限向右偏移和上限向左偏移分别表示对低血压和高血压的耐受性恶化（表 2）。在某些情况下，PA 可以得到改善（5, 29, 81, 154, 185）；然而，在大多数情况下，变异性导致恶化。

TABLE 2. Etiology, Mechanism, and Implications of Various Changes in Autoregulation

Component	Direction of Change	Etiology and Mechanism	Implications
Lower limit	Leftward shift	Acute sympathectomy (29), diabetes (136, 137)	Better tolerance of hypotension
	Rightward shift	Hypertension (5, 64, 125, 129), hypertrophy (5, 125), hypercapnia (102), volatile anesthesia (183)	Worse tolerance of hypotension
Upper limit	Leftward shift	Hypercapnia (102), volatile anesthesia (183)	Worse tolerance of hypertension
	Rightward shift	Hypertension (5, 65), hypertrophy (5)	Better tolerance of hypertension
Plateau	Upward shift	Increased metabolic activity (5, 19), myocardial hypertrophy (5, 125), hypercapnia (22), increased cardiac output (20), hemodilution (21), volatile anesthesia (26, 90, 183)	Increased requirement of organ perfusion
	Downward shift	Decreased metabolic activity (5), hypocapnia (22), decreased cardiac output (20), propofol anesthesia (25), hypothermia (81)	Decreased requirement of organ perfusion
	Steeper	Vasodilation (82, 184), volatile anesthesia (26, 33, 90, 183), hemodilution (21), diabetes mellitus (3, 17, 18), ischemic stroke (66), traumatic brain injury (67), aneurysmal subarachnoid hemorrhage (70–73), sepsis (74–76), out of hospital cardiac arrest (77, 78), acute bacterial meningitis (79), fulminant hepatic failure (80)	Worsening autoregulatory potency
	Narrowed	Increased metabolic activity (5), hypercapnia (22, 102), volatile anesthesia (183)	Shortened autoregulatory range

表 2. 自动调节的各种变化的病因、机制和影响

部位	变化方向	病因和机制	意义
下限	左移	急性交感神经切除 (29), 糖尿病 (136, 137)	低血压耐受性更好
	右移	高血压 (5, 64, 125, 129), 心肌肥厚 (5, 125), 高碳酸血症 (102), 吸入麻醉 (183)	低血压耐受性变差
上限	左移	高碳酸血症 (102), 吸入麻醉 (183)	高血压耐受性变差
	右移	高血压 (5, 65), 心肌肥厚 (5)	高血压耐受性更好
平台	上移	代谢活动增强 (5, 19), 心肌肥厚 (5, 125), 高碳酸血症 (22), 心输出量增加 (20), 血液稀释 (21), 吸入麻醉 (26, 90, 183)	组织灌注需求增加
	下移	代谢活动降低 (5), 低碳酸血症 (22), 心输出量下降 (20), 丙泊酚麻醉 (25), 低温 (81)	组织灌注需求降低
	变陡	扩血管 (82, 184), 吸入麻醉 (26, 33, 90, 183), 血液稀释 (21), 糖尿病 (3, 17, 18), 缺血性卒中 (66), 脑外伤 (67), 蛛网膜下腔出血 (70–73), 脓毒症 (74–76), 院外心跳骤停 (77, 78), 急性细菌性脑膜炎 (79), 爆发性肝衰竭 (80)	自动调节强度变差
	变窄	代谢活动增加 (5), 高碳酸血症 (22, 102), 吸入麻醉 (183)	自动调节范围变窄

The clinical relevance of PA's variability is corroborated by the abundant evidence showing a close relationship between impaired "cerebral" autoregulation and unfavorable outcomes in patients with TBI (174-180, 186-200), intracranial hemorrhage (72, 73, 201-212), or having major surgeries (173, 213-220). The available evidence is primarily based on observational single-cohort studies associating cerebral autoregulation with outcomes (Supplemental Table 2, Supplemental Digital Content 2, http://links.lww.com/CCM/E213 (opens new window)). Randomized controlled trials investigating the clinical care guided by the monitoring of cerebral PA (and perhaps the PA of noncerebral organs) are urgently needed. Currently, a prospective trial evaluating the feasibility of targeting optimal cerebral perfusion pressure in patients with severe TBI is ongoing (the CPPOpt Guided Therapy: Assessment of Target Effectiveness [COGiTATE] study at http://cppopt.org/research-projects-cogitate/ (opens new window)). Optimal perfusion pressure corresponds to the most robust PA of an organ (Fig. 4). Whether the strategy of maintaining an optimal perfusion pressure is feasible, generates beneficial outcomes, and is applicable to noncerebral organs remains to be elucidated.

大量的证据证实了 PA 的变异性的临床意义，这些证据显示 "大脑" 自动调节功能受损与创伤性休克患者的不良预后之间存在密切关系（174-180, 186-200)、颅内出血 (72, 73, 201-212) 或有重大手术 (173, 213-220) 的患者，其 "脑" 的自动调节功能受损与不良预后有密切关系。现有的证据主要是基于观察性的单队研究，将大脑血流自动调节与预后联系起来（补充表 2，补充数字内容 2，http://links.lww.com/CCM/E213 (opens new window)）。迫切需要进行随机对照试验，调查由监测脑 PA（也许还有非脑器官的 PA）指导的临床救治。目前，一项评估严重创伤性疾病患者最佳脑灌注压目标可行性的前瞻性试验正在进行（CPPOpt Guided Therapy: Assessment of Target Effectiveness [COGiTATE] 研究，见 http://cppopt.org/research-projects-cogitate/ (opens new window))。最佳灌注压力对应于一个器官最强的 PA（图 4）。保持最佳灌注压力的策略是否可行，是否能产生有益的结果，以及是否适用于脑以外的其他器官，还有待阐明。

Figure 4. Autoregulatory changes in vasomotor tone and the optimal perfusion pressure (PP). The abscissa is organ PP and the ordinate organ blood flow. Pressure autoregulation (PA) maintains a relatively stable organ blood flow (dark green curve) via vasodilation and vasoconstriction (dark red rings) when the PP is decreased and increased, respectively. An increasingly decreased PP gradually exhausts vasodilatory reserve until maximal vasodilation is reached (blue fonts and arrow). An increasingly increased PP gradually exhausts vasoconstrictive reserve until maximal vasoconstriction is reached (red fonts and arrow). Extreme hypertension frequently disrupts vasculature irreversibly (232). The balanced vasodilatory and vasoconstrictive reserve is accomplished somewhere in the middle (green bar). Different autoregulation indexes have been proposed to assess the strength of pressure reactivity or autoregulatory capacity (dashed black curve and axis) (233). Different organ PPs correspond to different values of predetermined autoregulation index. A U-shaped or V-shaped curve is normally formulated when plotting autoregulation index against PP, with the best PA performance located at the bottom of the curve and corresponding to the optimal PP (182, 191). In theory, the optimal PP defined by the autoregulation index-PP plot, and the PP that corresponds to the balanced vasodilatory and vasoconstrictive reserve, overlap or are in close proximity to each other.

图 4. 血管运动张力的自动调节变化和最佳灌注压（PP）。横轴是器官 PP，纵轴是器官血流。当 PP 降低和增加时，压力自动调节（PA）通过血管扩张和血管收缩（暗红色环）分别维持相对稳定的器官血流（深绿色曲线）。越来越小的 PP 会逐渐耗尽血管舒张储备，直到达到最大的血管舒张（红色字体和箭头）。越来越大的 PP 逐渐耗尽血管收缩储备，直到达到最大的血管收缩（蓝色字体和箭头）。极端高血压经常不可逆地破坏血管（232）。平衡的血管舒张和血管收缩储备是在中间某处完成的（绿色条）。人们提出了不同的自动调节指数来评估压力反应性或自动调节能力的强度（黑色虚线曲线和轴）（233）。不同的器官 PP 对应于不同的预定自动调节指数值。在绘制自动调节指数与 PP 的关系图时，通常会形成 U 型或 V 型曲线，最佳的 PA 性能位于曲线的底部，对应于最佳 PP（182, 191）。理论上，由自动调节指数 - PP 图定义的最佳 PP 和对应于平衡的血管舒张和血管收缩储备的 PP 是重叠的，或相互接近的。

It must be remembered that the blood flow of any organ is jointly regulated by multiple physiologic processes and patient/disease factors (20, 97, 221). The vasomotor tone is the post integration result of the effects exerted by these various processes and factors, which in turn determine the vascular reactivity to a specific modulator of organ blood flow (Fig. 5). The vascular reactivity (i.e., vasodilation or vasoconstriction initiated by a specific modulator) can be impaired by baseline vasodilation or vasoconstriction due to other modulators that result in exhaustion of the vasodilatory or vasoconstrictive reserve. It should be emphasized that PA is just one of the mechanisms modulating organ blood flow although, as being discussed in this review, its functional status is affected by various nonpressure processes and factors. For example, extreme hypercapnia abolishes cerebral autoregulation likely secondary to overzealous hypercapnia-related cerebral vasodilation (22, 36). Therefore, the integrative nature of organ blood flow regulation is probably responsible for most variations in PA.

必须记住，任何器官的血流都是由多种生理过程和病人 / 疾病因素共同调节的（20，97，221）。血管运动张力是这些不同过程和因素作用的整合结果，而这些因素又决定了血管对器官血流的特定调节器的反应性（图 5）。血管反应性（即由特定调节剂启动的血管扩张或血管收缩）可因其他调节剂引起的基线血管扩张或血管收缩而受损，导致血管扩张或血管收缩储备耗尽。应该强调的是，PA 只是调节器官血流的机制之一，尽管正如本评论所讨论的那样，其功能状态受到各种非压力过程和因素的影响。例如，极端的高碳酸血症消除了大脑的自动调节，可能是继发于过度的高碳酸血症相关的脑血管扩张（22，36）。因此，器官血流调节的综合性质可能是造成 PA 大多数变化的原因。

Figure 5. Regulation of cerebral blood flow (CBF) to illustrate the multifactorial and integrated nature of vascular modulation. The baseline vasomotor tone is the post integration result of the effects exerted by different modulators (20) and is one of the determinants of the cerebrovascular reactivity (i.e., vasodilation or vasoconstriction initiated by a specific modulator). Overzealous baseline vasodilation or vasoconstriction weakens cerebrovascular reactivity secondary to the exhaustion of the vasodilatory or vasoconstrictive reserve, for example, the vasculature cannot further dilate when it has been exceedingly dilated, and vice versa.

Hb = hemoglobin, SpO₂ = pulse oxygen saturation.

图 5. 脑血流（CBF）的调节，说明了血管调节的多因素和综合性质。基线血管运动张力是不同调节剂（20）作用的整合后的结果，是脑血管反应性的决定因素之一（即由特定调节剂启动的血管扩张或血管收缩）。过度的基线血管扩张或血管收缩会继发性削弱脑血管反应性，因为血管扩张或血管收缩储备已经耗尽，例如，当血管已经过度扩张时，就不能进一步扩张，反之亦然。

Hb = 血红蛋白，SpO₂ = 脉搏氧饱和度。

Hemodynamics can be considered as a ladder consisting of multiple yet interrelated steps, such as cardiac output, BP, and ultimately tissue perfusion (222). Organ perfusion is determined not only by BP via PA but also by distribution of cardiac output among different organs. Each organ's blood flow is a proportion of cardiac output (20, 223). As a result, reduced cardiac output leads to decreases of each organ's blood flow, with the magnitude of the decrease determined by how the reduced cardiac output is redistributed among different organs (224-226). The redistribution normally favors vital organs such as the brain (227). As a result of changes in organ blood flow secondary to changes in cardiac output, the PA of all organs including the brain is reshaped accordingly (20). The integrated regulation of organ blood flow by BP and cardiac output is clinically relevant and deserves more research.

血液动力学可被视为一个阶梯，由多个相互关联的步骤组成，如心输出量、血压和最终的组织灌注（222）。器官灌注不仅由血压通过 PA 决定，还由心输出量在不同器官间的分布决定。每个器官的血流量是心输出量的一个比例（20，223）。因此，心输出量的减少会导致每个器官血流的减少，而减少的程度取决于心输出量的减少如何在不同的器官间重新分配（224-226）。这种重新分配通常有利于重要的器官，如大脑（227）。由于继发于心输出量变化的器官血流变化，包括大脑在内的所有器官的 PA 都相应地被重塑（20）。血压和心输出量对器官血流的综合调节具有临床意义，值得进一步研究。

The collective evidence suggests that PA is a valid mechanism modulating the relationship between organ perfusion pressure and blood flow. Otherwise, after all, organ blood flow would be pressure passive with great risk of injury related to unstable perfusion. However, the traditional concept of cerebral static autoregulation has been questioned (221). The plateau may be sloped instead of flat (82, 228, 229). The width of the plateau may be overestimated (230, 231). These considerations could merely represent PA's variability.

集体证据表明，PA 是调节器官灌注压和血流之间关系的有效机制。否则，器官血流就随压力波动，不稳定的灌注导致损伤的风险很大。然而，传统的脑部静态自动调节的概念受到了质疑（221）。平台可能是倾斜的，而不是平坦的（82，228，229）。平台的宽度可能被高估了（230，231）。这些关注点可能只是代表了 PA 的变异性。

In summary, the relationship between organ perfusion pressure and blood flow is modulated by PA. Organ blood flow is jointly regulated by multiple physiologic processes and patient or disease factors, including PA. The pressure autoregulatory capacity is heterogeneous among different organs and varies in specific organs depending on nonpressure processes and factors. The knowledge of PA's heterogeneity and variability is instructive in clinical care because mismanaged BP, especially in the presence of an impaired PA in an individual patient, renders an organ at risk of ischemia or hyperperfusion-related injury. However, the value of PA monitoring and the organ to be prioritized for monitoring remain to be determined.

总之，器官灌注压和血流之间的关系是由 PA 调节的。器官血流由多种生理过程和病人或疾病因素共同调节，包括 PA。压力自动调节能力在不同的器官中是异质的，在特定的器官中也因非压力过程和因素而不同。PA 的异质性和变异性的知识在临床救治中是有指导意义的，因为错误的血压管理，特别是在个别病人的 PA 受损的情况下，使一个器官处于缺血或高灌注相关损伤的风险之中。然而，PA 监测的价值和优先监测的器官仍有待确定。

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脊髓血流的自动调节。脊髓是大脑的一个缩影吗？

46. Shaw RF, Mosher P, Ross J Jr, et al. Physiologic principles of coronary perfusion. J Thorac Cardiovasc Surg 1962; 44:608-616.
冠状动脉灌注的生理学原理。

47. Berne RM. Cardiodynamics and the coronary circulation in hypothermia. Ann N Y Acad Sci 1959; 80:365-383.
低温下的心脏动力学和冠状动脉循环。

48. Mosher P, Ross J Jr, Mcfate PA, et al. Control of coronary blood flow by an autoregulatory mechanism. Circ Res 1964; 14:250-259.
通过自动调节机制控制冠状动脉血流。

49. Lush DJ, Fray JC. Steady-state autoregulation of renal blood flow: A myogenic model. Am J Physiol 1984; 247:R89-R99.
肾脏血流的稳态自动调节。一个肌源性模型。

50. Waugh WH, Shanks RG. Cause of genuine autoregulation of the renal circulation. Circ Res 1960; 8:871-888.
肾脏循环真正自动调节的原因.

51. Feldberg R, Colding-Jorgensen M, Holstein-Rathlou NH. Analysis of interaction between TGF and the myogenic response in renal blood flow autoregulation. Am J Physiol 1995; 269:F581-F593.
肾血流自动调节中 TGF 和生肌反应之间的相互作用分析。

52. Iversen BM, Kvam FI, Matre K, et al. Resetting of renal blood autoregulation during acute blood pressure reduction in hypertensive rats. Am J Physiol 1998; 275:R343-R349.
高血压大鼠急性降压过程中肾脏血流自动调节的重新设定。

53. Turkstra E, Braam B, Koomans HA. Impaired renal blood flow autoregulation in two-kidney, one-clip hypertensive rats is caused by enhanced activity of nitric oxide. J Am Soc Nephrol 2000; 11:847-855.
双肾一夹式高血压大鼠肾血流自动调节功能受损是由一氧化氮活性增强引起的。

54. Rothe CF, Nash FD, Thompson DE. Patterns in autoregulation of renal blood flow in the dog. Am J Physiol 1971; 220:1621-1626.
狗肾血流自动调节的模式。

55. Cupples WA. Interactions contributing to kidney blood flow autoregulation. Curr Opin Nephrol Hypertens 2007; 16:39-45.
有助于肾脏血流自动调节的相互作用。

56. Cupples WA, Braam B. Assessment of renal autoregulation. Am J Physiol Renal Physiol 2007; 292:F1105-F1123.
肾脏自动调节的评估。

57. Hinshaw LB. Mechanism of renal autoregulation: Role of tissue pressure and description of a multifactor hypothesis. Circ Res 1964; 15(Suppl):120-131.
肾脏自动调节的机制。组织压力的作用和多因素假说的描述。

58. Burke M, Pabbidi MR, Farley J, et al. Molecular mechanisms of renal blood flow autoregulation. Curr Vasc Pharmacol 2014; 12:845-858.
肾脏血流自动调节的分子机制。

59. Forbes HS, Wolff HG. Cerebral circulation: III. The vasomotor control of cerebral vessels. Arch Neur Psych 1928; 19:1057-1086.
大脑血管的血管运动控制。

60. London MJ. Intraoperative mean blood pressure and outcome: Is 80 (mmHg) the "New" 60? Anesthesiology 2016; 124:4-6.
术中平均血压和结果。80（mmHg）是 "新"60 吗？

61. Kennedy C, Sokoloff L. An adaptation of the nitrous oxide method to the study of the cerebral circulation in children; normal values for cerebral blood flow and cerebral metabolic rate in childhood. J Clin Invest 1957; 36:1130-1137.
氧化亚氮法在儿童脑循环研究中的应用；儿童期脑血流和脑代谢率的正常值。

62. Lassen NA. Normal average value of cerebral blood flow in younger adults is 50 ml/100 g/min. J Cereb Blood Flow Metab 1985; 5:347-349.
年轻成年人的脑血流正常平均值为 50 毫升 / 100 克 / 分钟。

63. Deegan BM, Sorond FA, Galica A, et al. Elderly women regulate brain blood flow better than men do. Stroke 2011; 42:1988-1993.
老年妇女调节脑血流的能力比男性强。

64. Jones JV, Fitch W, MacKenzie ET, et al. Lower limit of cerebral blood flow autoregulation in experimental renovascular hypertension in the baboon. Circ Res 1976; 39:555-557.
狒狒实验性血管扩张性高血压的脑血流自动调节的下限。

65. Strandgaard S, Jones JV, MacKenzie ET, et al. Upper limit of cerebral blood flow autoregulation in experimental renovascular hypertension in the baboon. Circ Res 1975; 37:164-167.
狒狒实验性血管扩张性高血压的脑血流自动调节的上限。

66. Aries MJ, Elting JW, De Keyser J, et al. Cerebral autoregulation in stroke: A review of transcranial Doppler studies. Stroke 2010; 41:2697-2704.
脑卒中的脑血流自动调节。经颅多普勒研究的回顾。

67. Rangel-Castilla L, Gasco J, Nauta HJ, et al. Cerebral pressure autoregulation in traumatic brain injury. Neurosurg Focus 2008; 25:E7.
创伤性脑损伤中的脑压自动调节.

68. Mascia L, Andrews PJ, McKeating EG, et al. Cerebral blood flow and metabolism in severe brain injury: The role of pressure autoregulation during cerebral perfusion pressure management. Intensive Care Med 2000; 26:202-205.
严重脑损伤中的脑血流和代谢。脑灌注压管理过程中压力自动调节的作用.

69. Ter Minassian A, Dube L, Guilleux AM, et al. Changes in intracranial pressure and cerebral autoregulation in patients with severe traumatic brain injury. Crit Care Med 2002; 30:1616-1622.
严重脑外伤患者的颅内压和脑血流自动调节的变化。

70. Tseng MY, Czosnyka M, Richards H, et al. Effects of acute treatment with pravastatin on cerebral vasospasm, autoregulation, and delayed ischemic deficits after aneurysmal subarachnoid hemorrhage: A phase II randomized placebo-controlled trial. Stroke 2005; 36:1627-1632.
普伐他汀急性治疗对动脉瘤性蛛网膜下腔出血后脑血管痉挛、自动调节和延迟性缺血障碍的影响。一项 II 期随机安慰剂对照试验。

71. Soehle M, Czosnyka M, Pickard JD, et al. Continuous assessment of cerebral autoregulation in subarachnoid hemorrhage. Anesth Analg 2004; 98:1133-1139.
连续评估蛛网膜下腔出血的大脑血流自动调节功能。

72. Lang EW, Diehl RR, Mehdorn HM. Cerebral autoregulation testing after aneurysmal subarachnoid hemorrhage: The phase relationship between arterial blood pressure and cerebral blood flow velocity. Crit Care Med 2001; 29:158-163.
动脉瘤性蛛网膜下腔出血后的脑血流自动调节测试。动脉血压与脑血流速度的相位关系.

73. Jaeger M, Schuhmann MU, Soehle M, et al. Continuous monitoring of cerebrovascular autoregulation after subarachnoid hemorrhage by brain tissue oxygen pressure reactivity and its relation to delayed cerebral infarction. Stroke 2007; 38:981-986.
通过脑组织氧压反应性连续监测蛛网膜下腔出血后的脑血管自动调节及其与延迟性脑梗塞的关系.

74. Terborg C, Schummer W, Albrecht M, et al. Dysfunction of vasomotor reactivity in severe sepsis and septic shock. Intensive Care Med 2001; 27:1231-1234.
严重脓毒症和脓毒症休克中血管运动反应性的功能障碍。

75. Pfister D, Siegemund M, Dell-Kuster S, et al. Cerebral perfusion in sepsis-associated delirium. Crit Care 2008; 12:R63.
脓毒症相关的谵妄中的脑灌注。

76. Taccone FS, Castanares-Zapatero D, Peres-Bota D, et al. Cerebral autoregulation is influenced by carbon dioxide levels in patients with septic shock. Neurocrit Care 2010; 12:35-42.
脓毒症休克患者的脑部自动调节受二氧化碳水平的影响.

77. Sundgreen C, Larsen FS, Herzog TM, et al. Autoregulation of cerebral blood flow in patients resuscitated from cardiac arrest. Stroke 2001; 32:128-132.
心脏骤停患者复苏后的脑血流自动调节.

78. Nishizawa H, Kudoh I. Cerebral autoregulation is impaired in patients resuscitated after cardiac arrest. Acta Anaesthesiol Scand 1996; 40:1149-1153.
在心脏骤停后复苏的病人中，脑部自动调节功能受损。

79. Moller K, Larsen FS, Qvist J, et al. Dependency of cerebral blood flow on mean arterial pressure in patients with acute bacterial meningitis. Crit Care Med 2000; 28:1027-1032.
急性细菌性脑膜炎患者的脑血流对平均动脉压的依赖性。

80. Larsen FS, Strauss G, Knudsen GM, et al. Cerebral perfusion, cardiac output, and arterial pressure in patients with fulminant hepatic failure. Crit Care Med 2000; 28:996-1000.
暴发性肝衰竭患者的脑灌注、心输出量和动脉压。

81. Mutch WA, Sutton IR, Teskey JM, et al. Cerebral pressure-flow relationship during cardiopulmonary bypass in the dog at normothermia and moderate hypothermia. J Cereb Blood Flow Metab 1994; 14:510-518.
正常体温和中等体温下的狗在心肺分流过程中的脑压力 - 流量关系。

82. Lucas SJ, Tzeng YC, Galvin SD, et al. Influence of changes in blood pressure on cerebral perfusion and oxygenation. Hypertension 2010; 55:698-705.
血压变化对脑灌注和氧合的影响。

83. Wei EP, Moskowitz MA, Boccalini P, et al. Calcitonin gene-related peptide mediates nitroglycerin and sodium nitroprusside-induced vasodilation in feline cerebral arterioles. Circ Res 1992; 70:1313-1319.
降钙素基因相关肽介导硝化甘油和硝普钠诱导的猫科动物脑动脉血管扩张。

84. Joshi S, Duong H, Mangla S, et al. In nonhuman primates intracarotid adenosine, but not sodium nitroprusside, increases cerebral blood flow. Anesth Analg 2002; 94:393-399.
在非人类灵长类动物中，颈内腺苷而非硝普钠可增加脑血流量。

85. Joshi S, Young WL, Duong H, et al. Intracarotid nitroprusside does not augment cerebral blood flow in human subjects. Anesthesiology 2002; 96:60-66.
颈动脉内硝普钠不会增加人类的脑血流量。

86. Greenfield JC Jr, Tindall GT. Effect of norepinephrine, epinephrine, and angiotensin on blood flow in the internal carotid artery of man. J Clin Invest 1968; 47:1672-1684.
去甲肾上腺素、肾上腺素和血管紧张素对人的颈内动脉血流的影响。

87. Olesen J. The effect of intracarotid epinephrine, norepinephrine, and angiotensin on the regional cerebral blood flow in man. Neurology 1972; 22:978-987.
颈内肾上腺素、去甲肾上腺素和血管紧张素对人的区域脑血流的影响。

88. Moerman AT, Vanbiervliet VM, Van Wesemael A, et al. Assessment of cerebral autoregulation patterns with near-infrared spectroscopy during pharmacological-induced pressure changes. Anesthesiology 2015; 123:327-335.
在药物诱导的压力变化过程中用近红外光谱法评估大脑血流自动调节模式。

89. Meng L, Cannesson M, Alexander BS, et al. Effect of phenylephrine and ephedrine bolus treatment on cerebral oxygenation in anaesthetized patients. Br J Anaesth 2011; 107:209-217.
苯肾上腺素和麻黄素栓塞治疗对麻醉病人脑氧合的影响。

90. Conti A, Iacopino DG, Fodale V, et al. Cerebral haemodynamic changes during propofol-remifentanil or sevoflurane anaesthesia: Transcranial Doppler study under bispectral index monitoring. Br J Anaesth 2006; 97:333-339.
丙泊酚 - 瑞芬太尼或七氟烷麻醉过程中的脑血流动力学变化：双光谱指数监测下的经颅多普勒研究。

91. Lagerkranser M, Stange K, Sollevi A. Effects of propofol on cerebral blood flow, metabolism, and cerebral autoregulation in the anesthetized pig. J Neurosurg Anesthesiol 1997; 9:188-193.
丙泊酚对麻醉猪的脑血流、代谢和脑血流自动调节的影响。

92. Summors AC, Gupta AK, Matta BF. Dynamic cerebral autoregulation during sevoflurane anesthesia: A comparison with isoflurane. Anesth Analg 1999; 88:341-345.
七氟烷麻醉期间动态脑血流自动调节。与异氟烷的比较。

93. Cassaglia PA, Griffiths RI, Walker AM. Sympathetic nerve activity in the superior cervical ganglia increases in response to imposed increases in arterial pressure. Am J Physiol Regul Integr Comp Physiol 2008; 294:R1255-R1261.
颈部上神经节的交感神经活动因动脉压力的增加而增加。

94. Harper AM, Deshmukh VD, Rowan JO, et al. The influence of sympathetic nervous activity on cerebral blood flow. Arch Neurol 1972; 27:1-6.
交感神经活动对脑血流的影响。

95. Zhang R, Zuckerman JH, Iwasaki K, et al. Autonomic neural control of dynamic cerebral autoregulation in humans. Circulation 2002; 106:1814-1820.
人类动态脑血流自动调节的自主神经控制。

96. van Lieshout JJ, Secher NH. Point:Counterpoint: Sympathetic activity does/does not influence cerebral blood flow. Point: Sympathetic activity does influence cerebral blood flow. J Appl Physiol (1985) 2008; 105:1364-1366.
点。交感神经活动确实影响脑血流。

97. Willie CK, Tzeng YC, Fisher JA, et al. Integrative regulation of human brain blood flow. J Physiol 2014; 592:841-859.
人脑血流的综合调节。

98. Crystal GJ, Czinn EA, Salem MR. The mechanism of increased blood flow in the brain and spinal cord during hemodilution. Anesth Analg 2014; 118:637-643.
血液稀释时大脑和脊髓血流增加的机制。

99. Czinn EA, Salem MR, Crystal GJ. Hemodilution impairs hypocapnia-induced vasoconstrictor responses in the brain and spinal cord in dogs. Anesth Analg 1995; 80:492-498.
血液稀释会损害低碳酸血症引起的狗脑和脊髓的血管收缩反应。

100. Brown MM, Wade JP, Marshall J. Fundamental importance of arterial oxygen content in the regulation of cerebral blood flow in man. Brain 1985; 108(Pt 1):81-93.
动脉含氧量对人的脑血流调节的根本重要性。

101. Brown MM, Marshall J. Regulation of cerebral blood flow in response to changes in blood viscosity. Lancet 1985; 1:604-609.
对血液粘度变化的脑血流调节。

102. McCulloch TJ, Visco E, Lam AM. Graded hypercapnia and cerebral autoregulation during sevoflurane or propofol anesthesia. Anesthesiology 2000; 93:1205-1209.
七氟醚或丙泊酚麻醉期间的分级高碳酸血症和脑部自动调节。

103. Field EJ, Grayson J, Rogers AF. Observations on the blood flow in the spinal cord of the rabbit. J Physiol 1951; 114:56-70.
对兔子脊髓血流的观察。

104. Guha A, Tator CH, Rochon J. Spinal cord blood flow and systemic blood pressure after experimental spinal cord injury in rats. Stroke 1989; 20:372-377.
大鼠实验性脊髓损伤后的脊髓血流和全身血压。

105. Smith AJ, McCreery DB, Bloedel JR, et al. Hyperemia, CO₂ responsiveness, and autoregulation in the white matter following experimental spinal cord injury. J Neurosurg 1978; 48:239-251.
实验性脊髓损伤后白质中的高血症、二氧化碳反应性和自动调节。

106. Griffiths IR. Spinal cord blood flow after acute experimental cord injury in dogs. J Neurol Sci 1976; 27:247-259.
狗急性实验性脊髓损伤后的脊髓血流。

107. Werner C, Hoffman WE, Kochs E, et al. The effects of propofol on cerebral and spinal cord blood flow in rats. Anesth Analg 1993; 76:971-975.
丙泊酚对大鼠脑和脊髓血流的影响。

108. Kobrine AI, Evans DE, Rizzoli HV. The effect of alpha adrenergic blockade on spinal cord autoregulation in the monkey. J Neurosurg 1977; 46:336-341.
α 肾上腺素能阻断对猴子脊髓自动调节的影响。

109. Kobrine AI, Evans DE, Rizzoli HV. The effects of beta adrenergic blockade on spinal cord autoregulation in the monkey. J Neurosurg 1977; 47:57-63.
β 肾上腺素能阻断对猴子脊髓自动调节的影响.

110. Duncker DJ, Bache RJ. Regulation of coronary blood flow during exercise. Physiol Rev 2008; 88:1009-1086.
运动中冠状动脉血流的调节。

111. Berne RM. Regulation of coronary blood flow. Physiol Rev 1964; 44:1-29.
冠状动脉血流的调节。

112. Feigl EO. Coronary autoregulation. J Hypertens Suppl 1989; 7:S55-S58; discussion S59.
冠状动脉自动调节。

113. Canty JM Jr. Coronary pressure-function and steady-state pressure-flow relations during autoregulation in the unanesthetized dog. Circ Res 1988; 63:821-836.
未麻醉的狗在自动调节期间的冠状动脉压力 - 功能和稳态压力 - 流量关系。

114. Feigl EO. Coronary physiology. Physiol Rev 1983; 63:1-205.
冠状动脉生理学。

115. Hoffman JI, Spaan JA. Pressure-flow relations in coronary circulation. Physiol Rev 1990; 70:331-390.
冠状动脉循环中的压力 - 流量关系。

116. Westerhof N, Boer C, Lamberts RR, et al. Cross-talk between cardiac muscle and coronary vasculature. Physiol Rev 2006; 86:1263-1308.
心肌和冠状动脉血管之间的交叉对话。

117. Dole WP. Autoregulation of the coronary circulation. Prog Cardiovasc Dis 1987; 29:293-323.
冠状动脉循环的自动调节。

118. Yonekura S, Watanabe N, Caffrey JL, et al. Mechanism of attenuated pressure-flow autoregulation in right coronary circulation of dogs. Circ Res 1987; 60:133-141.
狗右冠状动脉循环中压力 - 流量自动调节减弱的机制。

119. Tani H, Saito D, Kusachi S, et al. Autoregulation by the right coronary artery in dogs with open chests; comparison with the left coronary artery. Pflugers Arch 1990; 416:442-447.
开胸狗的右冠状动脉的自动调节；与左冠状动脉的比较。

120. Guth BD, Schulz R, Heusch G. Pressure-flow characteristics in the right and left ventricular perfusion territories of the right coronary artery in swine. Pflugers Arch 1991; 419:622-628.
猪右冠状动脉的右心室和左心室灌注区的压力 - 流量特征。

121. Boatwright RB, Downey HF, Bashour FA, et al. Transmural variation in autoregulation of coronary blood flow in hyperperfused canine myocardium. Circ Res 1980; 47:599-609.
灌注过度的犬类心肌中冠状动脉血流自动调节的跨膜变化。

122. Guyton RA, McClenathan JH, Newman GE, et al. Significance of subendocardial S-T segment elevation caused by coronary stenosis in the dog. Epicardial S-T segment depression, local ischemia and subsequent necrosis. Am J Cardiol 1977; 40:373-380.
心外膜 S-T 段压低，局部缺血和随后的坏死。

123. Rouleau J, Boerboom LE, Surjadhana A, et al. The role of autoregulation and tissue diastolic pressures in the transmural distribution of left ventricular blood flow in anesthetized dogs. Circ Res 1979; 45:804-815.
自动调节和组织舒张压在麻醉犬左心室血流跨膜分布中的作用。

124. Yonekura S, Watanabe N, Downey HF. Transmural variation in autoregulation of right ventricular blood flow. Circ Res 1988; 62:776-781.
右心室血流自动调节的横断面变化。

125. Polese A, De Cesare N, Montorsi P, et al. Upward shift of the lower range of coronary flow autoregulation in hypertensive patients with hypertrophy of the left ventricle. Circulation 1991; 83:845-853.
左心室肥大的高血压患者的冠状动脉血流自动调节的低范围向上移动。

126. Canty JM Jr, Giglia J, Kandath D. Effect of tachycardia on regional function and transmural myocardial perfusion during graded coronary pressure reduction in conscious dogs. Circulation 1990; 82:1815-1825.
心动过速对意识清醒的狗在冠状动脉分级减压时区域功能和跨膜心肌灌注的影响。

127. Bian X, Williams AG Jr, Gwirtz PA, et al. Right coronary autoregulation in conscious, chronically instrumented dogs. Am J Physiol 1998; 275:H169-H175.
昏迷狗的右冠状动脉自动调节功能。

128. Hickey RF, Sybert PE, Verrier ED, et al. Effects of halothane, enflurane, and isoflurane on coronary blood flow autoregulation and coronary vascular reserve in the canine heart. Anesthesiology 1988; 68:21-30.
氟烷、恩氟烷和异氟烷对犬心脏冠状动脉血流自动调节和冠状动脉血管储备的影响。

129. Iversen BM, Sekse I, Ofstad J. Resetting of renal blood flow autoregulation in spontaneously hypertensive rats. Am J Physiol 1987; 252:F480-F486.
自发性高血压大鼠肾血流自动调节的复位。

130. Hayashi K, Epstein M, Loutzenhiser R. Pressure-induced vasoconstriction of renal microvessels in normotensive and hypertensive rats. Studies in the isolated perfused hydronephrotic kidney. Circ Res 1989; 65:1475-1484.
在分离的灌注水肾中的研究。

131. Hayashi K, Epstein M, Saruta T. Altered myogenic responsiveness of the renal microvasculature in experimental hypertension. J Hypertens 1996; 14:1387-1401.
实验性高血压中肾脏微血管的肌源反应性改变。

132. Hashimoto Y, Ideura T, Yoshimura A, et al. Autoregulation of renal blood flow in streptozocin-induced diabetic rats. Diabetes 1989; 38:1109-1113.
Streptozocin 诱导的糖尿病大鼠肾血流的自动调节。

133. Hayashi K, Epstein M, Loutzenhiser R, et al. Impaired myogenic responsiveness of the afferent arteriole in streptozotocin-induced diabetic rats: Role of eicosanoid derangements. J Am Soc Nephrol 1992; 2:1578-1586.
链脲霉素诱导的糖尿病大鼠传入动脉血管的肌源性反应性受损。二十烷烃类物质失调的作用。

134. Ishida K, Ishibashi F, Takashina S. Comparison of renal hemodynamics in early non-insulin-dependent and insulin-dependent diabetes mellitus. J Diabet Complications 1991; 5:143-145.
早期非胰岛素依赖型和胰岛素依赖型糖尿病的肾脏血流动力学比较。

135. Tolins JP, Shultz PJ, Raij L, et al. Abnormal renal hemodynamic response to reduced renal perfusion pressure in diabetic rats: Role of NO. Am J Physiol 1993; 265:F886-F895.
糖尿病大鼠肾血流动力学对肾灌注压降低的异常反应。NO 的作用。

136. De Micheli AG, Forster H, Duncan RC, et al. A quantitative assessment of renal blood flow autoregulation in experimental diabetes. Nephron 1994; 68:245-251.
实验性糖尿病中肾脏血流自动调节的定量评估.

137. Mauer SM, Brown DM, Steffes MW, et al. Studies of renal autoregulation in pancreatectomized and streptozotocin diabetic rats. Kidney Int 1990; 37:909-917.
胰腺切除和链脲霉素糖尿病大鼠肾脏自动调节的研究。

138. Parving HH, Kastrup H, Smidt UM, et al. Impaired autoregulation of glomerular filtration rate in type 1 (insulin-dependent) diabetic patients with nephropathy. Diabetologia 1984; 27:547-552.
1 型（胰岛素依赖型）糖尿病患者肾小球滤过率的自动调节功能受损。

139. New JP, Marshall SM, Bilous RW. Renal autoregulation is normal in newly diagnosed, normotensive, NIDDM patients. Diabetologia 1998; 41:206-211.
新诊断的、血压正常的 NIDDM 患者的肾脏自动调节功能是正常的。

140. Ogawa N, Ono H. Role of Ca channel in the renal autoregulatory vascular response analysed by the use of BAY K 8644. Naunyn Schmiedebergs Arch Pharmacol 1987; 335:189-193.
通过使用 BAY K 8644 分析 Ca 通道在肾脏自动调节血管反应中的作用。

141. Christensen PK, Akram K, Konig KB, et al. Autoregulation of glomerular filtration rate in patients with type 2 diabetes during isradipine therapy. Diabetes Care 2003; 26:156-162.
2 型糖尿病患者在接受伊拉地平治疗期间肾小球滤过率的自我调节。

142. Bugge JF, Stokke ES, Kiil F. Effects of bradykinin and papaverine on renal autoregulation and renin release in the anaesthetized dog. Acta Physiol Scand 1991; 143:431-437.
缓激肽和罂粟碱对麻醉狗肾脏自动调节和肾素释放的影响。

143. Ohmura A, Wong KC, Pace NL, et al. Effects of halothane and sodium nitroprusside on renal function and autoregulation. Br J Anaesth 1982; 54:103-108.
氟烷和硝普钠对肾功能和自动调节的影响。

144. Bastron RD, Perkins RM, Pyne JL. Autoregulation of renal blood flow during halothane anesthesia. Anesthesiology 1977; 46:142-144.
氟烷麻醉期间肾脏血流的自动调节。

145. Pappenheimer JR, Maes JP. A quantitative measure of the vasomotor tone in the hindlimb muscles of the dog. Am J Physiol 1942; 137:187-199.
对狗后肢肌肉血管运动张力的定量测量。

146. Folkow B. A critical study of some methods used in investigations on the blood circulation. Acta Physiologica 1953; 27:118-129.
对血液循环调查中使用的一些方法的批评研究。

147. Green HD, Lewis RN, Nickerson ND, et al. Blood flow, peripheral resistance and vascular tonus, with observations on the relationship between blood flow and cutaneous temperature. Am J Physiol 1944; 141:518-536.
血流、外周阻力和血管张力，以及对血流和皮肤温度之间关系的观察。

148. Folkow B. Intravascular pressure as a factor regulating the tone of the small vessels. Acta Physiologica 1949; 17:289-310.
血管内压是调节小血管张力的一个因素。

149. Faris I, Vagn Nielsen H, Henriksen O, et al. Impaired autoregulation of blood flow in skeletal muscle and subcutaneous tissue in long-term type 1 (insulin-dependent) diabetic patients with microangiopathy. Diabetologia 1983; 25:486-488.
长期患有微血管病的 1 型（胰岛素依赖型）糖尿病患者的骨骼肌和皮下组织的血流自动调节功能受损。

150. Kastrup J, Norgaard T, Parving HH, et al. Impaired autoregulation of blood flow in subcutaneous tissue of long-term type 1 (insulin-dependent) diabetic patients with microangiopathy: An index of arteriolar dysfunction. Diabetologia 1985; 28:711-717.
长期患有微血管病变的 1 型（胰岛素依赖型）糖尿病患者皮下组织的血流自动调节功能受损。动脉功能障碍的一个指标。

151. De Blasi RA, Palmisani S, Alampi D, et al. Microvascular dysfunction and skeletal muscle oxygenation assessed by phase-modulation near-infrared spectroscopy in patients with septic shock. Intensive Care Med 2005; 31:1661-1668.
用相位调制近红外光谱法评估脓毒症休克患者的微血管功能障碍和骨骼肌氧合情况。

152. Jacobson ED, Scott JB, Frohlich ED. Hemodynamics of the stomach. I. Resistance-flow relationship in the gastric vascular bed. Am J Dig Dis 1962; 7:779-785.
胃血管床的阻力 - 流量关系。

153. Bruggeman TM, Wood JG, Davenport HW. Local control of blood flow in the dog's stomach: Vasodilatation caused by acid back-diffusion following topical application of salicylic acid. Gastroenterology 1979; 77:736-744.
狗胃中血流的局部控制。局部使用水杨酸后酸液回渗引起的血管舒张。

154. Holm-Rutili L, Perry MA, Granger DN. Autoregulation of gastric blood flow and oxygen uptake. Am J Physiol 1981; 241:G143-G149.
胃血流和氧摄取的自动调节。

155. Perry MA, Murphree D, Granger DN. Oxygen uptake as a determinant of gastric blood flow autoregulation. Dig Dis Sci 1982; 27:675-679.
摄氧量是胃血流自动调节的一个决定因素。

156. Selkurt EE, Scibetta MP, Cull TE. Hemodynamics of intestinal circulation. Circ Res 1958; 6:92-99.
肠道循环的血流动力学。

157. Texter EC Jr, Merrill S, Schwartz M, et al. Relationship of blood flow to pressure in the intestinal vascular bed of the dog. Am J Physiol 1962; 202:253-256.
狗肠道血管床的血流与压力的关系。

158. Richardson DR, Johnson PC. Comparison of autoregulatory escape and autoregulation in the intestinal vascular bed. Am J Physiol 1969; 217:586-590.
肠道血管床的自动调节逃逸和自动调节的比较。

159. Shepherd AP, Granger HJ. Autoregulatory escape in the gut: A systems analysis. Gastroenterology 1973; 65:77-91.
肠道内的自动调节逃逸。一个系统分析。

160. Johnson PC, Hanson KM. Effect of arterial pressure on arterial and venous resistance of intestine. J Appl Physiol 1962; 17:503-508.
动脉压力对肠道的动脉和静脉阻力的影响。

161. Hanson KM, Johnson PC. Pressure-flow relationships in isolated dog colon. Am J Physiol 1967; 212:574-578.
分离的狗结肠中的压力 - 流量关系。

162. Hanson KM, Moore FT. Effects of intraluminal pressure in the colon on its vascular pressure-flow relationships. Proc Soc Exp Biol Med 1969; 131:373-376.
结肠腔内压力对其血管压力 - 流量关系的影响。

163. Richardson PD, Withrington PG. Pressure-flow relationships and effects of noradrenaline and isoprenaline on the hepatic arterial and portal venous vascular beds of the dog. J Physiol 1978; 282:451-470.
去甲肾上腺素和异丙肾上腺素的压力 - 流量关系和对狗肝动脉和门静脉血管床的影响。

164. Norris CP, Barnes GE, Smith EE, et al. Autoregulation of superior mesenteric flow in fasted and fed dogs. Am J Physiol 1979; 237:H174-H177.
空腹和进食的狗的肠系膜上层血流的自动调节。

165. Drummond JC. The lower limit of autoregulation: Time to revise our thinking? Anesthesiology 1997; 86:1431-1433.
自动调节的下限。是时候修改我们的想法了吗？

166. Bombardieri AM, Sharrock NE, Ma Y, et al. An observational study of cerebral blood flow velocity during hypotensive epidural anesthesia. Anesth Analg 2016; 122:226-233.
低血压硬膜外麻醉期间脑血流速度的观察性研究。

167. Larsen FS, Olsen KS, Hansen BA, et al. Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation. Stroke 1994; 25:1985-1988.
经颅多普勒对确定脑血流自动调节的下限是有效的。

168. Aronson S, Stafford-Smith M, Phillips-Bute B, et al; Cardiothoracic Anesthesiology Research Endeavors: Intraoperative systolic blood pressure variability predicts 30-day mortality in aortocoronary bypass surgery patients. Anesthesiology 2010; 113:305-312.
Aronson S, Stafford-Smith M, Phillips-Bute B, et al; Cardiothoracic Anesthesiology Research Endeavors: 术中收缩压变异性可预测主动脉冠状动脉搭桥手术患者 30 天的死亡率。

169. Aronson S, Dyke CM, Levy JH, et al. Does perioperative systolic blood pressure variability predict mortality after cardiac surgery? An exploratory analysis of the ECLIPSE trials. Anesth Analg 2011; 113:19-30.
围手术期收缩压变异性可预测心脏手术后的死亡率吗？对 ECLIPSE 试验的探索性分析。

170. Hirsch J, DePalma G, Tsai TT, et al. Impact of intraoperative hypotension and blood pressure fluctuations on early postoperative delirium after non-cardiac surgery. Br J Anaesth 2015; 115:418-426.
术中低血压和血压波动对非心脏手术后早期谵妄的影响.

171. Mascha EJ, Yang D, Weiss S, et al. Intraoperative mean arterial pressure variability and 30-day mortality in patients having noncardiac surgery. Anesthesiology 2015; 123:79-91.
非心脏手术患者的术中平均动脉压变异性和 30 天的死亡率。

172. Levin MA, Fischer GW, Lin HM, et al. Intraoperative arterial blood pressure lability is associated with improved 30 day survival. Br J Anaesth 2015; 115:716-726.
术中动脉血压的稳定性与 30 天生存率的提高有关。

173. Ono M, Arnaoutakis GJ, Fine DM, et al. Blood pressure excursions below the cerebral autoregulation threshold during cardiac surgery are associated with acute kidney injury. Crit Care Med 2013; 41:464-471.
心脏手术期间血压偏移低于脑血流自动调节阈值与急性肾脏损伤有关。

174. Overgaard J, Tweed WA. Cerebral circulation after head injury. 1. Cerebral blood flow and its regulation after closed head injury with emphasis on clinical correlations. J Neurosurg 1974; 41:531-541.
闭合性头部损伤后的脑血流及其调节，强调临床相关性。

175. Cold GE, Jensen FT. Cerebral autoregulation in unconscious patients with brain injury. Acta Anaesthesiol Scand 1978; 22:270-280.
昏迷中的脑损伤患者的脑自主调节.

176. Brady KM, Shaffner DH, Lee JK, et al. Continuous monitoring of cerebrovascular pressure reactivity after traumatic brain injury in children. Pediatrics 2009; 124:e1205-e1212.
儿童脑外伤后脑血管压力反应性的连续监测.

177. Bowles AP, Pasierb L, Simunich T, et al. Implications of neurophysiological parameters in persons with severe brain injury with respect to improved patient outcomes: A retrospective review. Brain Inj 2012; 26:1415-1424.
严重脑损伤患者的神经生理参数对改善患者预后的意义。一个回顾性的回顾。

178. Sorrentino E, Diedler J, Kasprowicz M, et al. Critical thresholds for cerebrovascular reactivity after traumatic brain injury. Neurocrit Care 2012; 16:258-266.
创伤性脑损伤后脑血管反应性的关键阈值。

179. Aries MJ, Czosnyka M, Budohoski KP, et al. Continuous monitoring of cerebrovascular reactivity using pulse waveform of intracranial pressure. Neurocrit Care 2012; 17:67-76.
使用颅内压的脉冲波形连续监测脑血管反应性。

180. Lang EW, Kasprowicz M, Smielewski P, et al. Outcome, pressure reactivity and optimal cerebral perfusion pressure calculation in traumatic brain injury: A comparison of two variants. Acta Neurochir Suppl 2016; 122:221-223.
创伤性脑损伤的结果、压力反应性和最佳脑灌注压计算。两种变体的比较。

181. Aries MJ, Wesselink R, Elting JW, et al. Enhanced visualization of optimal cerebral perfusion pressure over time to support clinical decision making. Crit Care Med 2016; 44:e996-e999.
增强最佳脑灌注压随时间变化的可视化，以支持临床决策。

182. Donnelly J, Czosnyka M, Adams H, et al. Individualizing thresholds of cerebral perfusion pressure using estimated limits of autoregulation. Crit Care Med 2017; 45:1464-1471.
利用估计的自动调节极限来确定脑灌注压的个体化阈值。

183. Bedforth NM, Girling KJ, Skinner HJ, et al. Effects of desflurane on cerebral autoregulation. Br J Anaesth 2001; 87:193-197.
地氟醚对大脑血流自动调节的影响。

184. Matta BF, Mayberg TS, Lam AM. Direct cerebrovasodilatory effects of halothane, isoflurane, and desflurane during propofol-induced isoelectric electroencephalogram in humans. Anesthesiology 1995; 83:980-985; discussion 27A.
氟烷、异氟烷和地氟烷在丙泊酚诱导的人体等电位脑电图中的直接脑血管扩张作用。

185. McCulloch TJ, Boesel TW, Lam AM. The effect of hypocapnia on the autoregulation of cerebral blood flow during administration of isoflurane. Anesth Analg 2005; 100:1463-1467.
异氟醚给药期间低碳酸血症对脑血流自动调节的影响。

186. Fieschi C, Battistini N, Beduschi A, et al. Regional cerebral blood flow and intraventricular pressure in acute head injuries. J Neurol Neurosurg Psychiatry 1974; 37:1378-1388.
急性颅脑损伤的区域脑血流和脑室内压。

187. Czosnyka M, Balestreri M, Steiner L, et al. Age, intracranial pressure, autoregulation, and outcome after brain trauma. J Neurosurg 2005; 102:450-454.
年龄、颅内压、自动调节和脑外伤后的结果。

188. Czosnyka M, Smielewski P, Kirkpatrick P, et al. Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery 1997; 41:11-17.
连续评估头部受伤时的脑血管运动反应性。

189. Czosnyka M, Smielewski P, Kirkpatrick P, et al. Monitoring of cerebral autoregulation in head-injured patients. Stroke 1996; 27:1829-1834.
监测头部受伤患者的脑部自动调节功能。

190. Lam JM, Hsiang JN, Poon WS. Monitoring of autoregulation using laser Doppler flowmetry in patients with head injury. J Neurosurg 1997; 86:438-445.
用激光多普勒血流仪监测头部受伤患者的自动调节功能。

191. Steiner LA, Czosnyka M, Piechnik SK, et al. Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury. Crit Care Med 2002; 30:733-738.
连续监测脑血管压力反应性可以确定脑外伤患者的最佳脑灌注压力。

192. Balestreri M, Czosnyka M, Steiner LA, et al. Intracranial hypertension: What additional information can be derived from ICP waveform after head injury? Acta Neurochir (Wien) 2004; 146:131-141.
颅内高血压。头部受伤后，从 ICP 波形中可以得到哪些额外信息？

193. Jaeger M, Schuhmann MU, Soehle M, et al. Continuous assessment of cerebrovascular autoregulation after traumatic brain injury using brain tissue oxygen pressure reactivity. Crit Care Med 2006; 34:1783-1788.
利用脑组织氧压反应性连续评估脑外伤后的脑血管自动调节功能。

194. Reinert M, Andres RH, Fuhrer M, et al. Online correlation of spontaneous arterial and intracranial pressure fluctuations in patients with diffuse severe head injury. Neurol Res 2007; 29:455-462.
弥漫性重度颅脑损伤患者的自发动脉和颅内压波动的在线相关性。

195. Radolovich DK, Aries MJ, Castellani G, et al. Pulsatile intracranial pressure and cerebral autoregulation after traumatic brain injury. Neurocrit Care 2011; 15:379-386.
脉动性颅内压和脑部自动调节在脑外伤后的应用。

196. Sorrentino E, Budohoski KP, Kasprowicz M, et al. Critical thresholds for transcranial Doppler indices of cerebral autoregulation in traumatic brain injury. Neurocrit Care 2011; 14:188-193.
创伤性脑损伤中经颅多普勒脑血流自动调节指数的临界值。

197. Depreitere B, Guiza F, Van den Berghe G, et al. Pressure autoregulation monitoring and cerebral perfusion pressure target recommendation in patients with severe traumatic brain injury based on minute-by-minute monitoring data. J Neurosurg 2014; 120:1451-1457.
基于每分钟的监测数据，严重脑外伤患者的压力自律监测和脑灌注压目标建议。

198. Dias C, Silva MJ, Pereira E, et al. Optimal cerebral perfusion pressure management at bedside: A single-center pilot study. Neurocrit Care 2015; 23:92-102.
最佳的床边脑灌注压管理。一个单中心的试点研究。

199. Petkus V, Krakauskaite S, Preiksaitis A, et al. Association between the outcome of traumatic brain injury patients and cerebrovascular autoregulation, cerebral perfusion pressure, age, and injury grades. Medicina (Kaunas) 2016; 52:46-53.
脑外伤患者的结局与脑血管自动调节、脑灌注压、年龄和损伤等级之间的关系。

200. Preiksaitis A, Krakauskaite S, Petkus V, et al. Association of severe traumatic brain injury patient outcomes with duration of cerebrovascular autoregulation impairment events. Neurosurgery 2016; 79:75-82.
严重脑外伤患者结局与脑血管自动调节功能受损事件持续时间的关系。

201. Jaeger M, Soehle M, Schuhmann MU, et al. Clinical significance of impaired cerebrovascular autoregulation after severe aneurysmal subarachnoid hemorrhage. Stroke 2012; 43:2097-2101.
严重动脉瘤性蛛网膜下腔出血后脑血管自动调节功能受损的临床意义。

202. Budohoski KP, Czosnyka M, Smielewski P, et al. Impairment of cerebral autoregulation predicts delayed cerebral ischemia after subarachnoid hemorrhage: A prospective observational study. Stroke 2012; 43:3230-3237.
大脑血流自动调节功能受损可预测蛛网膜下腔出血后的延迟性脑缺血。一项前瞻性的观察研究。

203. Rasulo FA, Girardini A, Lavinio A, et al. Are optimal cerebral perfusion pressure and cerebrovascular autoregulation related to long-term outcome in patients with aneurysmal subarachnoid hemorrhage? J Neurosurg Anesthesiol 2012; 24:3-8.
最佳脑灌注压和脑血管自动调节与动脉瘤性蛛网膜下腔出血患者的长期疗效有关吗？

204. Eide PK, Sorteberg A, Bentsen G, et al. Pressure-derived versus pressure wave amplitude-derived indices of cerebrovascular pressure reactivity in relation to early clinical state and 12-month outcome following aneurysmal subarachnoid hemorrhage. J Neurosurg 2012; 116:961-971.
压力衍生与压力波幅衍生的脑血管压力反应性指数与动脉瘤蛛网膜下腔出血后早期临床状态和 12 个月预后的关系。

205. Otite F, Mink S, Tan CO, et al. Impaired cerebral autoregulation is associated with vasospasm and delayed cerebral ischemia in subarachnoid hemorrhage. Stroke 2014; 45:677-682.
大脑血流自动调节功能受损与蛛网膜下腔出血的血管痉挛和延迟性脑缺血有关。

206. Diedler J, Santos E, Poli S, et al. Optimal cerebral perfusion pressure in patients with intracerebral hemorrhage: An observational case series. Crit Care 2014; 18:R51.
脑内出血患者的最佳脑灌注压。一个观察性的病例系列。

207. Calviere L, Nasr N, Arnaud C, et al. Prediction of delayed cerebral ischemia after subarachnoid hemorrhage using cerebral blood flow velocities and cerebral autoregulation assessment. Neurocrit Care 2015; 23:253-258.
利用脑血流速度和脑血流自动调节评估预测蛛网膜下腔出血后的延迟性脑缺血。

208. Reinhard M, Neunhoeffer F, Gerds TA, et al. Secondary decline of cerebral autoregulation is associated with worse outcome after intracerebral hemorrhage. Intensive Care Med 2010; 36:264-271.
大脑血流自动调节功能的继发性下降与脑内出血后较差的预后有关。

209. Barth M, Moratin B, Dostal M, et al. Correlation of clinical outcome and angiographic vasospasm with the dynamic autoregulatory response after aneurysmal subarachnoid hemorrhage. Acta Neurochir Suppl 2012; 114:157-160.
动脉瘤性蛛网膜下腔出血后临床结果和血管痉挛与动态自动调节反应的相关性。

210. Oeinck M, Neunhoeffer F, Buttler KJ, et al. Dynamic cerebral autoregulation in acute intracerebral hemorrhage. Stroke 2013; 44:2722-2728.
急性脑内出血的动态脑自主调节.

211. Fontana J, Moratin J, Ehrlich G, et al. Dynamic autoregulatory response after aneurysmal subarachnoid hemorrhage and its relation to angiographic vasospasm and clinical outcome. Neurocrit Care 2015; 23:355-363.
动脉瘤性蛛网膜下腔出血后的动态自动调节反应及其与血管痉挛和临床结果的关系。

212. Santos GA, Petersen N, Zamani AA, et al. Pathophysiologic differences in cerebral autoregulation after subarachnoid hemorrhage. Neurology 2016; 86:1950-1956.
蛛网膜下腔出血后脑部自动调节的病理生理学差异。

213. Newman MF, Croughwell ND, Blumenthal JA, et al. Effect of aging on cerebral autoregulation during cardiopulmonary bypass. Association with postoperative cognitive dysfunction. Circulation 1994; 90:II243-II249.
与术后认知功能障碍的关系。

214. Joshi B, Brady K, Lee J, et al. Impaired autoregulation of cerebral blood flow during rewarming from hypothermic cardiopulmonary bypass and its potential association with stroke. Anesth Analg 2010; 110:321-328.
低温心肺分流术后复温过程中的脑血流自动调节功能受损及其与中风的潜在联系。

215. Zheng Y, Villamayor AJ, Merritt W, et al. Continuous cerebral blood flow autoregulation monitoring in patients undergoing liver transplantation. Neurocrit Care 2012; 17:77-84.
肝移植患者的连续脑血流自动调节监测。

216. Ono M, Brady K, Easley RB, et al. Duration and magnitude of blood pressure below cerebral autoregulation threshold during cardiopulmonary bypass is associated with major morbidity and operative mortality. J Thorac Cardiovasc Surg 2014; 147:483-489.
在心肺分流过程中，血压低于大脑血流自动调节阈值的时间和幅度与主要的发病率和手术死亡率有关。

217. Hori D, Brown C, Ono M, et al. Arterial pressure above the upper cerebral autoregulation limit during cardiopulmonary bypass is associated with postoperative delirium. Br J Anaesth 2014; 113:1009-1017.
在心肺分流术期间，动脉压高于大脑血流自动调节上限与术后谵妄有关。

218. Hori D, Max L, Laflam A, et al. Blood pressure deviations from optimal mean arterial pressure during cardiac surgery measured with a novel monitor of cerebral blood flow and risk for perioperative delirium: A pilot study. J Cardiothorac Vasc Anesth 2016; 30:606-612.
用新型脑血流监测仪测量的心脏手术期间的血压偏离最佳平均动脉压和围手术期谵妄的风险。一个试点研究。

219. Laflam A, Joshi B, Brady K, et al. Shoulder surgery in the beach chair position is associated with diminished cerebral autoregulation but no differences in postoperative cognition or brain injury biomarker levels compared with supine positioning: The anesthesia patient safety foundation beach chair study. Anesth Analg 2015; 120:176-185.
沙滩椅体位下的肩部手术与脑自主调节功能减弱有关，但与仰卧位相比，术后认知能力或脑损伤生物标志物水平没有差异。麻醉病人安全基金会沙滩椅研究。

220. Goettel N, Burkhart CS, Rossi A, et al. Associations between impaired cerebral blood flow autoregulation, cerebral oxygenation, and biomarkers of brain injury and postoperative cognitive dysfunction in elderly patients after major noncardiac surgery. Anesth Analg 2017; 124:934-942.
老年非心脏大手术后患者脑血流自动调节功能受损、脑氧合、脑损伤生物标志物与术后认知功能障碍的关系。

221. Rickards CA. Cerebral blood-flow regulation during hemorrhage. Compr Physiol 2015; 5:1585-1621.
出血时的脑血流调节.

222. Meng L, Yu W, Wang T, et al. Blood pressure targets in perioperative care: Provisional considerations based on a comprehensive literature review. Hypertension 2018; 72:806-817.
围手术期救治中的血压目标。基于综合文献回顾的临时考虑。

223. Neutze JM, Wyler F, Rudolph AM. Use of radioactive microspheres to assess distribution of cardiac output in rabbits. Am J Physiol 1968; 215:486-495.
使用放射性微球来评估兔子的心输出量分布。

224. Neutze JM, Wyler F, Rudolph AM. Changes in distribution of cardiac output after hemorrhage in rabbits. Am J Physiol 1968; 215:857-864.
兔子出血后心输出量分布的变化.

225. Fell C. Changes in distribution of blood flow in irreversible hemorrhagic shock. Am J Physiol 1966; 210:863-868.
不可逆转的失血性休克中血流分布的变化。

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时域分析方法

• 1. 时域分析方法的定义：时域（time domain）分析方法主要是从序列自相关的角度揭示时间序列的发展规律。
• 2. 时域分析方法的优点：相当于谱分析方法，它具有理论基础扎实、操作步骤规范、分析结果易于解释等优点。目前它已广泛应用于自然科学和社会科学的各个领域，成为时间序列分析的主流方法。
• 3. 时域分析方法的基本思想：事件的发展通常具有一定的惯性，这种惯性用统计的语言来描述就是序列值之间存在着一定的相关关系，而且这种相关关系具有某种统计规律。我们分析的重点就是寻找这种规律，并拟合出适当的数学模型来描述这种规律，进而利用这个拟合模型来预测序列未来的走势。
• 时域很好理解，就是信号随时间的变化。 频域就是自变量是频率，因变量是信号的幅度，也就是通常所讲的频谱图。频谱图描述了信号的频率结构及频率与该频率信号幅度的关系。 空间域又称图像空间 (image space)。由图像像元组成的空间。在图像空间中以长度 (距离) 为自变量直接对像元值进行处理称为空间域处理。 频率域是由时间域求得的，表示相位随时间的变化；波数域是由空间域得来的，表示相位随空间位置的变化。 将空间 - 时间域进行二维傅里叶变换就得到频率 - 波数域。