降低动脉血压对狒狒脑血流的影响 | 交感神经系统的影响

Effects of Decreasing Arterial Blood Pressure on Cerebral Blood Flow in the Baboon ：INFLUENCE OF THE SYMPATHETIC NERVOUS SYSTEM

By William Fitch, Eric T. MacKenzie, and A. Murray Harper

Fitch W, MacKenzie ET, Harper AM. Effects of decreasing arterial blood pressure on cerebral blood flow in the baboon. Influence of the sympathetic nervous system. Circ Res. 1975;37(5):550-557. doi:10.1161/01.res.37.5.550

摘要

The influence of the sympathetic nervous system on the cerebral circulatory response to graded reductions in mean arterial blood pressure was studied in anesthetized baboons. Cerebral blood flow was measured by the ¹³³Xe clearance method, and arterial blood pressure was decreased by controlled hemorrhage. In normal baboons, the constancy of cerebral blood flow was maintained until mean arterial blood pressure was approximately 65% of the base-line value; thereafter, cerebral blood flow decreased when arterial blood pressure was reduced. Superior cervical sympathectomy of 2-3 weeks duration did not affect the normal response. In contrast, both acute surgical sympathectomy (cervical trunk division) and a-receptor blockade (1.5 mg/kg of phenoxybenzamine) enhanced the maintenance of cerebral blood flow in the face of hemorrhagic hypotension in that cerebral blood flow did not decrease until mean arterial blood pressure was approximately 35% of the base-line value. The results indicate that the sympathetic nervous system is not involved in the maintenance of cerebral blood flow in the face of a fall in arterial blood pressure. Indeed, the implication is that the sympathicoadrenal discharge accompanying hemorrhagic hypotension is detrimental to, rather than responsible for, cerebral autoregulation.

在麻醉的狒狒身上研究了交感神经系统对平均动脉压逐级降低的脑循环反应的影响。通过 ¹³³Xe 清除法^[1]测量脑血流量，并通过控制失血降低动脉血压。在正常的狒狒中，脑血流一直保持恒定直到平均动脉压约为基线值的 65%；此后，当动脉血压降低时，脑血流减少。颈上交感神经切除术 2-3 周内并不影响其正常反应。相反，急性外科交感神经切除术（颈部主干离断术）和 a 受体阻断术（1.5 mg/kg 苯氧苄胺）都增强了在失血性低血压时脑血流的维持，因为在平均动脉压约为基线值的 35% 之前，脑血流不会减少。结果表明，交感神经系统不参与动脉血压下降时的脑血流维持。事实上，这意味着伴随失血性低血压的交感神经放电不是负责而是不利于脑血流自身调节。

序言

Constancy of cerebral blood flow is maintained in the face of moderate variations in systemic arterial blood pressure (1-4), but the nature of this phenomenon is a matter of some debate. One view is that this mechanism is intrinsic. According to this view, cerebral blood flow is regulated by tissue metabolites (5, 6) or by a myogenic, Bayliss reflex (7-10). If either of these hypotheses is correct, then the blood pressure-flow relationship is a result of autoregulation. The other major view is that the characteristic blood pressure-flow relationship of the cerebral circulation is controlled or modified by the extrinsic innervation of the cerebral vasculature—the neurogenic hypothesis (4, 11, 12).

面对全身动脉血压的适度变化，脑血流保持恒定（1-4），但这一现象的性质还存在一些争议。一种观点认为这种机制是内在的。根据这种观点，脑血流是由组织代谢物（5，6）或由肌源性 —— 贝利斯反射（7-10）调节的。如果这些假说中的任何一个是正确的，那么血压 - 血流关系就是自动调节的结果。另一个主要观点是，脑循环的压力 - 血流关系是由脑血管的外在神经支配所控制或改变的 -- 神经源性假说（4，11，12）。

Some support for the extrinsic mechanism has been taken from morphological studies. Both fluorescent and electron microscopy have confirmed a dual adrenergic and cholinergic innervation of the cerebral circulation (13-15). Sympathetic nerves are the more abundant. The large arteries at the base of the brain receive the densest innervation and the pial vessels are moderately innervated, whereas autonomic nerves have rarely been noted in proximity to the intracerebral arteri- oles. However, under conditions of normocapnia and normotension, the largest fraction of the total vascular resistance in the brain is located in the parenchymal arteriolar vessels (16, 17).

外源性机制的一些支持来自于形态学研究。荧光和电子显微镜都证实了脑循环的肾上腺素和胆碱能的双重支配（13-15）。交感神经是比较丰富的。大脑底部的大动脉接受最密集的神经支配，皮层血管受到适度的神经支配，而自律神经在靠近脑内动脉的地方很少被发现。然而，在正常呼吸和正常血压的条件下，大脑总血管阻力的最大部分位于实质动脉血管中（16，17）。

The present study was undertaken to investigate the effects of surgical (acute and chronic) cervical sympathectomy and of a-receptor blockade (phenoxybenzamine) on the cerebral pressure-flow relationship existing during hypotension induced by hemorrhage.

本研究是为了研究手术（急性和慢性）颈交感神经切除术和 a 受体阻断术（苯氧苄胺）对失血引起的低血压期间大脑的压力 - 血流量关系的影响。

方法

This study was carried out on 31 young baboons (Papio cynocephalus or Papio anubis) weighing 8-12 kg The baboons were anesthetized with phencyclidine (12 mg, im) and sodium thiopental (7.5 mg/kg, iv). The> were then intubated and connected to an intermittent positive-pressure respiratory pump (Starling) which delivered a mixture of 75% N₂O-25% O2 in open circuit Phencyclidine (2 mg, im) and suxamethonium chloride (100 mg, im) were administered at 30-minute intervals Body temperature was controlled (36-38°C) by a heating lamp.

这项研究是在 31 只年轻的狒狒（Papio cynocephalus 或 Papio anubis）身上进行的，体重为 8-12 公斤，用苯环利定（12 毫克，im）和硫喷妥钠（7.5 毫克 / 公斤，iv）对狒狒进行麻醉。然后插管并连接到一个间歇性的正压呼吸泵（Starling），该泵在开路时输送 75% 的 N₂O-25% 的氧气混合物。 苯环利定（2 毫克，im）和氯化琥珀胆碱（100 毫克，im）每隔 30 分钟给药。

The scalp and the temporal muscle were removed frorr the right side of the cranium to ensure that no radioactiv ity was detected from extracranial tissues. The righi common carotid artery and its branches were ther exposed. All of the branches of the right external carotic artery were ligated except the linguofacial trunk, whict was cannulated with a fine polyethylene catheter.

头皮和颞部肌肉被从右侧颅骨上切除，以确保没有从颅外组织中检测到放射性物质。颈总动脉及其分支被暴露出来。除舌面主干外，右颈外动脉的所有分支都被结扎，置入细的聚乙烯导管。

Cerebral blood flow was measured by the intracarotic ¹³³Xe injection method and calculated by the height/area equation (18). A heavily collimated 2.5-cm scintillatior crystal was placed directly over the exposed skull anc angled in such a way that there was no possibility counting radioactivity from the surrounding tissues of the face and the neck. The scintillation crystal was connected to a ratemeter, a sealer, and a direct-writing recorder. The pulse-height analyzer was set at 81 kev with a gate of ±10%, i.e., with a lower limit of 73 kev. This setting effectively prevented any recording of Compton scatter. For each measurement of cerebral blood flow, 0.4-0.8 me of ¹³³Xe, dissolved in approximately 0.5 ml of saline, was injected into the internal carotid artery via the catheter in the linguofacial trunk. The recording was followed for 10 minutes on each occasion.

用颈内注射 ¹³³Xe 的方法测量脑血流，并通过高度 / 面积方程计算（18）。将一个高度准直^[2]的 2.5 厘米闪烁晶体直接放在暴露的颅骨上，其角度不会对面部和颈部周围组织的放射性进行计数。闪烁晶体与一个速率计、一个密封器和一个直接描记的记录器相连。脉冲高度分析仪被设定为 81 千伏，门限为 ±10%，即下限为 73 千伏。这一设置有效地防止任何康普顿散射记录。每次测量脑血流时，将 0.4-0.8 me 的 ¹³³Xe 溶解在大约 0.5ml 的生理盐水中，通过舌面干的导管注入颈内动脉。每次都要进行 10 分钟的记录。

The abdominal aorta was catheterized via the left femoral artery, and arterial blood pressure was monitored with a Statham strain-gauge transducer. During the operative procedure only, a slow intravenous infusion of normal saline was administered via a cannula in the right femoral vein. Arterial carbon dioxide tension (Pco₂) was measured frequently, using a direct-reading electrode system (Radiometer or Corning EEL). In each investigation, ventilation was controlled, and the minute volume was adjusted to maintain an arterial Pco₂ of approximately 40 mm Hg.

通过左股动脉对腹主动脉进行导管检查，用 Statham 应变仪传感器监测动脉血压。仅在手术过程中，通过右股静脉的插管缓慢地静脉注射正常盐水。使用直读电极系统（Radiometer 或 Corning EEL）经常测量动脉二氧化碳分压（Pco₂）。在每次调查中，都会控制通气量，并调整分钟通气量以保持动脉 Pco₂ 约为 40 mmHg。

Arterial blood pressure was lowered by bleeding the baboons into a reservoir, which was heparinized and kept at 37 °C, from a wide-bore catheter inserted in the right femoral artery. The reservoir was connected to a sphygmomanometer and could be held at any desired pressure. The baboons were heparinized during the experiments. Five groups of baboons were studied.

通过将狒狒从插入右股动脉的宽口径导管中放血到储器中来降低动脉血压，储器经过肝素化处理并保持在 37℃。储器与血压计相连，可以保持在任何需要的压力。实验期间对狒狒进行了肝素化处理。共研究了五组狒狒。

GROUP 1: HEMORRHAGIC HYPOTENSION ALONE

第一组：单纯失血性低血压

In ten baboons, stepwise reductions in mean arterial blood pressure were obtained by the intermittent withdrawal of blood. Sufficient blood was removed on each occasion to lower mean arterial blood pressure by approximately 10 mm Hg. This procedure took approximately 10-15 minutes to complete. Once the desired arterial blood pressure had been obtained, the pressure was held constant for 15-20 minutes. Cerebral blood flow was determined after each step reduction in pressure. The same protocol was followed in the other four groups.

在 10 只狒狒中，通过间歇性地抽血来获得平均动脉压的逐步降低。每次都抽出足够的血液，使平均动脉压降低大约 10 mmHg。这个过程大约需要 10-15 分钟来完成。一旦获得了所需的动脉血压，压力将保持恒定 15-20 分钟。在每一步压力降低后，测定脑血流量。其他四组也遵循同样的方案。

GROUP 2: HEMORRHAGIC HYPOTENSION PLUS CHRONIC CERVICAL SYMPATHECTOMY

第二组：失血性低血压加慢性颈交感神经切除术

In five baboons, the right cervical sympathetic trunk was divided in the neck 1 cm below the superior cervical ganglion. After 2-3 weeks, the baboons were subjected to a stepwise hemorrhage as was done in group 1.

在五只狒狒中，右颈交感神经干在颈部上神经节下方 1 厘米处被离断。2-3 周后，像第 1 组那样对狒狒进行分步失血。

GROUP 3: HEMORRHAGIC HYPOTENSION PLUS ACUTE CERVICAL SYMPATHECTOMY

第 3 组：失血性低血压加急性颈交感神经切除术

In six baboons, hemorrhagic hypotension was induced within 60 minutes of the division of the cervical sympathetic trunk on the right side.

在 6 只狒狒中，在右侧的颈部交感神经干被离断后 60 分钟内诱发失血性低血压。

GROUP 4: HEMORRHAGIC HYPOTENSION PLUS PHENOXYBENZAMINE

第四组：失血性低血压加苯氧苄胺

In five baboons, the a-receptor blocking agent phenoxybenzamine was given intravenously at a dose of 1.5 mg/kg. The baboons were then subjected to stepwise hemorrhage.

在五只狒狒中，静脉注射 a 受体阻断剂苯氧苄胺，剂量为 1.5 毫克 / 公斤。然后对狒狒进行分步放血。

GROUP 5: HEMORRHAGIC HYPOTENSION PLUS RETRANSFUSION

第五组：失血性低血压加再输血

In five baboons, an attempt was made to reproduce the protocol used by James et al. (4) by bleeding the baboons (in four stages) until arterial blood pressures between 30 and 40 mm Hg were established, retransfusing the withdrawn blood, and then repeating the hemorrhage. However, in contradistinction to the study by James et al. (4), the cervical sympathetic trunk was not divided after the retransfusion. In each baboon, the period of time at the lowest arterial blood pressure was limited to 20 minutes.

在五只狒狒中，试图重现 James 等人（4）所使用的方案，即给狒狒放血（分四个阶段），直到动脉血压建立在 30 和 40 mmHg 之间，将抽出的血液重新输注，然后重复放血。然而，与 James 等人（4）的研究不同的是，再输血后，颈部交感神经干没有被离断。在每只狒狒中，处于最低动脉血压的时间被限制在 20 分钟。

TREATMENT OF RESULTS Each baboon s resting cerebral blood flow and resting mean arterial blood pressure were used as its own control values and expressed as 100%. Changes in arterial blood pressure and cerebral blood flow in each baboon were expressed as a percent of its own control values. For ease of analysis, the blood flow results in each group of baboons were meaned at 10% intervals of the resting arterial blood pressure (for instance, 79-70 and 69-60% of base-line arterial blood pressure). Student's t-test was used for the statistical comparisons. The only exception to this procedure was in group 5 for which absolute values were used, since two separate hypotensive episodes were carried out in each baboon.

结果处理 每只狒狒的静息脑血流和静息平均动脉压被作为其自身的对照值，并以 100% 表示。每只狒狒的动脉血压和脑血流的变化表示为其自身对照值的百分比。为了便于分析，每组狒狒的血流结果是以静息动脉血压的 10% 的间隔为平均值（例如，基准动脉血压的 79-70% 和 69-60%）。t 检验被用于统计比较。这个过程的唯一例外是在第 5 组，使用了绝对值，因为每个狒狒都有两个单独的低血压发作。

结果

Table 1 shows the base-line values obtained in each of the first four groups studied. The groups mean control values for cerebral blood flow ranged from 44 to 54 ml/100 g min^-1 (average 49 ml/100 g min^-1 ). These values are comparable to those from other studies using the same method of measuring cerebral blood flow and similar conditions of anesthesia (19, 20). The groups mean arterial blood pressures ranged from 91 to 104 mm Hg (average 96 mm Hg). Arterial Pco₂ was consistently held at 40 mm Hg with a maximum standard deviation of 1.8 mm Hg. In each group, there was a decrease in arterial pH on bleeding. The decrease in pH ranged from 0.19 units in group 1 to 0.16 units in group 4. There were no significant differences in the degrees of acidosis which developed in any of the groups studied.

表 1 显示了在所研究的前四组中每组获得的基线值。各组脑血流的平均对照值在 44 至 54 ml/100 g min^-1 之间（平均 49 ml/100 g min^-1 ）。这些数值与其他使用相同方法测量脑血流和类似麻醉条件的研究的数值相当（19，20）。各组的平均动脉压在 91 到 104 mmHg 之间（平均 96 mmHg）。动脉 Pco₂ 始终保持在 40 mmHg，最大标准偏差为 1.8 mmHg。在每组中，失血时动脉 pH 值都有下降。pH 值的下降范围从第 1 组的 0.19 个单位到第 4 组的 0.16 个单位。 在研究的各组中，酸中毒的程度没有明显的差异。

TABLE 1 Base-Line Values for Mean Arterial Blood Pressure (MABP), Mean Cerebral Blood Flow (CBF), Arterial Carbon Dioxide Tension (Pco₂), and pH in Groups 1-4

表 1 第 1-4 组的平均动脉压（MABP）、平均脑血流（CBF）、动脉二氧化碳分压（Pco₂）和 pH 值的基线值

	Group 1	Group 2	Group 3	Group 4
MABP (mm Hg)	92 ± 7	97 ± 5	104 ± 14	91 ± 15
CBF (ml/100 g min-1)	52 ± 11	54 ± 11	45 ± 6	44 ± 10
Pco2 (mm Hg)	39.8 ± 1.8	40.3 ±1.8	40.6 ± 1.2	39.6 ± 1.0
PH	7.41 ±0.03	7.41±0.05	7.40 ± 0.03	7.39 ± 0.03

All values are means ± SD.

GROUP 1: HEMORRHAGIC HYPOTENSION ALONE

第一组：单纯失血性低血压

Prior to the induction of hypotension, base-line values for mean arterial blood pressure ranged from 77 to 103 mm Hg (mean ± SD 92 ± 7 mm Hg) in the individual baboons. At normal levels of Pco₂, mean cerebral blood flow ranged from 40 to 70 ml/100 g min^-1 (mean ± SD 52 ± 11 ml/100 g min^-1). Following the induction of hypotension, mean arterial blood pressure could be reduced to approximately 65-70% of the initial value before there was any decrease in cerebral blood flow, but at mean arterial blood pressures below this value cerebral blood flow was pressure dependent (Fig. 1).

在诱导低血压之前，各个狒狒的平均动脉压基线值在 77 至 103 mmHg 之间（平均 ±SD 92±7 mmHg）。在正常的 Pco₂ 水平下，平均脑血流量从 40 到 70 ml/100 g min^-1（平均 ±SD 52±11 ml/100 g min^-1）。在诱导低血压后，平均动脉压可降至初始值的约 65-70%，然后才有脑血流的减少，但在平均动脉压低于此值时，脑血流是压力依赖的（图 1）。

GROUP 2: HEMORRHAGIC HYPOTENSION PLUS CHRONIC CERVICAL SYMPATHECTOMY

第二组：失血性低血压加慢性颈交感神经切除术

The results obtained in this group as mean arterial blood pressure was decreased progressively were not significantly different from those observed in the baboons subjected to hemorrhagic hypotension alone (group 1) (Fig. 1).

该组在平均动脉压逐渐下降时得到的结果与单独接受失血性低血压的狒狒（第 1 组）观察到的结果没有明显区别（图 1）。

GROUP 3: HEMORRHAGIC HYPOTENSION PLUS ACUTE CERVICAL SYMPATHECTOMY

第 3 组：失血性低血压加急性颈交感神经切除术

In this group of baboons, the pressure-flow plateau persisted to lower levels of mean arterial blood pressure (Fig. 2). Cerebral blood flow remained relatively constant until a mean arterial blood pressure of approximately 40% of the initial value had been reached. At mean arterial blood pressures of 55% and 45% of the initial value, cerebral blood flow was significantly greater (P < 0.05 and P < 0.001, respectively) in the baboons subjected to hemorrhage plus acute surgical sympathectomy than it was in the baboons subjected to hemorrhage alone.

在这组狒狒中，压力 - 流量平台持续到平均动脉压的较低水平（图 2）。在达到平均动脉压约为初始值的 40% 之前，脑血流保持相对稳定。在平均动脉压为初始值的 55% 和 45% 时，接受失血加急性外科交感神经切除术的狒狒的脑血流比单独接受失血的明显增多（分别为 P<0.05 和 P<0.001）。

GROUP 4: HEMORRHAGIC HYPOTENSION PLUS PHENOXYBENZAMINE

第四组：失血性低血压加苯氧苄胺

The administration of phenoxybenzamine (1.5 mg/kg) reduced mean arterial blood pressure, in its own right, from 91 ± 15 (SD) mm Hg to 68 ± 11 mm Hg. Thereafter, the five baboons were subjected to a stepwise hemorrhage.

给予苯氧苄胺（1.5 mg/kg ）后，平均动脉压立刻（未放血）从 91±15（SD） mmHg 降至 68±11 mmHg。此后，这五只狒狒被置于逐步失血的状态下。

As did the baboons subjected to an acute surgical sympathectomy, this group of baboons showed a pressure-flow plateau that persisted to levels of mean arterial blood pressure lower than was the case in the baboons subjected to hemorrhagic hypotension alone (Fig. 3) or in those subjected to chronic cervical sympathectomy. Cerebral blood flow remained relatively steady despite the progressive changes in arterial blood pressure until a mean arterial blood pressure of 35-40% of the initial value had been reached. In fact, cerebral blood flow was significantly greater in this group than it was in those baboons subjected to hemorrhage alone at mean arterial blood pressures of less than 55% of the base-line value (P < 0.05).

与接受急性外科交感神经切除术的狒狒一样，这组狒狒表现出的压力 - 流量平台持续存在对应的平均动脉压低于单独接受失血性低血压的狒狒（图 3）或接受慢性颈交感神经切除术的狒狒的血压。尽管动脉血压在逐渐变化，但脑血流仍然相对稳定，直到平均动脉压达到初始值的 35-40%。事实上，该组的脑血流明显大于那些在平均动脉压低于基线值的 55% 时只接受失血的狒狒（P < 0.05）。

FIGURE 1 Effect of decreasing mean arterial blood pressure on mean cerebral blood flow (CBF) in the baboons subjected to hemorrhagic hypotension alone (solid circles) and those subjected to hemorrhagic hypotension plus chronic cervical sympathectomy (solid triangles). Values shown are means ± SE.

图 1 平均动脉压下降对单独接受失血性低血压的狒狒（实心圆）和接受失血性低血压加慢性颈交感神经切除术的狒狒（实心三角形）的平均脑血流量（CBF）的影响。所示数值为平均值 ±SE。

FIGURE 2 Effect of decreasing mean arterial blood pressure on mean cerebral blood flow (CBF) in the baboons subjected to hemorrhagic hypotension alone (solid circles) and those subjected to hemorrhagic hypotension plus acute cervical sympathectomy (open triangles). Cerebral blood flow at 55% and 45% of the initial value was significantly greater in the baboons subjected to hemorrhage plus an acute surgical sympathectomy (one asterisk = P < 0.05, and three asterisks = P < 0.001). Values are means ± SE.

图 2 单纯失血性低血压（实心圆）和失血性低血压加急性颈交感神经切除术（开放三角形）的狒狒，平均动脉压下降对平均脑血流（CBF）的影响。失血加急性手术交感神经切除的狒狒在初始值的 55% 和 45% 时脑血流量明显更大（ * =P<0.05， *** =P<0.001）。数值为平均值 ±SE。

FIGURE 3 Effect of decreasing mean arterial blood pressure on mean cerebral blood flow (CBF) in the baboons subjected to hemorrhagic hypotension alone (solid circles) and those subjected to hemorrhagic hypotension following the administration of phenoxybenzamine (1.5 mg/kg) {open squares). Cerebral blood flow was significantly greater in the phenoxybenzamine-treated baboons at all mean arterial blood pressures less than 55% of the base-line value (one asterisk = P < 0.05, and two asterisks = P < 0.01). Values are means ± SE.

图 3 平均动脉压下降对单纯失血性低血压的狒狒（实心圆圈）和给予苯氧苄胺（1.5mg/kg）后失血性低血压的狒狒的平均脑血流量（CBF）的影响 {开放方格）。在所有平均动脉压低于基线值的 55% 时，苯氧苄胺处理的狒狒的脑血流量明显更大（ * =P < 0.05， ** =P < 0.01）。数值为平均值 ±SE。

FIGURE 4 Effects of decreasing mean arterial blood pressure on mean cerebral blood flow (CBF) in the baboons subjected to hemorrhagic hypotension alone (solid circles), hemorrhagic hypotension plus chronic cervical sympathectomy (solid triangles), hemorrhagic hypotension plus acute cervical sympathectomy (open triangles), and hemorrhagic hypotension plus chemical sympathectomy (open squares).

图 4 单纯失血性低血压（实心圆）、失血性低血压加慢性颈交感神经切除术（实心三角形）、失血性低血压加急性颈交感神经切除术（开放三角形）和失血性低血压加化学交感神经切除术（开放正方形），平均动脉压下降对狒狒的平均脑血流（CBF）的影响。

Figure 4 summarizes the findings in these four groups of experiments and shows the difference found between the baboons subjected to hemorrhagic hypotension alone and hemorrhage plus chronic sympathectomy on the one hand and the baboons subjected to hemorrhage plus either acute surgical or chemical sympathectomy on the other.

图 4 总结了这四组实验的结果，并显示了一方面接受单独失血性低血压和失血加慢性交感神经切除术的狒狒与另一方面接受失血加急性外科或化学交感神经切除术的狒狒之间发现的差异。

GROUP 5: HEMORRHAGIC HYPOTENSION PLUS RETRANSFUSION

第五组：失血性低血压加再输血

First Hemorrhage.—As mean arterial blood pressure was reduced in steps from 86 ± 9 (SD) mm Hg to an average of 31 ± 1 mm Hg (Fig. 5), mean cerebral blood flow changed in a manner similar to that observed in the baboons previously subjected to hemorrhagic hypotension alone. Although there were only four steps in the arterial blood pressure decrease in this particular group of baboons, the pressure-flow plateau appeared to persist to levels of mean arterial blood pressure similar to those observed in the other baboons subjected to hemorrhage alone, namely to 65-70% of the initial value.

第一次失血。随着平均动脉压从 86±9（SD）mmHg 逐级降低到平均 31±1mmHg（图 5），平均脑血流的变化方式与之前单独接受失血性低血压的狒狒所观察到的相似。尽管在这组特定的狒狒中，动脉血压下降只有四个台阶，但压力 - 流量平台持续到平均动脉压的水平似乎与其他单独遭受失血的狒狒中观察到的相似，即达到初始值的 65-70%。

Second Hemorrhage.—The mean arterial blood pressure was held at the level gained following retransfusion for 20 minutes prior to the measurement of cerebral blood flow. Following the retransfusion of the blood removed during the first period of blood loss, mean cerebral blood flow was significantly greater than the value obtained at the start of the first period of hypotension (Fig. 5). The base-line arterial Pco₂ was 40.1 ± 2.3 (SD) mm Hg before retransfusion and 41.4 ± 1.3 mm Hg thereafter. This small and insignificant (P > 0.20) rise in Pco₂ is not great enough to explain the very considerable rise in cerebral blood flow following retransfusion.

第二次失血：在测量脑血流之前，平均动脉压被保持在再输血后获得的水平上 20 分钟。在重新输完第一次失血期间取出的血液后，平均脑血流量明显大于第一次低血压开始时的数值（图 5）。再输血前的动脉 Pco₂ 基线为 40.1±2.3（SD）mmHg，此后为 41.4±1.3mmHg。Pco₂ 的这一微小而不明显的上升（P>0.20）不足以解释再输血后脑血流量的大幅上升。

FIGURE 5 Comparison of the effect of decreasing mean arterial blood pressure on mean cerebral blood flow (CBF) during the first period of hemorrhage (solid circles) and the second period of hemorrhage, i.e., following retransfusion (solid diamonds). Cerebral blood flow was significantly higher at each level of mean arterial blood pressure except the lowest level after retransfusion (one asterisk = P < 0.05, two asterisks = P < 0.01, and three asterisks = P < 0.001). Values are means ± SE.

图 5 比较平均动脉压下降对平均脑血流（CBF）在第一次失血期（实心圆圈）和第二次失血期，即再输血后（实心菱形）的影响。除再输血后的最低水平外，每个水平的平均动脉压的脑血流都明显升高（ * =P<0.05， ** =P<0.01， *** =P<0.001）。数值为平均值 ±SE。

As the mean arterial blood pressure was decreased in steps for the second time, at arterial blood pressure values insignificantly different (P > 0.30) from those pertaining to the first hemorrhage and at normal levels of Pco₂, the mean cerebral blood flow was significantly greater at each pressure step than it had been during the first period of hemorrhage with the exception of the lowest arterial blood pressure level (Fig. 5). In addition, as mean arterial blood pressure was reduced progressively, mean cerebral blood flow decreased concomitantly: in other words, following retransfusion there was no pressure-flow plateau (Fig. 5). The linear correlation coefficient for mean cerebral blood flow against mean arterial blood pressure during this second hemorrhage was r = 0.79 (P < 0.001), indicating that flow was pressure dependent during the second hemorrhage.

当平均动脉压第二次逐级下降时，在与第一次失血相关的动脉血压值无明显差异（P>0.30）且 Pco₂ 水平正常的情况下，除最低动脉血压水平外，每个压力阶梯的平均脑血流量都明显大于第一次失血期间（图 5）。此外，随着平均动脉压的逐渐降低，平均脑血流也随之减少：换句话说，再输血后，没有压力 - 血流平台（图 5）。在第二次失血期间，平均脑血流与平均动脉压的线性相关系数为 r=0.79（P<0.001），表明在第二次失血期间血流与压力有关。

讨论

The purpose of the present study was to determine what influence, if any, the sympathetic nervous system had over the response of the cerebral circulation to induced hemorrhagic hypotension.

本研究的目的是确定交感神经系统对诱发失血性低血压的脑循环反应有什么影响（如果有的话）。

GROUP 1: HEMORRHAGIC HYPOTENSION ALONE

第 1 组：单纯失血性低血压

The lower limit of autoregulation found in the hemorrhagic hypotension group was in close agreement with that found in other studies in which hypotension has been induced by bleeding both in dogs (2, 3) and in primates (4, 21).

失血性低血压组中发现的自动调节的下限与其他研究中发现的接近一致，这些研究中的低血压是由狗（2，3）和灵长类动物（4，21）的失血引起的。

GROUP 2: HEMORRHAGIC HYPOTENSION PLUS CHRONIC CERVICAL SYMPATHECTOMY

第二组：失血性低血压加慢性颈交感神经切除术

In this group, the lower limit of autoregulation was again approximately 65 mm Hg. This value is consistent with that from the experiments of Waltz et al. (22) who studied cortical blood flow and pial vessel diameter in cats with chronic unilateral denervation of the cerebral vasculature. No side-to-side differences were noted in their study. When Eklbf et al. (21) used the ¹³³Xe clearance techniques in rhesus monkeys, they failed to identify any difference in the response to induced hemorrhagic hypotension between normal monkeys and monkeys with prior excision of the superior cervical ganglia.

在这组中，自动调节的下限又是大约 65 mmHg。这个数值与 Waltz 等人（22）的实验一致，他们研究了慢性单侧脑血管神经支配的猫的皮质血流和皮层血管直径。在他们的研究中没有注意到任何差异。当 Eklbf 等人（21）在恒河猴中使用 ¹³³Xe 清除技术时，他们未能发现正常猴子和事先切除颈上神经节的猴子对诱发失血性低血压的反应有任何差异。

GROUP 3: HEMORRHAGIC HYPOTENSION PLUS ACUTE CERVICAL SYMPATHECTOMY

第 3 组：失血性低血压加急性颈交感神经切除术

Various anatomical studies have shown that the superior cervical ganglia are the trophic centers for the adrenergic fibers that innervate the cerebral vessels (23-26). The fibers from one ganglion are distributed to the vessels of the ipsilateral hemisphere, and there is no overlapping. Thus, it would seem that either superior cervical ganglionectomy or cervical trunk division should effectively ablate the adrenergic pathways to the majority of vessels in the cerebral hemisphere from which blood flow is measured.

各种解剖学研究表明，颈上神经节是支配脑血管的肾上腺素能纤维的营养中心（23-26）。来自一个神经节的纤维分布在同侧半球的血管中，没有重叠。因此，无论是颈上神经节切除术还是颈神经干离断术，似乎都应该有效地消减大脑半球大多数血管的肾上腺素能通路，包含测量血流量的血管。

To our knowledge, there has only been one previous study of the effects of acute sympathectomy on cerebral autoregulation: that of James and his co-workers (4). Their findings differ from those of the present report on the following points. In the first instance, James et al. (4) found that cerebral blood flow was significantly elevated at normotension following acute sympathectomy, whereas we found no such difference. Second, James et al. (4) stated: "After sympathectomy . . . blood flow in gray matter fell steadily as mean arterial pressure was reduced in steps from 130 down to 70 mm Hg." Possible reasons for the discrepancies between the studies of James and his colleagues (4) and the present investigation will be discussed later.

据我们所知，以前只有一项关于急性交感神经切除术对大脑自动调节的影响的研究：詹姆斯和他的同事的研究（4）。他们的研究结果与本报告的研究结果有以下几点不同。首先，James 等人（4）发现在急性交感神经切除术后，脑血流在常压下明显升高，而我们没有发现这种差异。第二，James 等人（4）说。"交感神经切除术后...... 随着平均动脉压从 130 mmHg 逐级降低到 70 mmHg，灰质的血流量稳步下降"。詹姆斯和他的同事（4）的研究与本调查之间存在差异的可能原因将在后面讨论。

The concentration of norepinephrine in pial vessels decreases to almost zero within 2 weeks following either cervical sympathetic trunk division or superior cervical ganglionectomy; this change correlates with the destruction of the postganglionic adrenergic neurons (27). A plausible explanation for the difference between the effects of acute and chronic sympathectomy on cerebral autoregulation could be the phenomenon of denervation hypersensitivity. Denervation hypersensitivity reaches a maximum about 2 weeks after sympathectomy (28). In conditions of stress, such as extreme hemorrhagic shock, there is a considerable discharge of catecholamines from the suprarenal medullae. These circulating amines could then interact with the sensitized a-adrenoreceptors, resulting in a pressure-flow pattern in the chronically sympathectomized animal similar to that in the normal animal.

颈交感神经干离断术或颈上神经节切除术后 2 周内，小脑血管中去甲肾上腺素的浓度几乎降至零；这一变化与节后肾上腺素能神经元的破坏有关（27）。急性和慢性交感神经切除术对大脑自律性影响的不同，一个合理的解释可能是去神经的超敏现象。交感神经切除术后 2 周左右，神经支配超敏性达到最大值（28）。在应激条件下，如极度失血性休克，肾上腺髓质会有大量的儿茶酚胺排出。这些循环胺可能与敏感的 a - 肾上腺素受体相互作用，导致长期交感神经切除的动物出现与正常动物类似的压力 - 流量模式。

GROUP 4: HEMORRHAGIC HYPOTENSION PLUS PHENOXYBENZAMINE

第 4 组：失血性低血压加苯氧苄胺

Alpha-receptor blockade has been studied previously in humans (29, 30). The first of these studies showed that phentolamine does not affect the normal cerebral response to arterial blood pressure manipulations, although, on the average, arterial blood pressure was lowered by only 17%. Therefore, no statement could be made about the effects of a-receptor blockade on the lower limit of autoregulation. In the investigation by Meyer s group (30), the effects of intracarotid administration of phenoxybenzamine on the relationship of arterial blood pressure and cerebral blood flow were studied in a Circulation Research, Vol. 37, November, 1975 series of patients with impaired autoregulation. This impairment was associated with various degrees of cerebral ischemia and infarction. Their findings indicated an improved ability of the cerebral vessels to dilate during induced hypotension following a-receptor blockade.

以前曾在人类中研究过 α- 受体阻断的方法（29，30）。其中第一项研究表明，酚妥拉明并不影响大脑对动脉血压操作的正常反应，尽管平均而言，动脉血压只降低了 17%。因此，不能就 a 受体阻断对自动调节下限的影响做出说明。在 Meyer 小组（30）的调查中，在《循环研究》第 37 卷，1975 年 11 月，一系列自动调节功能受损的病人中，研究了颈内注射苯氧苄胺对动脉血压和脑血流关系的影响。这种损害与不同程度的脑缺血和梗塞有关。他们的研究结果表明，在 a 受体阻断后的诱导性低血压期间，脑血管的扩张能力有所提高。

GROUP 5: HEMORRHAGIC HYPOTENSION PLUS RETRANSFUSION

第 5 组：失血性低血压加再输血

The severe, although not extreme, hypotension induced on the first hemorrhage was followed by a progressive reduction in cerebral blood flow when arterial blood pressure was decreased for the second time. The probable reason for the observed increase in blood flow at normal blood pressures following hypotension and retransfusion is the cerebral hypoxia accompanying the first arterial blood pressure reduction. This posthypotensive loss of the usual pressure-flow relationship (and cerebral hyperemia at normotension) has been noted in both dogs (31) and primates (32), although in the primate study the duration of the hypotensive episode was more extreme. Other studies have confirmed this posthypoxic loss of the pressure-flow relationship, which may persist for several hours following the insult in both stagnant and hypoxic hypoxia (33, 34). Lassen (35) was the first to hypothesize that this phenomenon, which he termed "luxury perfusion," is due to the acute cerebral metabolic acidosis that accompanies hypoxia. Later studies have confirmed this concept: the reactive hyperemia after cerebral hypoxia is related to a tissue lactic acidosis (36, 37).

第一次失血时诱发的严重低血压虽然不是极端的，但当动脉血压第二次降低时，脑血流量逐渐减少。低血压和再输血后在正常血压下观察到的血流量增加的可能原因是伴随着第一次动脉血压降低的脑缺氧。在狗（31）和灵长类动物（32）中都注意到了这种降压后失去通常的压力 - 流量关系（和正常血压下的脑充血），尽管在灵长类动物的研究中，低血压发作的时间更为极端。其他研究也证实了这种缺氧后压力 - 流量关系的丧失，在瘀滞性缺氧和缺氧性缺氧的情况下，这种关系可能会持续数小时（33，34）。Lassen（35）是第一个假设这种现象的人，他称之为 "奢侈灌注"，是由于伴随缺氧的急性脑代谢性酸中毒造成的。后来的研究证实了这一概念：脑缺氧后的反应性充血与组织乳酸酸中毒有关（36，37）。

In all of the groups, there was a decrease in arterial pH, which was approximately the same in each group. However, it has been shown that systemic metabolic acidosis, even of a greater degree, will not affect cerebral blood flow as long as the arterial Pco₂ remains constant (38).

在所有的组别中，动脉 pH 值都有下降，每组都大致相同。然而，已经证明，只要动脉 Pco₂ 保持恒定，全身代谢性酸中毒，即使程度较重，也不会影响脑血流（38）。

A relatively constant cerebral blood flow was preserved to a lower absolute level of mean arterial blood pressure following both acute surgical sympathectomy and pharmacological adrenoreceptor blockade in these studies. Accordingly, we can offer little support for the neurogenic hypothesis of the nature of autoregulation (4, 12). Indeed, the implication of this study is that the sympathicoadrenal discharge that accompanies hemorrhagic hypotension is detrimental to, rather than responsible for, cerebral autoregulation.

在这些研究中，急性外科交感神经切除术和药物性肾上腺素受体阻断术后，相对恒定的脑血流被保留到较低的平均动脉压绝对水平。因此，我们可以为自律调节性质的神经源性假说提供很少的支持（4，12）。事实上，这项研究的含义是，伴随着失血性低血压的交感神经放电不利于，而不是负责脑部自动调节。

Similar situations occur in other organs, but to a greater extent. Using the kidney as an example, blood pressure reduction by either ganglionic blockade or graded occlusion of the abdominal aorta proximal to the renal arteries results in a relative constancy of renal blood flow over a wide range of arterial blood pressures, the lower limit being approximately 65 mm Hg in dogs. However, hemorrhagic hypotension alone results in a linear pressure-flow relationship. The conclusion is that sympathetic activity plays a major role in the vasoconstriction of the renal cortex which follows hemorrhage. This hypothesis has been confirmed in the kidney, since maintenance of a constant flow following bleeding is restored when a ganglionic blocking agent is given (39). It is also pertinent to note that the pressure-flow relationship in the kidney and in other tissues is now recognized as an intrinsic mechanism. This intrinsic mechanism has been termed "autoregulation" which is defined as the inherent ability of an organ or tissue to maintain a relatively constant blood flow in the face of moderate changes in perfusion pressure. There is now good evidence indicating that the normal response of the cerebral circulation to changes in arterial blood pressure can be properly termed autoregulation. (1) Acute sympathectomy does not impair autoregulation; in fact, in the present study, it improved it. Neither in this study nor in others does chronic sympathectomy affect autoregulation. (2) Autoregulation has been noted following the administration of ganglionic blocking agents, such as trimetaphan, which interrupt all autonomic pathways both in man (40) and in baboons (41). (3) Autoregulation is still present when cerebral perfusion pressure is lowered by increasing cerebrospinal fluid pressure rather than by lowering arterial blood pressure (6, 42). (4) Symon s group (10) has shown that an increase in pressure in an artery on the surface of the cortex results in a rapid autoregulatory change as seen by constant venous drainage from the area of cortex supplied by that artery.

类似的情况也发生在其他器官，但程度更深。以肾脏为例，通过神经节阻断或肾动脉近端腹主动脉的分级闭塞来降低血压，导致肾脏血流在很大的动脉血压范围内相对恒定，狗的下限大约是 65 mmHg。然而，仅失血性低血压就会导致压力 - 流量的线性关系。结论是交感神经活动在失血后肾皮质的血管收缩中起主要作用。这一假设已在肾脏中得到证实，因为当给予神经节阻断剂时，失血后恒定流量的维持就会恢复（39）。同样需要注意的是，肾脏和其他组织中的压力 - 流量关系现在被认为是一种内在的机制。这种内在机制被称为 "自动调节"，它被定义为一个器官或组织在面对适度的灌注压力变化时保持相对稳定的血流的内在能力。现在有很好的证据表明，脑循环对动脉血压变化的正常反应可以适当地称为自动调节。(1）急性交感神经切除术并不损害自动调节功能；事实上，在本研究中，它改善了自动调节功能。在本研究或其他研究中，慢性交感神经切除术都不影响自动调节。(2) 在使用神经节阻断剂，如曲美他芬，中断了人（40）和狒狒（41）的所有自律神经通路后，已经注意到自律神经的调节。(3) 当通过增加脑脊液压力而不是降低动脉血压来降低脑灌注压时，自动调节仍然存在（6，42）。(4) Symon 小组 (10) 已经证明，大脑皮层表面的动脉压力增加会导致快速的自动调节变化，这可以从该动脉所供应的皮层区域的持续静脉引流中看出。

The observation in the present study that areceptor blockade or surgical sympathectomy actually improved autoregulation can best be explained by the "dual control" hypothesis advanced by Harper and his colleagues (19). They observed that, whereas cervical sympathetic stimulation and norepinephrine have minimum effects on cerebral blood flow at normal resting conditions, there is a pronounced fall in cerebral blood flow when the cerebral vessels are already dilated during hypercapnia. They suggested that the cerebral circulation can be described as two resistances in series: the extraparenchymal vessels are influenced by the autonomic nervous system, but the intraparenchymal vessels are regulated by intrinsic metabolic or myogenic mechanisms. This theory has been sup- ported by a number of other more recent investigations (43-47). The intraparenchymal resistance vessels are the site of the principal autoregulatory adaptation to variations in arterial blood pressure (10, 17, 48). Before these vessels are near maximum dilation, that is, at the lower limit of autoregulation, it might be expected that any adrenergic vasoconstriction of the large arteries at the base of the brain would be met by a compensatory vasodilation of the intraparenchymal arterioles. When the lower limit of autoregulation is exceeded and the intraparenchymal vessels are already dilated, then any adrenergic influence on the larger, extraparenchymal arteries would tend to compromise cerebral blood flow. Evidence for this hypothesis can be adduced from angiographic studies in baboons which demonstrate that in hemorrhagic shock there is a constriction (not autoregulatory dilation) of the arteries at the base of the brain proportional to the degree of hypotension (49). Further evidence obtained from in vitro studies indicates that there is a shift of the flow-limiting resistance from the small arterioles to the larger arteries at the lower limit of autoregulation (J. K. Farrar, personal communication).

本研究中观察到的受体阻断或外科交感神经切除术实际上改善了自动调节，这可以用 Harper 和他的同事（19）提出的 "双重控制" 假说来解释。他们观察到，在正常休息状态下，颈部交感神经刺激和去甲肾上腺素对脑血流的影响最小，而在高碳酸血症时，脑血管已经扩张，脑血流会明显下降。他们提出，脑循环可以被描述为两个串联的电阻：实质外血管受自主神经系统的影响，但实质内血管受内在的代谢或肌源性机制的调节。这一理论已被其他一些最近的调查所证实（43-47）。实质内阻力血管是对动脉血压变化进行自我调节的主要部位（10, 17, 48）。在这些血管接近最大扩张之前，也就是在自动调节的下限时，可以预期，脑底部大动脉的任何肾上腺素能的血管收缩都会被实质内动脉血管的补偿性扩张所满足。当超过了自动调节的下限，并且实质内血管已经扩张，那么任何对较大的实质外动脉的肾上腺素影响都会损害脑血流。这一假设的证据可以从狒狒的血管造影研究中引出，该研究表明在失血性休克中，脑底动脉的收缩（而不是自动调节性扩张）与低血压程度成正比（49）。从体外研究得到的进一步证据表明，在自动调节的下限，限流阻力从小动脉血管转移到大动脉（J. K. Farrar，个人通讯）。

The current investigation gives no indication as to the functional significance of the sympathetic nerves that innervate the cerebral vessels. It could be that they are involved in the regulation of cerebral blood volume (50) or in the cerebrovascular mediation of the Cushing response (51). Thus, there exists the possibility that adrenergic nerves are important in the cerebral responses to changes in intracranial pressure.

目前的调查没有说明支配脑血管的交感神经的功能意义。可能是它们参与了脑血容量的调节（50）或参与了库欣反应的脑血管调解（51）。因此，存在着肾上腺素能神经在大脑对颅内压变化的反应中很重要的可能性。

Therefore, we believe that our results demonstrate that cerebral autoregulation is not controlled by the sympathetic nervous system. However, under conditions of hemorrhagic hypotension alone, sympathetic constriction of the extraparenchymal cerebral vessels decreases the possible range of autoregulation in the anesthetized baboon. A clinical implication of this work is that the cerebral circulation is at greater risk during a state of hemorrhagic or cardiogenic shock than it is if the hypotension is induced by autonomic blocking agents.

因此，我们认为，我们的结果表明，大脑的自动调节功能不受交感神经系统的控制。然而，仅在失血性低血压的条件下，交感神经对实质外脑血管的收缩降低了麻醉狒狒的自动调节的可能范围。这项工作的一个临床意义是，在失血性或心源性休克状态比自主神经阻断剂引起的低血压导致脑循环受损的风险更大。

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1. ¹³³Xenon(¹³³Xe，氙 - 133) 为脂溶性惰性气体，进入血循环后能自由通过正常血脑屏障，通过弥散方式被脑细胞摄取，继而迅速从脑组织清除，其在脑组织的清除率与 rCBF 成正相关，测定各区域脑组织 ¹³³Xe 的清除率，可以计算 rCBF 和 CBF。¹³³Xe 测定的 CBF 参考值为 67.83±8.95ml/100g/min，左右脑 rCBF 相近。 ↩︎

2. 准直通俗说就是保持光线之间是平行的。 ↩︎