α-肾上腺素能阻滞对出血后颅内压升高时脑血管反应的影响。

Effect of alpha-adrenergic blockade on the cerebrovascular response to increased intracranial pressure after hemorrhage.

作者信息

Rise I R, Kirkeby O J

机构信息

Institute for Surgical Research, The National Hospital, Oslo, Norway.

出版信息

J Neurosurg. 1998 Sep;89(3):454-9. doi: 10.3171/jns.1998.89.3.0454.

DOI:10.3171/jns.1998.89.3.0454

PMID:9724121

Abstract

OBJECT

In this study the authors tested the hypothesis that hemorrhagic hypotension and high intracranial pressure induce an increase in cerebrovascular resistance that is caused by sympathetic compensatory mechanisms and can be modified by alpha-adrenergic blockade.

METHODS

Continuous measurements of cerebral blood flow were obtained using laser Doppler microprobes placed in the cerebral cortex in anesthetized pigs during induced hemorrhagic hypotension and high cerebrospinal fluid pressure. Eight pigs received 2 mg/kg phentolamine in 10 ml saline, and 13 pigs served as control animals. During high intracranial pressure occurring after blood loss, cerebral perfusion pressure (CPP) (p < 0.01) and cerebral blood flow (p < 0.01) decreased in both groups. Cerebrovascular resistance increased (p < 0.05) in the control group and decreased (p < 0.005) in the phentolamine-treated group. The cerebrovascular resistance was significantly lower in the phentolamine-treated group (p < 0.05) than in the control group. Cerebrovascular resistance increased at lower CPPs in the control group (linear correlation, r = 0.39, p < 0.01) and decreased with decreasing CPP in the phentolamine-treated group (linear correlation, r = 0.76, p < 0.001).

CONCLUSIONS

This study shows that the deleterious effects on cerebral hemodynamics induced by blood loss in combination with high intracranial pressure are inhibited by alpha-adrenergic blockade. This suggests that these responses are caused by alpha-adrenergically mediated cerebral vasoconstriction.

摘要

目的

在本研究中，作者验证了以下假设，即出血性低血压和高颅内压会导致脑血管阻力增加，这是由交感神经代偿机制引起的，并且可以通过α-肾上腺素能阻滞剂进行调节。

方法

在麻醉猪诱导出血性低血压和高脑脊液压力期间，使用置于大脑皮层的激光多普勒微探头连续测量脑血流量。8只猪接受了2mg/kg酚妥拉明（溶于10ml生理盐水中），13只猪作为对照动物。在失血后出现高颅内压期间，两组的脑灌注压（CPP）（p<0.01）和脑血流量（p<0.01）均下降。对照组脑血管阻力增加（p<0.05），酚妥拉明治疗组脑血管阻力下降（p<0.005）。酚妥拉明治疗组的脑血管阻力显著低于对照组（p<0.05）。对照组在较低的CPP时脑血管阻力增加（线性相关，r = 0.39，p<0.01），而酚妥拉明治疗组脑血管阻力随CPP降低而下降（线性相关，r = 0.76，p<0.001）。