Trewby P N, Hanid M A, Mackenzie R L, Mellon P J, Williams R
Gut. 1978 Nov;19(11):999-1005. doi: 10.1136/gut.19.11.999.
The effects of arterial hypotension and a raised intracranial pressure on cerebral blood flow (CBF) have been investigated in an animal model of hepatic failure. Arterial hypotension was associated with a fall in CBF in the animals with liver failure but not in the controls. Significant differences in mean CBF between the two groups of animals could be demonstrated when the systolic blood pressure was in the 30-60, 60-90, and 90-120 mmHg range, but not in the 120-150 mmHg range. A raised intracranial pressure also resulted in a fall in CBF in the animals with liver failure, and a significant difference could be demonstrated between the two groups when the intracranial pressure was in the 20-40 mmHg range but not in the 0-20 mmHg range. Furthermore, in the animals with liver failure the cerebral metabolic rate for oxygen (CMRO(2)) fell as the CBF fell, there being a highly significant correlation between these two parameters. In the controls no such relation existed. Treatment with neither charcoal haemoperfusion nor high dose corticosteroids affected the fall in cerebral blood flow that occurred during arterial hypotension in the animals with liver failure. Corticosteroids, however, did reduce the fall in cerebral blood flow associated with a high intracranial pressure. These results suggest a disruption of the cerebral circulatory responses in hepatic failure. They also raise the possibility that CMRO(2) and cerebral blood flow may be maintained at normal levels in hepatic encephalopathy if cerebral oedema and arterial hypotension can be prevented.
在肝衰竭动物模型中,研究了动脉低血压和颅内压升高对脑血流量(CBF)的影响。在肝衰竭动物中,动脉低血压与CBF下降有关,而对照组则不然。当收缩压在30 - 60 mmHg、60 - 90 mmHg和90 - 120 mmHg范围内时,两组动物的平均CBF存在显著差异,但在120 - 150 mmHg范围内则无差异。颅内压升高也导致肝衰竭动物的CBF下降,当颅内压在20 - 40 mmHg范围内时,两组之间存在显著差异,但在0 - 20 mmHg范围内则无差异。此外,在肝衰竭动物中,随着CBF下降,脑氧代谢率(CMRO₂)也下降,这两个参数之间存在高度显著的相关性。在对照组中不存在这种关系。用活性炭血液灌注或高剂量皮质类固醇治疗均未影响肝衰竭动物在动脉低血压期间发生的脑血流量下降。然而,皮质类固醇确实减少了与高颅内压相关的脑血流量下降。这些结果表明肝衰竭时脑循环反应受到破坏。它们还提出,如果能预防脑水肿和动脉低血压,在肝性脑病中CMRO₂和脑血流量可能维持在正常水平。