Effects of cerebral oedema and arterial hypotension on cerebral blood flow in an animal model of hepatic failure

Abstract

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 (CMRO2) 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 hemoperfusion 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 CMRO2 and cerebral blood flow may be maintained at normal levels in hepatic encephalopathy if cerebral edema and arterial hypotension can be prevented.