Effects of hemorrhagic and pharmacologic hypotension on cerebral oxygen utilization and blood flow.

Cerebral oxygen utilization and blood flow were measured by the washout of oxygen-15 isotopes injected into the internal carotid artery in baboons during hypotension produced by acute hemorrhage, trimethaphan, and sodium nitroprusside. Acute hemorrhage, trimethaphan, and sodium nitroprusside lowered the mean arterial blood pressure to 52 per cent, 55 per cent, and 47 per cent, respectively, of control values. There were corresponding decreases in cerebral blood flow to 76 per cent (P less than 0.01), 81 per cent (P less than 0.05), and 79 per cent (P less than 0.01) of control values. When the mean arterial blood pressure was decreased 11 per cent with hemorrhage, auto-regulation of the cerebral vasculature was preserved and cerebral oxygen utilization increased 10 per cent (P less than 0.01). When cerebral autoregulation was lost with acute hemorrhage, cerebral oxygen utilization declined 17 per cent (P less than 0.05). When cerebral autoregulation was lost with pharmacologic hypotension, cerebral oxygen utilization was preserved with trimethaphan and increased 17 per cent (P less than 0.05) with sodium nitroprusside. The increase in cerebral oxygen utilization seen with sodium nitroprusside and hemorrhagic (autoregulation preserved) hypotension may be due to stimulation of the sympathetic nervous system with release of circulating catecholamines. However, the mechanism by which circulating catecholamines mediate an increase in cerebral oxygen metabolism during hypotension is not clear.