Effects of Hemorrhagic and Pharmacologic Hypotension on Cerebral Oxygen Utilization and Blood Flow

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Abstract
Cerebral O2 utilization and blood flow were measured by the washout of 15O2 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%, 55% and 47%, respectively, of control values. There were corresponding decreases in cerebral blood flow to 76% (P < 0.01), 81% (P < 0.05) and 79% (P < 0.01) of control values. When the mean arterial blood pressure was decreased 11% with hemorrhage, autoregulation of the cerebral vasculature was preserved and cerebral O2 utilization increased 10% (P < 0.01). When cerebral autoregulation was lost with acute hemorrhage, cerebral O2 utilization declined 17% (P < 0.05). When cerebral autoregulation was lost with pharmacologic hypotension, cerebral O2 utilization was preserved with trimethaphan and increased 17% (P < 0.05) with sodium nitroprusside. The increase in cerebral O2 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. The mechanism by which circulating catecholamines mediate an increase in cerebral O2 metabolism during hypotension is unclear.