Hemodynamic and metabolic concomitants of brain swelling and cerebral edema due to experimental cerebral infarction.

Abstract

✓ Severe cerebral ischemia was produced in 25 baboons by clamping the carotid and vertebral arteries bilaterally for 10 minutes. Cerebral hemodynamics and metabolism were monitored throughout. Cerebral anoxia was less severe in animals in which a marked pressor response occurred due to ischemia of the vasomotor center, and a reversible type of brain swelling was usual. In those with more severe ischemic anoxia, progressive cerebral edema was a pathological entity. Evidence is presented that cerebral edema was caused by loss of autoregulation of cerebral blood flow (CBF) concomitant with hyperemia and an increase of water and chloride content of brain tissue. Cerebral edema began when CBF was reduced during occlusion and progressed for several hours after termination of occlusion. Evidence is adduced that uncoupling of oxidative phosphorylation may be an important concomitant of cerebral edema.