Abstract
Cerebral ischemia provokes sequential changes that include EEG suppression, anoxic depolarization (AD) with maximal increases in extracellular potassium ion activity (K+o), and anoxia with maximal decreases in tissue oxygen tension (tPO2) and increases in the reduction/oxidation (redox) ratios of the mitochondrial electron transport carriers. Studies were directed toward relationships among these events during cerebral ischemia (“four-vessel occlusion model”) in pentobarbital anesthetized rats. Results demonstrate that EEG suppression and anoxic depolarization do not occur as a simple function of progressive oxygen decline during cerebral ischemia. Rates of K+ elevation, tPO2 decline, and cytochrome a,a3 reduction were decreased in the immediate period following EEG suppression. Latency to EEG suppression was inversely correlated with latency to maximal cytochrome reduction. In contrast, AD was associated with increased rates of tPO2 decline and cytochrome a,a3 reduction. Latency to AD was related to latency of subsequent maximal cytochrome a,a3 reduction. These data suggest that EEG suppression spares oxygen while AD accelerates the progression to energy failure by accelerating the decline in oxygen stores in brain following global ischemia.
