Delayed hypometabolism induced by bilateral ischemia in the gerbil: regional metabolic thresholds.

The common carotid arteries were occluded in gerbils for 5 min and the metabolic rate was estimated by measuring the loss of high-energy phosphate equivalents at 4 days of reperfusion in the cerebral cortex, hippocampus, and striatum. Metabolites values at 4 days of reperfusion were not different from those of controls with the exception of glycogen, which was significantly elevated in the hippocampus. The metabolic rate, as determined by the "closed-box" method at 4 days of reflow, was decreased by more than 50% in all three regions after 5 min of bilateral ischemia. The ischemic time necessary to elicit the hypometabolic response at 4 days of reflow was 2, 3 and 4 min for the striatum, hippocampus, and cortex, respectively. It is suggested that delayed postischemic hypometabolism may be a component of an adaptive process which counteracts, to varying degrees, the deleterious effects of ischemia depending on the region examined.