Ischemic preconditioning preserves mitochondrial function after global cerebral ischemia in rat hippocampus

Ischemic tolerance in brain develops when sublethal ischemic insults occur before "lethal" cerebral ischemia. Two windows for the induction of toleran ce by ischemic preconditioning (IPC) have been proposed: one that occurs wi thin 1 hour after IPC, and another that occurs 1 or 2 days after IPC. The a uthors tested the hypotheses that IPC would reduce or prevent ischemia-indu ced mitochondrial dysfunction. IPC and ischemia were produced by bilateral carotid occlusions and systemic hypotension (50 turn Hg) for 2 and 10 minut es, respectively. Nonsynaptosomal mitochondria were harvested 24 hours afte r the 10-minute "test" ischemic insult. No significant changes were observe d in the oxygen consumption rates and activities for hippocampal mitochondr ial complexes I to IV between the IPC and sham groups. Twenty-four hours of reperfusion after 10 minutes of global ischemia (without IPC) promoted sig nificant decreases in the oxygen consumption rates in presence of substrate s for complexes I and II compared with the IPC and sham groups. These data suggest that IPC protects the integrity of mitochondrial oxidative phosphor ylation after cerebral ischemia.