Journal
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
Volume 21, Issue 12, Pages 1401-1410Publisher
SAGE PUBLICATIONS INC
DOI: 10.1097/00004647-200112000-00004
Keywords
anoxia; cell death; free radicals; tolerance
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Funding
- NINDS NIH HHS [NS38276, NS30037, 3P01NS05820-35A1, 5R29NS34773-04] Funding Source: Medline
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Ischemic tolerance in brain develops when sublethal ischemic insults occur before lethal cerebral ischemia. Two windows for the induction of tolerance by ischemic preconditioning (IPC) have been proposed: one that occurs within 1 hour after IPC, and another that occurs 1 or 2 days after IPC. The authors tested the hypotheses that IPC would reduce or prevent ischemia-induced mitochondrial dysfunction. IPC and ischemia were produced by bilateral carotid occlusions and systemic hypotension (50 turn Hg) for 2 and 10 minutes, respectively. Nonsynaptosomal mitochondria were harvested 24 hours after the 10-minute test ischemic insult. No significant changes were observed in the oxygen consumption rates and activities for hippocampal mitochondrial complexes I to IV between the IPC and sham groups. Twenty-four hours of reperfusion after 10 minutes of global ischemia (without IPC) promoted significant decreases in the oxygen consumption rates in presence of substrates for complexes I and II compared with the IPC and sham groups. These data suggest that IPC protects the integrity of mitochondrial oxidative phosphorylation after cerebral ischemia.
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