title: Ischemic preconditioning preserves mitochondrial function after global cerebral ischemia in rat hippocampus.
abstract: 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 mm 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.
authors.affiliation: Cerebral Vascular Disease Research Center, Department of Neurology, University of Miami School of Medicine, Miami, Florida, USA.
authors.forename: K R
authors.initials: KR
authors.lastname: Dave
authors.forename: I
authors.initials: I
authors.lastname: Saul
authors.forename: R
authors.initials: R
authors.lastname: Busto
authors.forename: M D
authors.initials: MD
authors.lastname: Ginsberg
authors.forename: T J
authors.initials: TJ
authors.lastname: Sick
authors.forename: M A
authors.initials: MA
authors.lastname: Pérez-Pinzón
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D016923:Cell Death; D003342:Corpus Striatum / Q000378:metabolism; D042967:Electron Transport Complex I; D042963:Electron Transport Complex II; D014450:Electron Transport Complex III / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D019194:Ischemic Preconditioning; D008297:Male; D008928:Mitochondria / Q000201:enzymology*; D009097:Multienzyme Complexes / Q000378:metabolism; D009247:NADH, NADPH Oxidoreductases / Q000378:metabolism; D010088:Oxidoreductases / Q000378:metabolism; D010101:Oxygen Consumption; D051381:Rats; D017208:Rats, Wistar; D013385:Succinate Dehydrogenase / Q000378:metabolism
chemical_list: D005609:Free Radicals; D009097:Multienzyme Complexes; D010088:Oxidoreductases; D042963:Electron Transport Complex II; D013385:Succinate Dehydrogenase; D009247:NADH, NADPH Oxidoreductases; D003576:Electron Transport Complex IV; D042967:Electron Transport Complex I; D014450:Electron Transport Complex III