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

K. R. Dave, I. Saul, R. Busto, M. D. Ginsberg, T. J. Sick, M. A. Pérez-Pinzón

Research output: Contribution to journalArticlepeer-review

91 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1401-1410
Number of pages10
JournalJournal of Cerebral Blood Flow and Metabolism
Volume21
Issue number12
DOIs
StatePublished - 2001

Keywords

  • Anoxia
  • Cell death
  • Free radicals
  • Tolerance

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)
  • Endocrinology, Diabetes and Metabolism

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