Endotoxin pretreatment increases endogenous myocardial catalase activity and decreases ischemia-reperfusion injury of isolated rat hearts

J. M. Brown, M. A. Grosso, L. S. Terada, G. J R Whitman, A. Banerjee, C. W. White, A. H. Harken, J. E. Repine

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254 Scopus citations

Abstract

Hearts isolated from rats pretreated 24 hr before with endotoxin had increased myocardial catalase activity, but the same superoxide dismutase, gluthatione peroxidase, gluthatione reductase, and glucose-6-phosphate dehydrogenase activities, as hearts from untreated rats. Hearts isolated from rats pretreated with endotoxin 24 hr before also had increased myocardial function (decreased injury) after ischemia and reperfusion (Langendorff apparatus, 37°C), as assessed by measurement of ventricular developed pressure, contractility (+dP/dt), and relaxation rate (-dP/dt), compared to control hearts. In contrast, hearts isolated from rats pretreated with endotoxin 1 hr before isolation or hearts perfused with endotoxin did not have increased catalase activity or decreased injury following ischemia and reperfusion. Aminotriazole pretreatment prevented increases in myocardial catalase activity and myocardial function after ischemia-reperfusion in hearts from endotoxin-pretreated rats. The results suggest that endotoxin pretreatment decreases cardiac ischemia-reperfusion injury and that increases in endogenous myocardial catalase activity contribute to protection.

Original languageEnglish (US)
Pages (from-to)2516-2520
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume86
Issue number7
DOIs
StatePublished - 1989

ASJC Scopus subject areas

  • General

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