Endotoxin pretreatment increases endogenous myocardial catalase activity and decreases ischemia-reperfusion injury of isolated rat hearts.
- 1 April 1989
- journal article
- research article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 86 (7), 2516-2520
- https://doi.org/10.1073/pnas.86.7.2516
Abstract
Hearts isolated from rats pretreated 24 hr before with endotoxin had increased myocardial catalase activity, but the same superoxide dismutase, glutathione peroxidase, glutathione 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 degrees 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.This publication has 12 references indexed in Scilit:
- Heat-shock response is associated with enhanced postischemic ventricular recovery.Circulation Research, 1988
- Xanthine oxidase produces hydrogen peroxide which contributes to reperfusion injury of ischemic, isolated, perfused rat hearts.JCI Insight, 1988
- Cachectin/tumor necrosis factor regulates hepatic acute-phase gene expression.JCI Insight, 1986
- Myocardial reperfusion: a double-edged sword?JCI Insight, 1985
- Reactive oxygen species may cause myocardial reperfusion injuryBiochemical and Biophysical Research Communications, 1985
- Oxygen-Derived Free Radicals in Postischemic Tissue InjuryNew England Journal of Medicine, 1985
- Interleukin-1 and the Pathogenesis of the Acute-Phase ResponseNew England Journal of Medicine, 1984
- Protection from Oxygen Toxicity with EndotoxinJCI Insight, 1980
- [41] Preparation and assay of superioxide dismutasesMethods in enzymology, 1978
- The Statistical MethodNew England Journal of Medicine, 1966