Why the study?
Does exogenous glutathione reduce infarct size in a canine model of permanent myocardial ischaemia without reperfusion?
Does exogenous glutathione reduce infarct size in a canine model of permanent myocardial ischaemia without reperfusion?
Exogenous glutathione provides only minor, transient benefits in reducing infarct size during permanent myocardial ischemia without reperfusion in a canine model.
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Transient reduction in canine permanent ischemia does not support clinical translation; leaves open efficacy in reperfused models.
The present study was to evaluate the effect of exogenous glutathione on myocardial damage resulting from permanent (no reperfusion) coronary ligation (3 or 6 h) in anaesthetized dogs. Haemodynamics, infarct size and myocardial glutathione content were determined. Erythrocyte superoxide dismutase (SOD) activity was also determined in coronary venous blood samples. Glutathione was administered by the intraperitoneal route, 100 mg kg-1 as initial dose given 5 min before coronary ligation, and successive doses of 25 mg kg-1 every 40 min throughout the study period. Saline-treated dogs showed myocardial infarction, a decrease in myocardial glutathione content, and a transient increase in SOD activity. Three hours occlusion in glutathione-treated dogs resulted in a small reduction of infarct size, and no changes in myocardial glutathione content and SOD activity. By contrast, administration of glutathione failed to reduce infarct size and failed to prevent myocardial glutathione decrease in dogs subjected to 6 h occlusion. These results indicate that exogenous glutathione is of minor beneficial effect for myocardial damage resulting from permanent coronary occlusion and suggest that endogenous glutathione has a limited role in protecting against myocardial ischaemia without reperfusion.
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Such et al. (1993) studied this question.
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