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Abstract
Cardiac ischemia–reperfusion injury results in oxidative stress and poor physiological recovery. This study examined the amount of lipid and protein oxidation during ischemia–reperfusion to assess the degree of oxidative stress. Selenium supplementation was used to alter the antioxidant status of rats and the recovery of myocardial function post ischemia–reperfusion was investigated. Male Wistar rats were fed diets containing 0, 50, and 1000 μg/kg sodium selenite for 5 weeks, whilst controls received normal rat food containing 240 μg/kg selenium. Langendorff-perfused hearts were subjected to 22.5 min global ischemia and 45 min reperfusion, with functional recovery assessed. Heart tissues were assayed for the presence of lipid peroxides and protein carbonyls and correlated to cardiac recovery. Following ischemia and reperfusion there was a significant increase in both protein oxidation and lipid peroxidation. Hearts from selenium-deficient animals demonstrated higher levels of both protein carbonyls and lipid peroxides and were more susceptible to ischemia–reperfusion injury when compared to controls (38% versus 47% recovery of rate pressure product (RPP)). Selenium supplementation lowered the levels of protein carbonyls and lipid peroxides and resulted in improved recovery of cardiac function post ischemia–reperfusion (57% recovery of RPP). These data suggest that selenium supplementation may provide an effective method for reducing oxidative damage post cardiac ischemia–reperfusion.