Background-Although most previous studies have attempted to correlate plasma concentrations of vitamins with specific cardiovascular end points, metabolic considerations suggest that changes in myocardial tissue and storage organs may be better indicators of myocardial oxidative stress. Methods and Results-Rats fed commercial chow or a diet enriched with vitamin E for 2 weeks were subjected to either a surgical myocardial infarction (MI) or a sham procedure. Rats were hemodynamically assessed 16 weeks after surgery, and their heart, liver, kidney, and plasma were analyzed for antioxidant vitamins E (tocopherol) and A (retinol and total retinyl esters). At 16 weeks, MI rats on a control diet showed depressed peak systolic and elevated diastolic pressures in both right and left ventricles compared with their sham controls. Plasma concentrations of vitamins E and A in MI rats were not different from sham controls fed the same diet. However, concentrations of vitamin E in left ventricle and liver and of vitamin A in liver (retinol) and kidney (retinyl esters) were decreased in rats with MI compared with the sham controls. Vitamin E supplementation improved hemodynamic function in rats with MI and increased plasma, myocardial, liver, and kidney concentrations of vitamin E. The vitamin E diet also prevented the loss of total retinyl esters from the kidney but not of retinol from the liver in MI rats.
Conclusions-Dietary
Heart failure is considered to be a complex clinical syndrome, with alterations in the multiple neurohumoral systems and subcellular cardiac sites that correlate with abnormal cardiac function. Strong evidence for the role of oxidative stress in the pathogenesis of heart failure has been provided by studies on experimental animals as well as humans. This concept is gaining more acceptance due to the fact that during heart failure, changes in different neurohormones, cytokines, nitric oxide, and activated inflammatory cells are closely linked to oxidative stress at the cellular and molecular levels. The present article provides a simple description of oxygen free radicals as well as the antioxidant defense system. Evidence for the role of oxidative stress in the pathogenesis of heart failure is reviewed in a concise manner.
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