Vitamin E and the heart: possible role as antioxidant.
When cardiac muscle becomes hypoxic the cells become oedematous and the fine ultrastructure is altered. Developed tension declines and resting tension increases. The cellular stores of ATP and CP are depleted and the mitochondria exhibit an altered respiration, characterized by a reduced state III respiration and a lowered respiratory control index. Reoxygenation results in a further increase of the hypoxic damage. Using these changes in function as indices of the severity of the damage caused by hypoxia and reoxygenation, we have investigated whether the administration of alfa-tocopherol provides protection. Adult male New Zealand white rabbits were used. The hearts were isolated, Langendorff perfused and then made hypoxic. Alfa-tocopherol acetate was infused directly into the aorta inflow cannula, 20 minutes before the onset of hypoxia and was continued for the remainder of the perfusion. Hypoxia was established by substituting 95% N2 and 5% CO2 + CO2 in the gas mixture. The alfa-tocopherol-treated rabbits hearts were protected in that during hypoxia and particularly during reoxygenation had a lower rate or rise of resting tensions and of ATP and CP depletion. This treatment also maintained mitochondrial function after hypoxia and reoxygenation and it resulted in the preservation of the fine ultrastructure of the myocardium as electronmicroscopic examination of the hearts revealed a marked reduction in oedema, contracture-band formation and mitochondria alterations.
D000332:Aerobiosis; D000818:Animals; D000975:Antioxidants; D006321:Heart / Q000187:drug effects*; D008297:Male; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D010100:Oxygen / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D011817:Rabbits; D014810:Vitamin E / Q000494:pharmacology*
D000975:Antioxidants; D014810:Vitamin E; D010100:Oxygen