Effect of vitamin E on the response to ischemia-reperfusion of langendorff heart preparations from hyperthyroid rats (original) (raw)

Hypet-thyroidism has been reported to decrease heart antioxidant capacity and increase its susceptibility to in vitro oxidative stress. This may affect the heart response to &hernia-reperfusion, a condition that increases free radical production. We compared the functional recovery from in vitro ischemia-repermsion (Langendorff) of hearts from euthyroid (E), hyperthyroid (H, ten daily intraperitoneal injections of T,, 10 ug/lOOg body weight), vitamin E-treated (VE, ten daily intramuscular injections, 20 mg/lOOg body weight) and hyperthyroid vitamin Etreated (HVE) rats. We also determined lipid peroxidation, tissue antioxidant capacity and the tissue capability to face an oxidative stress in vitro. A significant tachycardia was displayed during reperfusion following 20 min ischemia by the hyperthyroid hearts, together with a low recovery of left ventricular developed pressure (LVDP) and left ventricular dPid$,,,. When H hearts were paced at 300 beats/min, the functional recovery (LVDP and dPidt,,_J was close to 100% and significantly higher than in E paced hearts. At the end of the ischemia-reperfusion protocol, myocardium antioxidant capacity was significantly lower, whereas lipid peroxidation and the susceptibility to in vitro oxidative stress were higher in the T, treated (H) than in euthyroid rats. The in vifro tachycardic response, the reduction in the antioxidant capacity and the increase in lipid peroxidation were prevented by treatment of hyperthyroid rats with vitamin E (HVE). These results suggest that the tachycardic response to reperfusion following chronic T, pretreatment was associated with the reduced capability of the heart to face oxidative stresses in hyperthyroidism. Key K&K hyperthyroidism, heart ischemia-reperfision, vitamin E, antioxidant capacities Hyperthyroidism has been associated with a hyperdynamic state of the heart characterized by tachycardia (1, 2) and increased contractile performance (3). These changes in the electrical and mechanical activity of the heart result in an increased total cardiac output and work which match the increased oxygen demand by peripheral tissues owing to the thyroid hormone-induced increase in their metabolism. These changes in heart function and tissue metabolism may represent an integrate, suitable response to physiological increases in thyroid state, such as those elicited by seasonal