title: Effect of vitamin E on the response to ischemia-reperfusion of Langendorff heart preparations from hyperthyroid rats.
abstract: Hyperthyroidism has been reported to decrease heart antioxidant capacity and increase its susceptibility to in vitro oxidative stress. This may affect the heart response to ischemia-reperfusion, a condition that increases free radical production. We compared the functional recovery from in vitro ischemia-reperfusion (Langendorff) of hearts from euthyroid (E), hyperthyroid (H, ten daily intraperitoneal injections of T3, 10 microg/100g body weight), vitamin E-treated (VE, ten daily intramuscular injections, 20 mg/100g body weight) and hyperthyroid vitamin E-treated (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 dP/dt(max). When H hearts were paced at 300 beats/min, the functional recovery (LVDP and dP/dt(max)) 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 T3 treated (H) than in euthyroid rats. The in vitro 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 T3 pretreatment was associated with the reduced capability of the heart to face oxidative stresses in hyperthyroidism.
authors.affiliation: Dipartimento di Fisiologia Generale ed Ambientale, Università di Napoli, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Venditti
authors.forename: P
authors.initials: P
authors.lastname: Masullo
authors.forename: C
authors.initials: C
authors.lastname: Agnisola
authors.forename: S
authors.initials: S
authors.lastname: Di Meo
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D001881:Borates / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects; D004562:Electrocardiography; D006321:Heart / Q000503:physiopathology*; D006980:Hyperthyroidism / Q000473:pathology / Q000503:physiopathology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008566:Membranes / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D014810:Vitamin E / Q000378:metabolism / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D001881:Borates; D014810:Vitamin E; C027707:sodium perborate