Background: Previous studies have shown that use of supraphysiologocal doses of anabolic adrogenic steroids (AAS) associated with detrimental cardiovascular effects including ventricular hypertrophy, increased susceptibility to ischaemia/reperfusion injury, impairment of exercise-induced cardioprotection and sudden cardiac death. The aim of the present study was to evaluate the impact of 8 weeks treatment of AAS nandrolone decanoate (10 mg/kg/week), on ischemic preconditioning (IPC) phenomena in isolated hearts of sedentary rats. Materials and Methods: Three groups of animals were studied in the present study. Control ischemia/reperfusion injury group (IR), 2- Ischemic preconditioned group before main test ischemia and reperfusion (IPC+IR), and 3- Nandrolone treated ischemic preconditioned group before main test ischemia and reperfusion (Nan+IPC+IR). After two months of nandrolone and/or its solvent, the isolated Langendorff perfused rat hearts were subjected to 30 min of ischemia followed by 120 min reperfusion. The IPC was induced by three cycles of 3-min occlusion and 3-min reperfusion of the left anterior descending coronary artery (LAD) before main test ischemia. Heart rate, left ventricular developed pressure (LVDP), rate pressure product (RPP), Max dp/dt, Min dp/dt and coronary flow were recorded during experiment. Infarction size was measured after 120 min reperfusion by TTC staining. Results: Eight weeks’ nandrolone treatment decreased body weight and increased cardiac to body weight ratio in treated rats. Nandrolone increased pre-ischemic base line cardiac function parameters in the rat hearts. Cardiac function recovery parameters in different time points during reperfusion were also greater in nandrolone treated rats compared to their respective controls. IPC decreased infarct size in the rats (P<0.05). Nandrolone could not significantly change the infarct size lowering effect of IPC in the rat heart. Conclusion: The present study revealed that chronic supraphysiological doses of AAS nandrolone, could not impair cardioprotective effects of ischemic preconditioning in isolated rats heart.
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