Although reperfusion of an ischemic organ is essential to prevent irreversible tissue damage, it may amplify tissue injury. This study investigates the role of endogenous testosterone in myocardial ischemia reperfusion and apoptosis in male rats. Material and method. Twenty four male rats were randomized into 4 equal groups: Group (1), sham group, rats underwent the same anesthetic and surgical procedure as the control group except for LAD ligation; Group (2), Active control group, rats underwent LAD ligation; Group (3), castrated, rats underwent surgical castration, left 3wks for recovery, and then underwent LAD ligation; and Group (4), Goserelin acetate treated, rats received 3.6？mg of Goserelin 3？wks before surgery and then underwent LAD ligation. At the end of experiment, plasma cTn I, cardiac TNF-α, IL1-β, ICAM-1, and Apoptosis level were measured and histological examination was made. Results. Compared to sham group, the levels of myocardial TNF-α, IL-1β, ICAM-1, apoptosis, and plasma cTn I were significantly increased ( ) in control group and all rats showed significant myocardial injury ( ). Castration and Goserelin acetates significantly counteract the increase in myocardial levels of TNF-α, IL-1β, ICAM-1, plasma cTn I, and apoptosis ( ) and significantly reduce ( ) the severity of myocardial injury. We conclude that castration and Goserelin acetates ameliorate myocardial I/R injury and apoptosis in rats via interfering with inflammatory reactions. 1. Introduction Ischemic heart disease is one of the major leading causes of death for both men and women. Depriving the organ from its blood supply has long been documented as a critical factor in the clinical outcome of stroke, hemorrhagic shock, myocardial infarction, and organ transplantation. Although the restoration of blood flow to an ischemic organ is essential to prevent permanent tissue damage, reperfusion may increase tissue injury in excess of that produced by ischemia alone. Restoration of blood flow to ischemic myocardium results in the ischemia reperfusion (I/R) injury [1]. Cellular damage after reperfusion of previously viable ischemic tissue is defined as ischemia reperfusion (I/R) injury [2]. I/R injury may occur in a variety of clinical situations, including reperfusion after thrombolytic therapy, coronary angioplasty, organ transplantation, and cardiopulmonary bypass. Reperfusion of ischemic tissue results in both a local and systemic inflammatory responses that, in turn, may give rise to wide spread microvascular dysfunction and changed tissue barrier and function. If sever
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