ABSTRACT
Beta-endorphins [BE] were recently detected in the heart. Since the incidence of cardiac disease in premenopausal females is by far less frequent than males and since opioid peptides were found to be affected by sex hormones in the CNS, the aim of this study was to investigate whether they also modulate the BE-response to acute stress in the isolated rabbit hearts subjected to ischemia and reperfusion injury. Stressed rabbits were divided into male and female groups with and without naloxone and castrated males and tamoxifen [estrogen-receptor blocker] pretreated females with and without naloxone. BE was found to have a cardioprotective effect during stress which is sex-related. It has a negative chronotropic and inotropic effect. It prolongs the time until cardiac arrest during ischemia and reduces reperfusion arrhythmia. However, the presence of testosterone has a detrimental effect on the cardiac response to stress, which may be due to inhibition of BE release. In addition, testosterone directly decreases contractility and shortens the duration until cardiac arrest during ischemia. It probably causes coronary vasoconstriction. Estrogen, on the other hand, possess protective properties in ischemic stressed heart and prevents reperfusion arrhythmia independent of BE. The effects of estrogen may be caused by a direct action or by release of opioid peptides, which act via non- mu-receptors