الفهرس 
Heart rate following ischemia-reperfusionOnly 14 pages are availabe for public view
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Abstract
Cardioregulatory actions of androgens have been documented. However, it is uncertain whether it has beneficial or deleterious effects on the heart. Therefore, the present study was designed to explore the role of testosterone on the heart, through studying the cardiac performance under basal condition as well as following ischemia-reperfusion in androgen deprived animals. The oxidant-antioxidant activity of cardiac tissue was also investigated.
Experimental androgen deprivation was induced in adult male Wistar rats by bilateral orchidectomy. Sham-operated control rats were subjected to all surgical procedures as the orchidectomized group except for removal of the testes.
Four weeks following orchidectomy, rats were subjected to measurement of body weight, ECG recording, plasma testosterone level estimation as well as heart isolation on Langendorff preparation for assessment of the basal cardiac activities and cardiac responses to 30 minutes reperfusion following 30 minutes total global ischemia. Thereafter, cardiac muscle was assessed for its content of the oxidative stress marker malondialdhyde as well as the antioxidant catalase enzyme activity.
The results obtained revealed significant reduction in the final body weight and final body mass index in the androgen deprived rats compared to their sham-operated controls; this might be attributed to loss of the anabolic effect of testosterone on muscle mass. Such significant reduction in body weight was accompanied with insignificant reduction in the absolute cardiac weights, pointing to sparing of cardiac muscle mass with androgen deprivation.
The changes in ECG parameters were insignificantly different between both groups, indicating maintained electrophysiological properties of androgen deprived hearts.
Hearts isolated from orchidectomized rats (ORX) exhibited significantly higher baseline myocardial flow rate, denoting better cardiac perfusion with androgen deprivation. This was accompanied with maintained chronotropic, inotropic, systolic and diastolic functions of these hearts compared to those isolated from rats with normal androgen level.
Following ischemia-reperfusion, significant bradycardia was observed in both groups of rats; however the deterioration in chrontropic activity was less evident in androgen deprived hearts as indicated by the significantly higher heart rate during
5 and 15 minutes of reperfusion in comparison to the control values.
Following 30 minutes of ischemia-reperfusion, hearts with normal testosterone level showed significant reduction in absolute and relative peak tension compared to preischemia values. The marked deterioration of the inotropic activity could be attributed to the increase in the reactive oxygen species with marked alteration in calcium (Ca++) homeostasis in the form of Ca++ overload. On the contrary, the reduction in peak tension was insignificant in androgen deprived hearts, denoting less inotropic deterioration and more protection against ischemia-reperfusion injury in androgen deprived state.
Significant prolongation in time to peak tension, half relaxation time and contraction time existed in the two studied groups during the whole period of reperfusion compared to their initial preischemia values, denoting systolic and diastolic dysfunction on exposure to ischemia-reperfusion. The contraction time that indicates the time needed to accomplish both systolic and diastolic time components was less prolonged in androgen deprived hearts confirming better Ca++ handling on exposure to ischemia-reperfusion in androgen deprived state.