ABSTRACT
Several research works have been done on the last two decades to limit the damaging effect of ischemic episodes of the heart. Brief cycles of coronary artery reperfusion alternating with re-occlusion applied during the first few minutes of reperfusion, reduce irreversible post ischemic injury vice infarct size, endothelial dysfunctions, apoptosis and was termed post conditioning [postC]. It was reported that administration of some potent compounds at the start of reperfusion could protect the heart against injury and one of these is adenosine. The present study was performed to assess the effect of postC with adenosine on the degree of apoptosis among rats subjected to intermittent coronary ischemia. The present study was conducted on 30 male albino rats that were divided into 3 groups [n10]:-Group 1 consisted of normal healthy rats served as control group and they were sham operated. Group2 consisted of rats that undergone coronary ischemia/reperfusion [PR] by3O minutes occlusion of left anterior descending [LAD] artery. Group3 consisted of rats that received adenosine in a dose 200 pg per minute by i.v infusion for 15 minutes after induction of ischemia. Then, postC procedure was done by 3 cycles of 30 seconds reperfusion and 30 seconds re-occlusion of LAD artery that started immediately after the initial reperfusion. The following parameters were estimated in the rats of all groups: myocardial levels of both mitogen activated protein kinase p.38 [MAP kinase p38] and caspase 3 as well as the serum levels of lactate dehydrogenase [LDH], creatine kinase [CK] and soluble Fas-ligand [sFas-L]. The Findings of the present study revealed that exposure of the myocardium to 30 minutes of ischemia followed by 3 hours of reperfusion was associated with increased levels of the markers of myocardial necrosis vice LDH and CK. In addition apoptosis was stimulated as evidenced by increased serum soluble Fas-L and increased myocardial tissue levels of Caspase-3 and the death kinase MAP kinase P38. Treatment of rats in group 3 with adenosine and postC was associated with decreased LDH and CK levels Furthermore, the apoptotic cell loss was also attenuated as evidenced by decreased myocardial caspase-3 and MAP kinase p38 in the treated group. So, postC was reported to delay the wash out of endogenous adenosine and administration of exogenous adenosine was thought to cause myocardial protection by preservation of ATP, improved nucleotide repletion on perfusion, stimulation of glycolysis and limiting myocardial oxygen demand. It was concluded that adenosine and postC technique could be used as an important clinical therapeutic option to attenuate myocardial apoptosis which could decrease the subsequent myocardial dysfunction and heart failure. But further preclinical and clinical studies on human patients are still needed to test this therapeutic approach