ve To investigate the effect of ischemic preconditioning (IPC) on apoptosis induced by acute myocardial ischemia/reperfusion and expressions of Bcl-2 and Bax protein which were known to modulate apoptosis. Methods Twenty-four healthy SD rats of either sex, weighing (200()20)g were anesthetized with intraperitoneal pentobarbital 4.5mg?100g-1. The animals were tracheotomized and mechanically ventilated. Respiratory rate was 20 bpm and tidal volume 2 ml?100g-1. Myocardial ischemia/ reperfusion(I/R) model was established by ligation and untying of the anterior descending branch of left coronary artery. The animals were randomly divided into three equal groups with eight animals each. Group I : (control group) anterior descending branch was exposed and dissected but not ligated and was exposed for 50 min. Group II (I/R group): anterior descending branch was double ligated for 30 min and then untied for reperfusion which lasted 2h. Group III (IPC group): The anterior descending branch was tied for 5 min then untied for 5 min and the process was repeated 4 times according to Murray's method, then I/R was produced as in group II. A piece of myocardium of 2 mm thick was cut from ischemia-infarct area. Apoptotic myocardial cells were detected by TdT-mediated dUTP-biotin nick end labeling (TUNEL) and the expressions of Bcl-2 and Bax protein were measured by immunohistochemical technique. Results I/R increased the percentage of apoptotic myocardial cells and the optical density (OD) value of Bax protein and decreased the OD value of Bcl-2 protein as compared with those in the control group. IPC reduced the increased percentage of apoptotic myocardial cells and OD value of Bax protein induced by I/R and increased the OD value of Bcl-2 protein as compared with those in the I/R group. Conclusions IPC can inhibit the apoptosis induced by myocardial I/R by modulating the expression of Bcl-2 and Bax protein.

Objective:To explore the relationship between the nitric oxide(NO)and the pathogenesis of the pulmonary hypertension(PH)induced by congenital heart disease(CHD). Method:NO content in plasma of CHD patient's pulmonory artery and superior vena cava was detected with NO kit. Result:NO content in the pulmonary artery of the patients with PH was much higher than that of patients without PH(37.58?9.99?mol/L vs 19.03?15.25?mol/L,P0.5). Conclusion:NO content in the pulmonary artery of CHD patients with PH increase,which may be involved in the pathogenesis of PH induced by CHD.