ABSTRACT
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.
ABSTRACT
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.