| Background and objectiveChronic hypoxia results in such pathologic changes as right ventricle reconstitution, hypoxic pulmonary vascular remodeling, hypoxic pulmonary hypertension, etc. It is very important to study pathologic changes of myocardium undergoing ischemia reperfusion in patients with cyanotic congenital heart defect. Current investigations proved that endothelial nitric oxide synthase and inducive nitric oxide synthase (eNOS/iNOS) expressed disturbedly in myocardium suffered from ischemia reperfusion, which led to disorder of nitric oxide (NO) metabolism. So far, changes and effects of NO pathway in chronic hypoxic myocardium subjected to ishcemia reperfusion have not reported. This study was designed to detect the changes of cardiac fuction, myocardal enzyme and some importment factors inculding NOS, iNOS, NO, NT and MDA in chronic hypoxic myocardium undergoing ischemia reperfusion by establishing chronic hypoxia rat model and isolated perfused left-side working heart model, and to verify the significance of NO pathway and the effects of L-arginine (a prosoma of NO).MethodsThe study was conducted by two steps. In the first step, chronic hypoxic rat model was established. Adult male Sprague-Dawley rats were bred under enviroment of normal pressure intermittent hypoxia (10 percent oxygen concentration) for 10 hours every day. After 28 days, arterial blood gas, hematocrit (HCT), mean pulmonary arterial pressure (mPAP) and right ventricular hypertrophy index (RVHI) were detected in rats. The hypoxic pulmonary vascular remodeling was analyzed with hematoxylin-eosin staining. The ratio of the thickness of pulmonary arteriolae wall to external diameter of pulmonary arteriolae (MT%) was observed.In the second step, isolated perfused left-side working heart model was prepared. Normoxic and chronic hypoxic rats were assigned to four groups (n=10), in which all isolated rat hearts subjected to ischemia for 90 minutes and reperfusion for 60 minutes. In...
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