动物造模,肾缺血再灌注后心肌损伤 z-bio 2022-06-28 320

　　Objective: To investigate the effect of vitamin E on myocardial injury after renal ischemia-reperfusion in rats.

　　Methods: The RIR model of rats was replicated, and some animals were given VE500mg/kg/24h by gavage 4 weeks before reperfusion, and the myocardial tissue malondialdehyde (MDA), myeloperoxidase (MPO), and xanthine oxidase (XO) were observed. Changes in , superoxide dismutase (SOD), nitric oxide (NO) and plasma creatine kinase (CK) and creatine kinase isoenzyme (CK-MB); measurement of mean arterial pressure (MAP), left ventricular contraction pressure (LVSP), the maximum rate of systolic left ventricular pressure rise (dp /dt max) and the maximum rate of diastolic left ventricular pressure fall (-dp /dt max); light microscopy and immunohistochemistry were used to observe myocardial morphology and endothelial monoxide The expression of nitrogen synthase (eNOS). Western blot was used to detect the expression of P47phox protein in cardiomyocytes.

　　RESULTS: After RIR, myocardial tissue MDA content, MPO and XO activities and NO concentration increased while SOD activity decreased, plasma CK and CK-MB increased, hemodynamic indexes decreased, myocardial cell edema and eNOS positive cells under microscope After administration of VE, the content of MDA, the activity of MPO and XO in the rat myocardial tissue decreased while the activity of SOD increased, the plasma CK and CK-MB decreased, the hemodynamic indexes increased, and the NO concentration increased. , Myocardial injury was alleviated under microscope, the number of eNOS positive cells was increased, and the expression of p47phox protein was decreased, and the differences were statistically significant.

　　Conclusion: VE may play a protective effect on the myocardium after RIR through anti-inflammatory, anti-oxidative, increasing NO content, and reducing P47phox expression.