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目的:研究合成的口山酮化合物3,4,5,6四羟基口山酮对离体大鼠心肌缺血再灌注损伤的保护作用及其机制。方法:离体大鼠心脏采用Langendorff法灌流,停灌30min再灌30min造成心肌缺血再灌注损伤模型。左心室插入水囊导管,记录左室内压(LVP)、左室内压最大上升速率(+dpdtmax)和心率(HR),定时收集冠脉流出液,测定冠脉流量(CF)和肌酸激酶(CK)活性。心脏灌流结束后心脏称重,计算单位心脏湿重的CK释放量。心肌组织制备匀浆,用放射免疫法测定心肌组织TNFα含量。结果:预先给予3,4,5,6四羟基口山酮(30、100或300μmol·L-1)可显著改善缺血再灌注所致的心功能损伤,减少CK的释放和心肌组织TNFα的产生。结论:3,4,5,6四羟基口山酮对心肌缺血再灌注损伤具有保护作用,其作用机制可能与抑制TNFα的产生有关。
OBJECTIVE: To study the protective effect and mechanism of the synthetic triamcinolone compound 3,4,5,6-tetrahydroxyguanosine on myocardial ischemia-reperfusion injury in isolated rat hearts. METHODS: Rat hearts were perfused with Langendorff method. After 30 minutes of reperfusion for 30 minutes, myocardial ischemia-reperfusion injury model was established. The left ventricle was inserted into a balloon catheter and the left ventricular pressure (LVP), the maximum rate of increase of left ventricular pressure (+dpdtmax), and heart rate (HR) were recorded. Coronary effluent was collected periodically to determine coronary flow (CF) and creatine kinase ( CK) activity. The heart was weighed after cardiac perfusion and the CK release of the unit’s wet heart weight was calculated. Myocardium was homogenized and the content of TNFα in myocardial tissue was measured by radioimmunoassay. RESULTS: Pretreatment with 3,4,5,6-tetrahydroxy-ketoglutaraldehyde (30, 100, or 300 μmol·L-1) significantly ameliorated the damage of cardiac function induced by ischemia-reperfusion, decreased the release of CK and the expression of TNFα in myocardial tissue. produce. Conclusion: 3,4,5,6-tetrahydroxy-ketosonone has a protective effect on myocardial ischemia-reperfusion injury, and its mechanism may be related to the inhibition of TNFα production.