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目的 :检测地尔硫对心肌缺血再灌注损伤中一氧化氮 (NO) ,丙二醛 (MDA)动态变化曲线及对心肌超微结构的影响 ,探讨地尔硫对心肌缺血再灌注损伤的保护作用及其机制。方法 :结扎大鼠左冠状动脉前降支 30min后复灌 180min ,制成心肌缺血再灌注模型。Wistar大鼠 4 8只 ,随机分成假手术组 ,MIR组 ,地尔硫组 :地尔硫 (1mg kg)在缺血前 5min经颈静脉 35min内缓慢注入。各组于缺血前、缺血 30min、再灌 90min、180min检测NO ,MDA ,并做电镜标本。结果 :NO、MDA在缺血期无明显变化。NO再灌后下降 ,以再灌 90min内下降明显 (P <0 0 5 ) ,地尔硫组NO活性高于MIR组 (P <0 0 5 )。再灌后MDA合成持续上升 ,再灌 180min与缺血 30min时相比 ,P <0 0 1,高于同期的地尔硫组 (P <0 0 5 )。电镜观察地尔硫能减少超微结构的损伤。结论 :地尔硫对心肌缺血再灌注损伤具保护作用
Aims: To investigate the dynamic changes of nitric oxide (NO) and malondialdehyde (MDA) in myocardial ischemia-reperfusion injury induced by diltiazem and its effect on myocardium ultrastructure. To investigate the effect of diltiazem on myocardial ischemia Protective effect of perfusion injury and its mechanism. Methods: The left anterior descending coronary artery of rats was ligated for 30 minutes and then reperfused for 180 minutes to make myocardial ischemia-reperfusion model. Forty-eight Wistar rats were randomly divided into sham-operation group, MIR group and diltiazem group. Diltiazem (1 mg kg) was slowly injected into the jugular vein within 35 min 5 min before ischemia. Each group before ischemia, ischemia 30min, reperfusion 90min, 180min detection of NO, MDA, and do electron microscopy. Results: There was no significant change of NO and MDA during ischemia. NO decreased after reperfusion, decreased significantly within 90 min after reperfusion (P <0.05), NO activity in diltiazem group was higher than that in MIR group (P <0.05). After reperfusion MDA synthesis continued to rise, reperfusion 180min compared with 30min ischemia, P <0.01, higher than the same period of diltiazem group (P <0 05). Electron microscopy Diltiazem can reduce the ultrastructure damage. Conclusion: Diltiazem has a protective effect on myocardial ischemia-reperfusion injury