【摘要】 目的　探讨核黄素(riboflavin)对再灌注损伤心肌保护作用的机制。方法　通过结扎左冠状动脉前降支复制在体心肌缺血再灌注损伤动物模型。将家兔随机分为4组,即假手术组(SC组)、缺血再灌注组(IRI组)、缺血预处理组(IPC组)和核黄素干预组(RBF组) ,检测不同时间点血清中一氧化氮(NO)和丙二醛(MDA)的含量以及缺血区心肌组织匀浆中一氧化氮合酶(NOS)的活性。结果　与IRI组相比,RBF组在缺血后各时点血清中NO含量升高明显(P <0 .0 5 ,P <0 .0 1) ,心肌组织匀浆中各型NOS检测结果示:RBF组cNOS的活性较高,与IRI组相比有显著性意义(P <0 .0 1)。结论　核黄素对再灌注损伤干预作用的部分机制是通过保护冠脉血管内皮,维持cNOS活性,增加NO的释放,从而对再灌注损伤的心肌有保护作用。更多还原

【Abstract】 Objective To explore the mechanism of riboflavin in resisting myocardial ischemia reperfusion injury. Methods The models of myocardial ischemia reperfusion injury were replicated in vivo by tightening and subsequently releasing a silk suture which was placed around the left anterior descending coronary artery. 32 male rabbits were randomly divided into four groups: sham-operation control group(SC, n=8), ischemia reperfusion injury group(IRI, n=8), ischemia preconditioning group(IPC, n=8), riboflavin pretreatment group(RBF, n=8). The content of NO, malondialdehyde(MDA) in serum at regular intervals and the activity of NOS in myocardium homogenate were determined respectively. Results As was compared with IRI group, the content of NO was significantly higher at each point after ischemia in RBF group(P<0.05,P<0.01). The activity of NOS in myocardium homogenate showed that cNOS activity increased markedly in RBF group compared with IRI group. Conclusion The partial mechanism of riboflavin pretreatment resisting ischemia reperfusion injury was through protecting coronary artery vascular endothelium, maintaining the activity of cNOS and increasing NO releasing.更多还原