【摘要】 【目的】探讨PPARγ激动剂对大鼠心肌缺血-再灌注心律失常的影响及相关机制。【方法】将雄性SD大鼠60只随机分成假手术(Sham)组、缺血再灌注(I/R)组、缺血再灌注+罗格列酮(I/R+Ros)组、缺血再灌注+罗格列酮+缓激肽B2受体拮抗剂HOE140(I/R+Ros+HOE140)组,每组15只。麻醉大鼠后,结扎大鼠冠状动脉前降支根部30min,再灌注40min,观察缺血再灌注前后心律失常发生情况,检测心肌组织丙二醛(MDA)、超氧化物歧化酶(SOD)、总一氧化氮合酶(tNOS)、还原型一氧化氮合酶(eNOS)、诱导型一氧化氮合酶(iNOS)和一氧化氮(NO)水平。【结果】罗格列酮预处理组的大鼠恶性室性心律失常的发生时间(13min),持续时间(14.37s),室性早搏的发生次数(47次)和心律失常评分等指标均得到改善(P<0.05);提前应用Hoe140可部分或全部阻断缺血-再灌注时罗格列酮的抗心律失常作用(P<0.05);I/R+Ros组与I/R组相比心肌组织eNOS、NO、和SOD活性水平明显提高,而iNOS活性和MDA水平显著下降(P<0.05);HOE140可阻断此作用(P<0.05)。【结论】PPARγ激动剂罗格列酮有抗大鼠心肌缺血再灌注心律失常作用,这可能是通过缓激肽-一氧化氮途径实现的。更多还原

【Abstract】 Objective To determine the effects and possible mechanism of peroxisome proliferators-activated receptor γ(PPAR γ) activator rosiglitazone on myocardial ischemia-reperfusion induced arrhythmia in rats.Method Sixty adult male Sprague Dawley rats were randomly subjected to Sham operation(n= 10),ischemia-reperfusion(I/R,n= 10),I/R plus rosiglitazone(n = 13) or I/R plus rosiglitazone and a selective bradykinin B2 receptor antagonist HOE140(n=11).Myocardial injury was produced by the occlusion of the left anterior descending coronary artery for 30 min followed by 40 min reperfusion.Then the measurements of arrhythmia were assessed,as well as the maleic dialdehyde(MDA),superoxide dismutase(SOD),nitric oxide synthase(NOS),and nitric oxide(NO) levels in homogenate of rat heart tissue.Result Compared with I/R group,the measurements of arrhythmia in I/R plus rosiglitazone group were improved significantly(P< 0.05),which can be,at least partially,abolished by pretreatment with HOE140(P< 0.05).The eNOS,NO,and SOD levels of the heart tissue were clearly up regulated in I/R plus rosiglitazone group(P< 0.05),while the iNOS and MDA levels were reduced markedly(P< 0.05) in the same group,these effects can also be prevented by HOE140.Conclusion PPAR γ activator rosiglitazone exerts its myocardial protection against ischemia-reperfusion induced arrhythmia in rats at least partially through the bradykinin-NO mechanism.更多还原