摘要
目的探讨ＡＴＰ敏感性钾通道开放剂Ｃｒｏｍａｋｌｉｍ和其阻断剂优降糖对缺血／再灌注心肌的作用。方法在氨基甲酸乙酯麻醉家兔心肌缺血／再灌注模型上，观察ＡＴＰ敏感性钾通道开放剂Ｃｒｏｍａｋｌｉｍ和其阻断剂优降糖对家兔血流动力学、心功能、心肌耗氧量、心外膜电图、心肌梗塞范围的影响。结果在缺血／再灌注过程中，血流动力学，心功能，心肌耗氧量均明显持续性降低；各组心外膜电图ＳＴ段在缺血过程中明显抬高；单纯缺血／再灌注组的心肌梗塞范围为３２．３％，ＡＴＰ敏感性钾通道开放剂Ｃｒｏｍａｋｌｉｍ降低心肌梗塞范围至２３．３％（Ｐ＜０．０１），其阻断剂优降糖对心肌梗塞范围无影响，但可取消Ｃｒｏｍａｋｌｉｍ的心肌保护效应。结论ＡＴＰ敏感性钾通道开放剂Ｃｒｏｍａｋｌｉｍ减轻心肌损伤，对缺血／再灌注心肌有保护作用。
Objective To investigate the role of the ATP sensitive potassium channel opener cromaklim and its blocker glibenclimde on rabbit heart with ischemia-reperfusion.Methods The effects of ischemia-reperfusion ,the ATP sensitive potassium channel opener cromaklim and its blocker glibenclimde on the hemodynamics, cardic function,myocardial oxygen consumption, epicardial electrography,infarct size were examined in urethane-anesthetized rabbit models.[WTHZ〗Results In the course of ischemia(30 min)/reperfusion(180 min),all hemodynamic parameters,cardic function and myocardial oxygen consumption were decreased progressively significantly. The epicardial electrographic ST-segment in all groups were markedly increased during myocardial ischemia. The myocardial infarct size of the left ventrical by ischemia-reperfusion was 32.2% , the ATP sensitive potassium channel opener cromaklim reduced myocardial infarct size to 23.3%(P<0.01); The blocker glibenclimde had no injury effect on ischemical-reperfused myocardium, but it abolished the cardioprotection of cromaklim.Conclusion The ATP sensitive potassium channel opener cromaklim could reduce injury on myocardium; this indicated the ATP sensitive potassium channel played cardioprotection during ischemia-reperfusion.
出处
《新乡医学院学报》
CAS
1998年第3期241-242,245,共3页
Journal of Xinxiang Medical University
关键词
缺血
再灌注
ATP
敏感性钾通道
心肌梗塞
ischemia-reperfusion
ATP sensitive potassium channel
Cromaklim
glibenclimde
myocardial infarct size
rabbit
urethane
