二氮嗪后处理对离体大鼠心功能及线粒体心磷脂的影响

发布时间：2018-01-24 19:30

  本文关键词： 心磷脂 二氮嗪 缺血/再灌注损伤　出处：《中国病理生理杂志》2015年05期 　论文类型：期刊论文

【摘要】：目的:建立离体大鼠心肌缺血/再灌注损伤模型,观察二氮嗪(diazoxide,D)后处理对缺血/再灌注损伤离体大鼠心功能及线粒体心磷脂的影响,并探讨ATP敏感性钾通道在二氮嗪后处理心肌保护中的作用。方法:采用Langendorff装置建立离体大鼠心肌缺血/再灌注损伤模型,将SD大鼠随机分为对照组(control)、缺血再灌注模型组(I/R)、二氮嗪后处理组(I/R+D)、5-羟葵酸拮抗二氮嗪后处理组(I/R+5-HD+D),每组8只,均先灌注平衡20 min。Control组:灌注平衡后续灌70 min;I/R组:缺血前灌注4℃ST.Thomas停跳液,全心缺血40 min,再灌30 min;I/R+D组:全心缺血40 min,缺血后给予含二氮嗪(50μmol/L)的K-H液灌注5 min后,再灌25 min;I/R+5-HD+D组:二氮嗪后处理前给予含5-羟葵酸(100μmol/L)的K-H液灌注5 min,再灌20 min。观察各组续(再)灌注末心率、冠脉流出液量、心功能、心肌酶学及心肌线粒体心磷脂的变化。结果:各组续(再)灌注末比较,I/R组较control组及I/R+D组心率减慢、冠脉流出液量降低,心功能明显受损,心肌酶增加,心磷酯含量减少,但与I/R+5-HD+D无明显差异。结论:二氮嗪后处理通过增加线粒体心磷脂含量,减少心肌酶的释放,改善心脏功能,减轻心肌的再灌注损伤,产生心肌保护作用。5-羟葵酸能够完全阻断二氮嗪的心肌保护作用。
[Abstract]:Objective: to establish an isolated rat model of myocardial ischemia / reperfusion injury and to observe the effects of diazoxide-diazide-diazide (DZ) treatment on cardiac function and mitochondrial cardiolipin in isolated rats with ischemia / reperfusion injury. To investigate the role of ATP sensitive potassium channel in myocardial protection after diazazine treatment. Methods: the model of isolated myocardial ischemia / reperfusion injury in rats was established by Langendorff device. Sprague-Dawley rats were randomly divided into control group (control group), ischemia reperfusion model group (I / R), diazazine post-treatment group (I / R). 5-hydroxyanilic acid antagonized diazazine post-treatment group (n = 8): I / R 5-HD DU group (n = 8), each group was perfused with equilibrium for 20 min.Control, followed by perfusion equilibrium for 70 minutes; In the I / R group, 4 鈩，

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