本文關(guān)鍵詞： 心磷脂 二氮嗪 缺血/再灌注損傷　出處：《中國病理生理雜志》2015年05期 　論文類型：期刊論文

【摘要】：目的:建立離體大鼠心肌缺血/再灌注損傷模型,觀察二氮嗪(diazoxide,D)后處理對缺血/再灌注損傷離體大鼠心功能及線粒體心磷脂的影響,并探討ATP敏感性鉀通道在二氮嗪后處理心肌保護中的作用。方法:采用Langendorff裝置建立離體大鼠心肌缺血/再灌注損傷模型,將SD大鼠隨機分為對照組(control)、缺血再灌注模型組(I/R)、二氮嗪后處理組(I/R+D)、5-羥葵酸拮抗二氮嗪后處理組(I/R+5-HD+D),每組8只,均先灌注平衡20 min。Control組:灌注平衡后續(xù)灌70 min;I/R組:缺血前灌注4℃ST.Thomas停跳液,全心缺血40 min,再灌30 min;I/R+D組:全心缺血40 min,缺血后給予含二氮嗪(50μmol/L)的K-H液灌注5 min后,再灌25 min;I/R+5-HD+D組:二氮嗪后處理前給予含5-羥葵酸(100μmol/L)的K-H液灌注5 min,再灌20 min。觀察各組續(xù)(再)灌注末心率、冠脈流出液量、心功能、心肌酶學(xué)及心肌線粒體心磷脂的變化。結(jié)果:各組續(xù)(再)灌注末比較,I/R組較control組及I/R+D組心率減慢、冠脈流出液量降低,心功能明顯受損,心肌酶增加,心磷酯含量減少,但與I/R+5-HD+D無明顯差異。結(jié)論:二氮嗪后處理通過增加線粒體心磷脂含量,減少心肌酶的釋放,改善心臟功能,減輕心肌的再灌注損傷,產(chǎn)生心肌保護作用。5-羥葵酸能夠完全阻斷二氮嗪的心肌保護作用。
[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，

本文編號：1460845