mito-KATP通道在吡那地尔后处理减轻大鼠心肌缺血再灌注损伤中的作用：离体实验  

Role of mitO-KATp channel in pinacidil postconditioning-induced reduction of myocardial ischemia-reperfusion injury in rats： an in vitro experiment

作　　者：周雯静 李进 喻田[1] 王海英[3] Zhou Wenfing, Li Jin, Yu Tian, Wang Haiying,(1 Guizhou Key Laboratory of Anesthesia and Organ Protection, Zunk4 Medical College, Zunyi 563000, China; 2Department of Anesthesiology, Affiliated Hospital of Zunyi Medical College, Zunyi 563000, China ;3 Department of Anesthesiology, Affiliated Hospital of Southwest Medical University, Luzhou 646000, China)

机构地区：[1]遵义医学院贵州省麻醉与器官保护基础研究重点实验室,563000 [2]西南医科大学附属医院麻醉科,泸州市646000 [3]遵义医学院附属医院麻醉科,563000

出　　处：《中华麻醉学杂志》2018年第5期627-630,共4页Chinese Journal of Anesthesiology

基　　金：贵州省科学技术基金项目（黔科合J字2014-2188号）

摘　　要：目的评价线粒体ATP敏感性钾通道（mito-K。通道）在吡那地尔后处理减轻大鼠心肌缺血再灌注损伤中的作用。方法SPF级健康雄性SD大鼠，16～20周龄，体重250～300g，取离体灌注模型制备成功的心脏32个，采用随机数字表法分为4组（n=8）：对照组（C组）、缺血再灌注组（I／R组）、吡那地尔后处理组（P组）和5-羟葵酸＋吡那地尔后处理组（5-HD＋P组）。采用俘灌40min再灌注60min的方法制备大鼠心肌缺血再灌注损伤模型。于再灌注即刻，P组灌注含50μmol／L吡那地尔的K-H液2min，再灌注K．H液58min；5-HD＋P组先灌注含100μmol／L5-羟葵酸的K-H液5min，随后灌注含50“mol／L吡那地尔的K-H液2min，再灌注K-H液53min。于平衡灌注20min（T1）和再灌注结束（T2）时记录HR、左室舒张末压（LVEDP）、左室舒张压（LVDP）、左室内压最大上升速率（＋dp／dtmax）。于T：时取心肌组织，采用TTC法确定心肌梗死面积百分比，观察心肌超微结构，行线粒体Flameng评分。结果与C组比较，I／R组T2时HR、LVDP和＋dp／dtmax降低，LVEDP、心肌梗死面积百分比和线粒体Flameng评分升高（P〈0.05）。与I／R组比较，P组L时HR、LVDP和＋dp／dtmax升高，LVEDP、心肌梗死面积百分比和线粒体Flameng评分降低（P〈0．05），心肌病理学损伤减轻；5-HD＋P组上述指标差异无统计学意义（P〉0．05）。与P组比较，5-HD＋P组rrl时HR、LVDP和＋dp／dtmap降低，LVEDP、肌梗死面积百分比和线粒体Flameng评分升高（P〈0．05），心肌病理学损伤加重。结论吡那地尔后处理减轻大鼠心肌缺血再灌注损伤的全部机制与促进mito-Katp通道开放有关。Objective To evaluate the role of mitochondrial KAyF （ mitO-KATP ） channel in pinacidil postconditioning-induced reduction of myocardial ischemia-reperfusion （I/R） injury in rats. Methods SPF healthy male Sprague-Dawley rats, aged 16-20 weeks, weighing 250-300 g, were anesthetized with pentobarbital. Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95% 02-5% CO2 at 36.5-37.5 °C. Thirty-two Langendorff-perfused hearts were divided into 4 groups （ n = 8 each） using a random number table ： control group （ group C） , group I/R, pinaeidil posteonditioning group （group P） and 5-hydroxy deeanoie acid plus pinacidil posteonditioning group （group 5-HD＋P）.Myocardial ischemia was induced by interrupting perfusion for 40 min followed by 60 rain reperfusion. Im- mediately after onset of reperfusion, hearts were perfused with K-H solution containing 50 μmol/L pinacidil for 2 rain and then with K-H solution for 58 rain in group P, hearts were perfused with K-H solution contai- ning 100 p.mol/L 5-HD for 5 rain, with K-H solution containing 50 μmol/L pinacidil for 2 rain and then with K-H solution for 53 rain in group 5-HD＋P. The heart rate （HR） , left ventrieular developed pressure （LVDP） , left ventricular end-diastolic pressure （ LVEDP ） and the maximum rate of increase in left ven- tricular pressure （ ＋dp/dtm^x ） were recorded at 20 rain of equilibration （ T1 ） and at the end of reperfusion （T2 ）. Myocardial tissues were obtained at T2 for determination of myocardial infarct size and for examina- tion of myocardial uhrastructure and Flameng scoring of the mitochondria was performed. Results Com- pared with group C, the HR, LVDP and ＋dp/dt were significantly decreased, and the LVEDP, myo- cardial infarct size and mitochondrial Flameng score were increased at T2 in group I/R （P〈0. 05）. Com- pared with group I/R, the HR, LVDP and ＋dp/dtm~ were significantly increased and the LVEDP, myocar- dial infarct size and

关 键 词：心肌再灌注损伤 吡那地尔 线粒体 KATP通道 

分 类 号：R542.2[医药卫生—心血管疾病]