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三十烷醇对大鼠离体心脏缺血再灌注损伤的影响
引用本文:郭艳,易思思,胡长平. 三十烷醇对大鼠离体心脏缺血再灌注损伤的影响[J]. 医学临床研究, 2014, 0(8): 1522-1525
作者姓名:郭艳  易思思  胡长平
作者单位:郭艳 (中南大学药学院药理学系,湖南 长沙,410078); 易思思 (中南大学药学院药理学系,湖南 长沙,410078); 胡长平 (中南大学药学院药理学系,湖南 长沙,410078);
摘    要:
【目的】观察三十烷醇(triacontanol ,TRIA)对心肌缺血再灌注损伤(IRI)的影响。【方法】采用Langendorff灌流装置建立大鼠离体心脏IRI模型。将大鼠随机分为正常组、缺血再灌注(IR)组、不同剂量T RIA+IR组及T RIA (2.5μg/mL)组。正常组全心持续灌流90 min;IR组平衡灌注30 min ,缺血30 min后再灌注30 min;TRIA+IR组在缺血前5 min分别给予(25,15,5,2.5)μg/mL TRIA之后处理同IR组;TRIA组平衡灌注30 min后给药5 min ,之后持续灌流30 min。观测各组心率(HR)、冠脉流量(CF)、左室内压(LVP)和左室内压变化最大速率(± dp/dtmax),测定冠脉流出液中肌酸激酶(CK)释放量。【结果】与正常组比较,IR组引起明显的心功能损伤,表现为再灌注期间 HR、CF、LVP、± dp/dtmax降低以及CK释放量增加;心脏灌注不同剂量TRIA(25,15,5,2.5μg/mL)5 min可加重IRI所致心功能损伤,甚至心脏停跳,表现为LVP、± dp/dtmax进一步降低,CF显著减少,HR减慢以及CK释放量增加;单独灌注TRIA(2.5μg/mL)对大鼠心功能也有明显抑制作用,抑制作用持续30 min不能恢复。【结论】离体大鼠心脏灌流 T RIA可抑制心功能及加重心肌IR后心功能的损伤。

关 键 词:醇类/药理学  心肌缺血  疾病模型  ,动物  心肌再灌注损伤/预防和控制  大鼠,Sprague-Dawley

Effect of Triacontanol on Myocardial Ischemia-reperfusion Injury in Isolated Rat Heart
C_O Yan,YI Si-si,HU Chang-ping. Effect of Triacontanol on Myocardial Ischemia-reperfusion Injury in Isolated Rat Heart[J]. Journal of Clinical Research, 2014, 0(8): 1522-1525
Authors:C_O Yan  YI Si-si  HU Chang-ping
Affiliation:( Department of Pharmacology, School of Pharmaceutical Sciences, Central South University, Changsha 410078, China )
Abstract:
[Objective]To explore the effect of triacontanol(TRIA) on myocardial ischemia-reperfusion injury(IR) in isolated rat cardiac IR model .[Methods]Langendorff perfusion device was used to establish rat isolated heart IR model .All rats were randomly divided into normal group ,different dose TRIA+IR group and TRIA(2 .5 g/ml) group .The normal group was given whole heart continuous perfusion for 90min .The IR group was given the balance for 30min and then reperfusion for 30min after 30min-ischemia .The TRIA-IR group was given 25 ,15 ,5 and 2 .52 .5 g/ml TRIA at 5min before ischemia and then the same treatment as IR group .The TRIA group was given the medication for 5min after 30min-balance and then continuous perfusion for 30min .Heart rate(HR) ,coronary flow (CF) ,left ventricular pressure (LVP) and maximum velocity of LVP variation(dp/dtmax ) were observed .The level of creatine kinase(CK) in coronary effluent was measured .[Results]Compared with normal group ,IR could induce the obvious heart dysfunction as shown by a decrease in HR ,CF ,LVP and dp/dtmax and an increase in CK level .Heart perfusion with different doses of TRIA (25 , 15 ,5 and 2 .5 g/mL) for 5min aggravated IR-induced cardiac dysfunction and even heart arrest as shown by a further decrease in HR ,CF ,LVP and dp/dtmax and an increase in CK level .TRIA(2 .5 g/mL) alone also inhibited rat cardiac function which was not recovered for continuous 30min .[Conclusion]TRIA can inhibit cardiac function and aggravate myocardial IR injury in Langendorff rat .
Keywords:Alcohols/PD  Myocardial Ischemia  Disease Models,Animal  Myocardial Reperfu-sion Injury/PC  Rats,Sprague-Dawley
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