[1]邓胜利,喻田,余志豪.缺血预处理对离体大鼠心肌线粒体心磷脂及心功能的影响[J].陆军军医大学学报(原第三军医大学学报),2009,31(18):1736-1739.
 DENG Sheng-li,YU Tian,YU Zhi-hao.Ischemic preconditioning maintains myocardial mitochondria cardiolipin and attenuates heart impairment in isolated rat hearts[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(18):1736-1739.
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缺血预处理对离体大鼠心肌线粒体心磷脂及心功能的影响(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
31卷
期数:
2009年第18期
页码:
1736-1739
栏目:
论著
出版日期:
2009-09-30

文章信息/Info

Title:
Ischemic preconditioning maintains myocardial mitochondria cardiolipin and attenuates heart impairment in isolated rat hearts
作者:
邓胜利喻田余志豪
遵义医学院麻醉学系药理学教研室
Author(s):
DENG Sheng-li YU Tian YU Zhi-hao
Department of Pharmacy, Faculty of Anesthesiology, Zunyi Medical College, Zunyi 563003, Guizhou Province, China
关键词:
缺血预处理线粒体心功能再灌注损伤心磷脂
Keywords:
ischemic preconditioning mitochondria heart functionreperfusion injury cardiolipin
分类号:
R322.11;R329.25;R457.9
文献标志码:
A
摘要:
目的   探讨缺血预处理(ischemic preconditioning ,IP)对缺血再灌注损伤大鼠心肌线粒体心磷脂(cardiolipin)及心功能的影响。    方法   清洁级SD大鼠72只,体质量200~300 g,雌雄各半,用随机数字表法分为正常组、对照组、缺血预处理组(IP组)、5-羟葵酸(5-HD)拮抗缺血预处理组(HD组),每组18只。采用Langendorff灌流装置建立大鼠离体心脏缺血再灌注模型,正常组灌注平衡20 min,持续灌注100 min;对照组灌注平衡20 min,持续灌注30 min,缺血40 min,再灌注30 min;IP组灌注平衡20 min后,给予2次间断缺血预处理,每次缺血5 min再灌注5 min,余缺血再灌注同对照组;HD组在预处理前灌注5-HD 10 min,余同IP组。各组分别于灌注平衡末(T1)、缺血前即刻(T2)、再灌注末(T3)记录心率(HR)、左心室发展压(LVDP)和左心室舒张末压(LVEDP),采用高效液相色谱仪测定心肌线粒体心磷脂含量。   结果   与T1、T2时比较,各组T3时HR、LVDP明显降低,LVEDP明显升高,心肌线粒体心磷脂含量明显降低(P<0.05,P<0.01);与正常组比较,余3组T3时HR、LVDP明显降低,LVEDP明显升高,心肌线粒体心磷脂含量明显降低(P<0.05,P<0.01);与对照组比较,IP组及HD组T3时HR、LVDP明显升高,LVEDP明显降低,心肌线粒体心磷脂含量明显升高(P<0.05,P<0.01);与IP组比较,HD组T3时HR、LVDP明显降低,LVEDP明显升高,心肌线粒体心磷脂含量明显降低(P<0.05,P<0.01)。   结论   IP可维护心肌线粒体心磷脂含量的相对稳定,改善大鼠离体缺血再灌注心脏功能,其机制主要与mito-KATP通道的激活有关。
Abstract:
Objective   To investigate the effect of ischemic preconditioning (IP) on the content of myocardial mitochondria cardiolipin and the heart function in isolated rat hearts.    Methods   Seventy-two healthy SD rats of both sexes (36 males, 36 females) weighing 200 to 300 g were randomly divided into 4 groups (n=18 for each group): normal group, control group, IP group (IP) and 5-hydroxydecanoate (5-HD) plus IP group (HD). Langendorff apparatus were used to establish the model of ischemia/reperfusion in isolated rat hearts. The hearts were perfused for 20 min to get stabilization followed by continuous perfusion in normal group for 100 min. In control group, after perfusing of 20 min for stabilization followed by continuous perfusion for 30 min, the hearts were then reperfused for 30 min after 40 min ischemia. In IP group, the hearts were given a 5-minute ischemia and 5-minute reperfusion for twice in order within a brief intermittent period, and ischemia reperfusion was carried out in the same way as that in control group. In HD group, the hearts were perfused with 100 μmol/L 5-HD before IP, and the following procedures were carried out as those in IP group. HR, left ventricular end-diastolic pressure (LVEDP), left ventricular developed pressure (LVDP) were recorded at the end of stable perfusion (T1), immediately before ischemia (T2) and at the end of reperfusion (T3) in all the groups. The content of myocardial mitochondria cardiolipin was measured with HPLC.    Results   When the parameters at T3 were compared with those at T1 and T2, HR and LVDP were decreased, LVEDP was increased and the content of myocardial mitochondria cardiolipin was decreased. All these changes were significant (P<0.05, P<0.01). The changes mentioned above were also significant at T3 in control, IP and HD groups than in normal group (P<0.05,P<0.01). Conversely, HR and LVDP were increased, LVEDP was decreased, and the content of myocardial mitochondria cardiolipin became higher at T3 in IP group than in control group and HD group (P<0.05, P<0.01). The values were also significant at T3 in HD group than in control group (P<0.05, P<0.01).    Conclusion   IP maintains the stable level of myocardial mitochondria cardiolipin and improves the cardiac function during ischemia/reperfusion in isolated rat hearts. The protective effect of IP probably may result from the activation of mitochondrial ATP sensitive potassium channels.

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更新日期/Last Update: 2009-09-16