Ischemic preconditioning maintains myocardial mitochondria cardiolipin and attenuates heart impairment in isolated rat hearts

邓胜利; 喻田; 余志豪

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Ischemic preconditioning maintains myocardial mitochondria cardiolipin and attenuates heart impairment in isolated rat hearts

更新时间：2026-01-09

- Ischemic preconditioning maintains myocardial mitochondria cardiolipin and attenuates heart impairment in isolated rat hearts
- Journal of Army Medical University Vol. 31, Issue 18, Pages: 1736-1739(2009)
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  CLC： R322.11;R329.25;R457.9
- Published：2009
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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.
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. DOI：

　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. DOI：

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（T

）、缺血前即刻（T

）、再灌注末（T

）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T

、T

时比较，各组T

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（P0.05，P0.01）；与正常组比较，余3组T

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（P0.05，P0.01）；与对照组比较，IP组及HD组T

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（P0.05，P0.01）；与IP组比较，HD组T

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（P0.05，P0.01）。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 isola

ted 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 (T

)

immediately before ischemia (T

) and at the end of reperfusion (T

) in all the groups. The content of myocardial mitochondria cardiolipin was measured with HPLC. Results When the parameters at T

were compared with those at T

and T

HR and LVDP were decreased

LVEDP was increased and the content of myocardial mitochondria cardiolipin was decreased. All these changes were significant (P0.05

P0.01). The changes mentioned above were also significant at T

in control

IP and HD groups than in normal group (P0.05，P0.01). Conversely

HR and LVDP were increased

LVEDP was decreased

and the content of myocardial mitochondria cardiolipin became higher at T

in IP group than in control group and HD group (P0.05

P0.01). The values were also significant at T

in HD group tha

n in control group (P0.05

P0.01). 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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