摘要
【目的】研究SEA0400对离体大鼠心肌缺血再灌注损伤的效应及作用机制。【方法】SD大鼠随机分为正常对照组(NC组)、缺血再灌注组(IR组)及SEA0400处理组(SEA0400+I/R组),每组动物10只。离体大鼠心脏采用Langendorff法灌流,停灌40 min再灌60 min造成心肌缺血再灌注损伤模型。全程连续记录左心室发展压(LVDP)和左心室内压最大变化速率(±dp/dtmax)。心脏灌流结束后测定心肌组织ATP含量以及心肌线粒体膜电位(ΔΨ)和基质钙离子浓度([Ca2+]m)。【结果】灌注液加入SEA0400可显著改善缺血再灌注所致的心功能损伤,抑制缺血再灌注造成的心肌组织ATP含量下降、线粒体钙超载以及线粒体膜电位去极化。【结论】SEA0400可通过抑制缺血再灌注所致线粒体钙超载维持线粒体功能和心肌组织ATP含量,从而起到心肌保护的效应。
[Objective] To study the cardioprotective effects and mechanisms of SEA0400 on myocardial ischemia-reperfusion injury in isolated rat hearts. [Methods] Ischemia-repeffusion injury was induced by 40 rain of global ischemia and 60 min of reper-fusion in isolated rat hearts. Left ventricular developed pressure （LVDP） and the first derivative （±dp/dtmax） were recorded. Tissue ATP content, mitochondrial Ca^2＋ concentration （ [ Ca^2＋ ]m ） and mitochondrial membrane potential （ΔΨ） were measured. [Results] SEA0400 enhanced the recovery of contractile force and attenuated tissue ATP content decrease during ischemia-reper-fusion. Ischemia-reperfusion resulted in the depolarization of the mitochondrial membrane potential and an increase in mitochondrial Ca^2＋ concentration, and SEA0400 significantly delayed these changes. [ Conclusions] SEA0400 maintains mitoehondrial function and tissue ATP content during ischemia through the inhibition mitochondrial Ca^2＋ overload
出处
《武警医学院学报》
CAS
2009年第2期101-105,共5页
Acta Academiae Medicinae CPAPF
