异丙酚对兔缺血/再灌注损伤心肌m-calpain激活线粒体膜通透性转换的影响

目的观察异丙酚对缺血-再灌注损伤心肌细胞中线粒体膜通透性转换（MPT）和细胞凋亡的影响,探讨异丙酚对缺血-再灌注损伤心肌的保护机制。方法4月龄健康雄性新西兰大耳白兔24只,体重2.1～2.3 kg,随机分为3组：假手术组（Sham组）、缺血-再灌注组（I-R组）和丙泊酚组（P组）,每组8只。实验结束取缺血区心肌标本,免疫组织化学方法（SP法）检测m型钙激活蛋白酶（m-calpain）的表达,采用Motic 6.0图像分析系统进行处理,采集平均光密度值（AO值）进行统计分析;JC-1检测线粒体膜电位（Δψm）,流式细胞术（AnnexinⅤ-PI双染色法）测定细胞凋亡。结果Sham组中m-calpain低程度表达,可见少量凋亡细胞;与Sham组比较,I-R组和P组m-calpain值、凋亡细胞数升高,Δψm降低（P〈0.05）;与I-R组比较,P组m-calpain、凋亡细胞数降低,Δψm升高（P〈0.05）。结论异丙泊酚抑制心肌缺血-再灌注损伤时m-calpain的激活,降低线粒体膜通透性转换,对缺血-再灌注心肌产生保护作用。

Effects of propofol on the activation of m-calpain and mitochobdrial permeability transition in the damaged myocardium due to ischemia-reperfusion in rabbits

Objective To investigate the effect of propofol on the activation of mcalpain, mitochobdrial permeability transition （MPT） and apoptosis induced by myocardial ischemia/reperfusion in rabbits. Methods Twenty four male New-Zealand rabbits weighed 2.1 - 2.3 kg were randomly divided into three groups： sham operation group （sham group）, isehemia-reperfusion group（ I-R group） and propofol group（P group）, 8 animals in each group. The expression of m-calpain was detected by immunohistochemistry, and the average optical value of these images was analysised by medical image analysis software （Motic 6.0）. The flow cytometry method （FCM） was used for detecting apoptosis of myocardium and △ψm. Results The activated m-Calpain expressed at low degree, a few apoptotic myocytes were detected by Annexin Ⅴ-propidium iodide staining in sham group. The expression of m-calpain and the number of apoptotic myocytes in I-R group and P group were significantly higher and△ψm was lower than those in sham group （P 〈 0.05） . As compared with those in I-R group, the expression of m-calpain and the number of apoptotic myocytes of P group were significantly lower and the △ψm was higher（ P 〈 0.05）. Conclusion Propofol can inhibit the activition of m-calpain and decrease the MPT, reduce MPT, as a result, which has a protective effect on damaged myocardium due to isehemia-reperfusion in rabbits.