关键词:

再灌注心律失常, 心室肌, 电传导, 应激诱导磷蛋白1, 连接蛋白43

Abstract:

Objective To investigate the changes of ventricular myoelectric conduction and its possible mechanism in hypothermic ischemia⁃reperfusion arrhythmia rats. Methods Healthy male SD rats aged 2 ~ 3 months were selected to prepare isolated heart perfusion models（n = 16）. The rat models were randomly divided into normal control group（C group，continuous perfusion of 37 ℃ K⁃H solution for 120 min）and hypothermic ischemia⁃reper⁃ fusion group（IR group，continuous perfusion of 37 ℃ K⁃H solution for 30 min，reperfusion stopped for 60 min， and then reperfusion for 30 min），with 8 rats in each group. Heart rate（HR），conduction velocity（CV）and elec⁃ trical conduction chart at the timepoint of continuous perfusion for 15 min（T0），continuous perfusion for 30 min （T1），reperfusion for 15 min（T2）and reperfusion for 30 min（T3）were collected，and the arrhythmia was recorded. The expression and distribution of STIP1 and Cx43 in the anterior wall of left ventricle after reperfusion were detected by western blot and immunohistochemistry. Results IR group had 7 cases of arrhythmia during reperfusion. Anlayis on IR group showed，HR and CV were decreased significantly at T2 and T3 when compared with T0 and T1（all P < 0.05）and the conduction direction showed divergent change. The expression of STIP1 and Cx43 protein in myocar⁃ dial tissue of IR group were apparently decreased when compared with C group（both P < 0.05），and Cx43 positive stained particle numbers in IR group were also decreased，in which the phenomenon of lateralization was observed. Conclusions STIP1 may affect ventricular myoelectric conduction after hypothermic ischemia⁃reperfusion by regu⁃ lating the expression of Cx43.

Key words:

reperfusion arrhythmia, ventricular myocardium, electrical conduction, stress induced phosphoprotein 1, connexin 43