高海拔地区房颤模型大鼠心房肌细胞I_(ks)的表达

The expression of the slowly activating delayed rectifier K^+currents(I_(ks) ) in the myocardial organization of AF rats at the height of 2300m

目的检测房颤大鼠心房肌细胞膜上缓慢延迟整流钾电流(Iks)通道的表达变化,进一步探讨Iks通道在房颤发病机制中的作用。方法采用经尾静脉注射乙酰胆碱、氯化钙混合液的方式建立房颤大鼠模型,对照组按同样方法注射等剂量的生理盐水。在第7天造模成功后,测定各组大鼠心房肌组织Iks通道基因表达量及心房肌组织超微结构的变化。结果①将实验组大鼠连续给药7天,第4天开始记录大鼠心电图,在第7天后房颤模型趋于稳定;②RT-PCR后荧光法检测大鼠缓慢延迟整流钾电流(Iks)通道的基因表达变化,正常组与实验组Iks通道在大鼠心房肌均有广泛分布,实验组心房肌Iks通道的表达均较正常组明显增加(p<0.05)。而实验组两两比较均无明显差异(p>0.05);③实验组大鼠心房肌组织切片显示为心房肌细胞心肌纤维纤维化,片状淋巴细胞浸润、灶性坏死,对照组无明显改变。结论心房肌Iks通道对心房颤动可能是一种保护机制,避免发生严重的电生理紊乱。

Objective To explore the changes of the slowly activating delayed rectifier K＋currents（Iks） expression in the myocardial organization of AF rats, and the effect of Iks in atrial fibrillation pathogenesis. Methods The model rats of atrial fibrillation were injected drugs of combinations including Ach and CaCl2 through the caudal vein, and the rats in control group were injected the isodose physiological saline by the same methods. When the model rats of atrial fibrillation were successful at the seventh day, we measure the expression of Iks and the ultra microstructure changes in the myocardial organization of rats in every group. Results ①The rats of experimental group were injected drugs one time per day and the total process continued one week, at the fourth day to record the ECG of rats, and the ECG of model rats of atrial fibrillation tend to stable after seven days; ②To measure the expressive change of the slowly activating delayed rectifier K＋currents（Iks） of rats by fluorescent quantitation after RT-PCR, the slowly activating delayed rectifier K＋currents（Iks） are widely distributed in the myocardial organization between the experimental group and control group, but with the comparison of control group, the mRNA express level of Iks in experimental group heightened obviously（p0.05）, and no obvious difference of the change in the experimental group（p0.05）; ③The tissue slice in the experimental group shows that myocardial organization has been fibrosis, infiltrated piece of lymphocyte and piece of necrotic tissues, but nothing was changed in control group. Conclusions The slowly activating delayed rectifier K＋currents（Iks） in the myocardial organization may be a protection mechanism to AF, and protect from occurring serious electrophysiological disorders.