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目的:研究缝隙连接开放剂抗心律失常肽(AAP10)抗肥厚心肌室性心律失常的作用并探讨缝隙连接蛋白43(Cx43)与心律失常的关系。方法:30只日本大耳白兔随机分为假手术组(Sham组)、左室肥厚组(LVH组)、AAP10组。LVH组和AAP10组行腹主动脉缩窄术,Sham组开腹但不行腹主动脉缩窄术。术后喂养8周。制备左室楔形心肌块灌注模型。Sham组和LVH组灌注正常台式液,AAP10组灌注含100 nmol/L的AAP10台式液。利用浮置玻璃微电极法同步记录楔型心肌块跨壁心电图和内外膜心肌细胞跨膜动作电位,程序电刺激起搏,记录早期后除极及室性心律失常的发生率。采取Western blot检测3组Cx43表达;采取免疫荧光方法显示3组Cx43的分布。结果:Sham组、LVH组、AAP10组室性心律失常的发生率分别为0、40%、10%。与Sham组相比,LVH组Cx43表达下降(50.7±6.1)%(P<0.05),AAP10组与LVH组相比,Cx43表达上升(20.9±4.7)%,P<0.05。免疫荧光显示肥厚心肌Cx43分布紊乱,由正常的端端分布成为细胞表面随机分布,加入AAP10后可改善其分布。结论:肥厚心肌有较高的心律失常发生率,肥厚心肌细胞Cx43表达下降并且排列紊乱,AAP10可提高Cx43的表达及改善其分布,降低室性心律失常的发生率。
Objective: To investigate the effect of gap junction opener antiarrhythmic peptide (AAP10) on hypertensive ventricular arrhythmia and to explore the relationship between connexin 43 (Cx43) and arrhythmia. Methods: Thirty Japanese white rabbits were randomly divided into sham operation group (Sham group), left ventricular hypertrophy group (LVH group) and AAP10 group. The abdominal aorta constriction was performed in the LVH group and the AAP10 group, but the abdominal aorta constriction was not performed in the Sham group. After 8 weeks of feeding. Preparation of left ventricular wedge myocardial block model. Sham group and LVH group were perfused with normal table liquid, and AAP10 group was perfused with 100 nmol / L AAP10 table liquid. The floating electrocardiogram and the transmembrane action potentials of cardiomyocytes were recorded synchronously by floating glass microelectrode method. The procedure was electrically stimulated and paced, and the incidence of depolarization and ventricular arrhythmia was recorded. Western blot was used to detect the expression of Cx43 in three groups. Immunofluorescence staining was used to detect the distribution of Cx43 in the three groups. Results: The incidence of ventricular arrhythmia in Sham group, LVH group and AAP10 group were 0, 40% and 10% respectively. Compared with Sham group, Cx43 expression decreased (50.7 ± 6.1)% in LVH group (P <0.05). Compared with LVH group, Cx43 expression increased (20.9 ± 4.7)% in AAP10 group, P <0.05. Immunofluorescence showed that the distribution of Cx43 in hypertrophic myocardium was disordered and distributed randomly from the normal end to the cell surface. The addition of AAP10 could improve its distribution. CONCLUSION: Hypertrophic myocardium has a higher incidence of arrhythmia. Cx43 expression in hypertrophic cardiomyocytes is decreased and disordered. AAP10 can increase the expression of Cx43 and improve its distribution, and reduce the incidence of ventricular arrhythmia.