摘要
目的观察慢性心力衰竭(简称心衰)兔心房肌细胞钠离子通道电流的变化及分子机制和厄贝沙坦的干预作用,探讨心衰房性心律失常及厄贝沙坦抑制心律失常的可能机制。方法90只兔随机分为假手术组、心衰组、厄贝沙坦组。通过结扎左室支建立兔心衰模型,厄贝沙坦组于术后第2天行厄贝沙坦干预。用全细胞膜片钳记录兔心房肌细胞钠通道电流的变化;用定量聚合酶链式反应(PCR)方法测定兔心房肌细胞钠通道α亚单位mRNA表达。结果兔心房肌细胞钠离子通道峰电流密度心衰组和厄贝沙坦组低于假手术组(-22.04±1.94pA/pF,-26.24±-2.36pA/pFvs-32.22±-2.22pA/pF),厄贝沙坦组高于心衰组。假手术组、心衰组、厄贝沙坦组钠离子通道α亚单位mRNA分别为1.7±0.35(×10-1),1.1±0.22(×10-1),1.24±0.31(×10-1)。结论兔慢性心衰心房肌细胞钠离子通道电流下调,其机制之一可能与通道α亚单位mRNA表达的减少有关,而厄贝沙坦则可抑制其下调。
Objective To explore the possible mechanisms for the atrial arrhythmia in chronic heart failure(CHF) and for antiarrhythmic effects of irbesartan by observating the change of atrial myocyte INa and INa αsubunit mRNA expression. Methods A total of 90 rabbits were randomly divided into sham-operated group,CHF group and irbesartan group. The CHF rabbit model was established by ligation of ventricular branch of the left coronary arteries. The INa and the INa current densities of left atrial myocytes in three groups were recorded with whole-cell patch clamp technique. The messenger ribonucleic acid(mRNA) of atrial sodium channel α subunit were measured by real-time reverse transcription-polymerase chain reaction. Results The peak INa current densities of atrial myocytes in CHF group and irbesartan group decreased when compared with sham-operated group( - 22.04 ± 1.94 pA/pF, - 26.24 ± - 2.36 pA/pF vs - 32.22 ±- 2.22 pA/pF), irbesartan group increased compared with CHF group. The INa α subunit mRNA expression of atrial myocytes in sham-operated group,CHF group and irbesartan group were 1.7 ±0.35( ×10^-1) ,1.1 ±0.22(×10^-1) ,1.24 ±0.31( × 10^-1). Conclusion The INa current density of left atrial myocytes reduced in CHF; The down-regulation of sodium channel α subunit mRNA level might be one of major mechanisms of down-regulation of INa current density. Irbesartan could prevent the remodeling of INa of atrial myocte with CHF.
出处
《中国心脏起搏与心电生理杂志》
2008年第3期248-251,共4页
Chinese Journal of Cardiac Pacing and Electrophysiology