糖尿病大鼠不同阶段心肌电学的改变  

Electrophysiological changes in rat ventricular myocardium at different stages of experimental diabetes

作　　者：陈章强[1] 胡申江[1] 杜娟[1] 史维雅[1] 金希[1] 沈岳良[2] 夏强[2] 

机构地区：[1]浙江大学医学院附属第一医院心内科,浙江杭州310003 [2]浙江大学医学院生理教研室,浙江杭州310031

出　　处：《中国病理生理杂志》2004年第2期247-250,共4页Chinese Journal of Pathophysiology

基　　金：国家教育部留学回国人员科研启动基金资助项目 (No 1999- 74 7)

摘　　要：目的 :探讨糖尿病 (DM)易出现心律失常的可能机制。方法 :SD雄性大鼠尾静脉注射四氧嘧啶 (al loxan ,5 0mg·kg-1以生理盐水稀释 )复制糖尿病模型 ,选择以年龄相匹配健康成年SD雄性大鼠尾静脉注射相同剂量的生理盐水作为对照组。分别观察 2、4、6和 8周 4个不同时段。记录大鼠右心室乳头肌跨膜电位。结果 :在糖尿病成模后第 2周起 ,右室乳头肌动作电位时程 (APD)复极化各水平均不同程度地长于正常大鼠 (P <0 0 1) ,8周时较 2周时更明显 (P <0 0 5 )。而去极化最大速率 (Vmax)超射值 (OS)和动作电位幅度 (APA)以及静息膜电位 (RP)水平均无明显变化。结论 :糖尿病大鼠右室乳头肌动作电位时程明显延长 ,而动作电位的过度延长可能是糖尿病易导致心律失常以及心源性猝死的主要原因 ,尤其是糖尿病晚期阶段。AIM: To explore the probable mechanisms of diabetes-induced arrhythmias. METHODS: Diabetes was induced in male SD rats,using a single injection of alloxan into tail vein. Untreated age-matched animals were used as controls. All animals were observed by 2,4,6 and 8 weeks,respectively. Transmembrane potentials were recorded with conventional glass microelectrodes. RESULTS: Action potential duration(APD) at all level (APD10,APD20,APD30,APD50,APD70,APD90) was significantly lengthened in right ventricular papillary muscle from week 2 of diabetes. At week 8,APD was more lengthened at any level of repolarization than that at week 2. No differences were observed in the maximum rate of depolarization(V_ max ),overshoot(OS) and action potential amplitude(APA) as well as the resting membrane potential(RP) from the 2th to 8th week of diabetes. CONCLUSION: The results indicate that prolongation of APD may be prominently responsible for the increased incidence of cardiac re-entry-arrhythmias and sudden death,especially at late stages of diabetes.

关 键 词：动作电位 糖尿病 大鼠 乳头肌 心脏 

分 类 号：R587.1[医药卫生—内分泌]