摘要
目的:以Sprague-Dawley大鼠为研究对象,观察经过1d、3d、5d及7d睡眠剥夺(Sleep Deprivation,SD)大鼠心电图及其心室肌组织KV2.1钾离子通道水平,探索SD致心律失常的发生机制。方法:以改良多平台睡眠剥夺法(MMPM)建立睡眠剥夺模型,设笼养对照组,大平台对照组,睡眠剥夺1 d、3 d、5 d、7 d组,实时PCR定量监测各组大鼠心肌组织KV2.1钾离子通道基因mRNA水平随SD时间变化趋势。结果:SD后大鼠心电图改变以心律失常为主,心肌组织KV2.1钾离子通道的水平随SD时间的延长持续下调(笼养对照组,大平台对照组,睡眠剥夺1 d,3 d,5 d,7d组的2-△△ct值依次为1,0.84,0.60,0.35,0.1,0.06,各睡眠剥夺组的较两对照组显著下降(P<0.05)。结论:SD可致大鼠发生心律失常,心肌组织K2.1钾离子通道水平的下调可能是SD致心律失常的机制之一。
Objective： To observe the changes in rats ECG after sleep deprivation （SD）, and to examine the level of Kv 2.1 voltage-gated potassium channel, and severity of arrhythmia in different SD duration, and research the mechanism of arrhythmia which caused by SD. Methods： Rat models of SD were established by modified multiple platform method, ECG were recorded on 1 d, 3 d, 5 d and 7 d respectively. The levels of Kv2.1 voltage-gated potassium channel were analyzed quantitatively after SD by Real-time PCR. Results： Main changes in ECG after SD were arrhythmia. The levels of Kv2.1 voltage-gated potassium channel were all decreased, and became lower （value of 2^-△△ct of normal cage control group, tank control groups, SD1 d, 3 d, 5 d, 7 d group was 1, 0.84, 0.60, 0.35, 0.1, 0.06 respectively, compared with that of two control group that of every SD group significantly decreased, P〈0.05 all） with the increasing SD duration. Conclusion： SD could cause arrhythmia in rats, the decreasing levels of Kv2.1 voltage-gated potassium channel maybe one mechanism of arrhythmia which caused by SD.
出处
《心血管康复医学杂志》
CAS
2009年第3期224-226,共3页
Chinese Journal of Cardiovascular Rehabilitation Medicine
关键词
睡眠剥夺
心律失常
逆转录聚合酶联反应
Sleep deprivation
Arrhythmia
Reverse transcriptase polymerase chain reaction
