低温对离体大鼠心室肌复极时程的影响及其机制

doi:10.12047/j.cjap.5914.2020.050

摘要/Abstract

摘要： 目的: 观察低温对离体大鼠心室肌复极时程及Kir2.1蛋白表达的影响,探讨Kir2.1蛋白在其中的作用。方法:18只健康雄性SD大鼠, 随机分为3组(n=6),即正常对照组(C组)、35℃低温组(H₁组)和32℃低温组(H₂组)。制备Langendorff离体心脏灌注模型,37℃ K-H液平衡灌注15 min后,C组继续灌注37℃ K-H液30 min;H₁组继续灌注35℃的K-H液30 min,H₂组继续灌注32℃的K-H液30 min。记录各组平衡灌注15 min(T₁)和继续灌注30 min(T₂)时HR、左心室前壁三层心肌单相动作电位,计算单相动作电位复极50％、90％的时程(MAPD₅₀、MAPD₉₀)和跨室壁复极离散度(TDR),同时记录心律失常发生情况。取测量电生理的心室肌部位组织以Western blot测定Kir2. 1蛋白表达,以免疫组织化学法测量Kir2. 1蛋白的平均光密度值(AOD)及分布情况。结果: 与T₀比较,T₁时H₁组和H₂组HR显著减慢(P＜0.05), MAPD₅₀、MAPD₉₀显著延长(P＜0.05),TDR显著增大(P＜ 0.05);与C组比较,T₁时H₁组和H₂组HR显著减慢(P＜0.05),MAPD₉₀显著延长(P＜0.05),TDR显著增大(P＜ 0.05),Kir2.1蛋白表达显著减少(P＜0.05), AOD值显著减少(P＜0.05)。与H₁组比较,T₁时H₂组心率显著减慢(P＜0.05),MAPD₅₀、MAPD₉₀显著延长(P＜0.05),TDR显著增大(P＜0.05)。C组Kir2.1蛋白分布正常,H₁、H₂组蛋白分布紊乱。结论: 低温会延长心室复极时程,增加复极离散度,其机制与低温下调Kir2.1蛋白表达、改变Kir2.1蛋白分布有关。

关键词: 低温, 单相动作电位时程, 跨室壁复极离散度, 心律失常, Kir2.1, 心脏电生理技术

Abstract: Objective: To observe the effects of hypothermia on the repolarization duration and the expression of Kir2.1 protein of ventricular myocytes in isolated rat heart and explore the role of Kir2.1 protein.Methods: Eighteen healthy adult male Sprague-Dawley rats were randomly divided into three groups (n=6 per group): Control group (C group), 35℃ group (H₁ group), 32℃ group (H₂ group). Langendorff isolated heart models were established. After 15 min 37℃ K-H fluid banlanced perfusion, C group continued to perfuse the K-H solution at 37℃ for 30 minutes, H₁ group continued to perfuse the K-H solution at 35℃ for 30 minutes, H₂ group continued to perfuse the K-H solution at 32℃ for 30 minutes. At 15 min of balanced perfusion (T₁), and 30 min of continuous perfusion (T₂), the heart rate,and the MAP in the three layers of the left ventricular anterior wall were recorded, the action potential duration at 50% repolarization (MAPD₅₀), the action potential duration at 90% repolarization (MAPD₉₀) and transmural dispersion of repolarization(TDR) were calculated. At the same time, the occurrence of arrhythmia was recorded. The expression of Kir2.1 protein was measured by Western blot. The average optical density (AOD) and the distribution of Kir2.1 protein were measured by immunohistochemistry in the ventricular tissue measured by electrophysiology. Results: Compared with T₀, the heart rate was decreased, MAPD₅₀ and MAPD₉₀ were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) in H₁ group, H₂group at T₁. Compared with C group, the HR was decreased, the MAPD₉₀ was prolonged significantly (P＜0.05), TDR was increased significantly (P＜0.05),the expression and the AOD of Kir2.1 protein were decreased significantly (P＜0.05) in H₁group, H₂group at T₁. Compared with H₁ group, the heart rate of H₂ group was decreased significantly (P＜0.05), MAPD₅₀ and MAPD₉₀ were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) at T₁. The distribution of Kir2.1 protein in group C was normal, while the distribution of Kir2.1 in H₁ group and H₂ group was disordered. Conclusion: Hypothermia prolonged the ventricular duration of repolarization and increased the dispersion of repolarization. The mechanism is related to the down-regulation the expression of Kir2.1 protein and the disorder of the distribution of Kir2.1 protein.

Key words: hypothermia, monophasic action potential, transmural dispersion of repolarization, arrhythmia, Kir2.1, electrophysiological techniques

中图分类号:

R614.1

符校魁, 刘艳秋, 高鸿, 王贵龙, 李华宇, 代东君. 低温对离体大鼠心室肌复极时程的影响及其机制[J]. 中国应用生理学杂志, 2020, 36(3): 228-231.

FU Xiao-kui, LIU Yan-qiu, GAO Hong, WANG Gui-long, LI Hua-yu, DAI Dong-jun. Effects of hypothermia on the repolarization duration of ventricular myocytes in rats and its mechanism[J]. CJAP, 2020, 36(3): 228-231.

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