二十二碳六烯酸对心房颤动大鼠心房肌生理改变及双孔钾通道TASK-1蛋白表达的影响

目的：探讨二十二碳六烯酸（DHA）对大鼠心房颤动（AF）模型心房肌生理特性的影响及相关机制研究。方法：80只乙酰胆碱-氯化钙混合液敏感的SD大鼠分为对照组（CTL组）、DHA处理组（DHA组）、房颤组（AF组）和房颤+DHA处理组（DHA+AF组），观察房颤持续时间；采用全细胞膜片钳技术记录大鼠心房肌细胞动作电位时程（APD）和双孔钾通道TASK-1电流，Western blot测定大鼠心房组织TASK-1蛋白表达。结果：大鼠尾静脉注射乙酰胆碱-氯化钙混合液后，房颤持续时间随实验天数增加而逐渐延长，DHA干预缩短房颤持续时间。与CTL组相比，AF组大鼠心房肌细胞复极50%时的动作电位时程（APD₅₀）和复极90%时的动作电位时程（APD₉₀）明显缩短，心房肌细胞TASK-1电流密度升高，蛋白表达升高（P<0.05）。与AF组相比，DHA+AF组大鼠心房肌细胞APD₅₀和APD₉₀明显延长，TASK-1电流密度和蛋白表达降低（P<0.05）。结论：DHA具有延长房颤大鼠心房肌细胞APD的作用，可能与其下调心房肌TASK-1蛋白的表达从而降低心房肌细胞TASK-1电流密度有关。

Effects of docosahexaenoic acid on atrial physiological parameter and TASK-1 protein expression in atrial fibrillation rats

Objective: To investigate the effect of docosahexaenoic acid (DHA) on atrial physiological parameter and its related mechanisms in atrial fibrillation rats. Methods: Eighty Sprague-Dawley (SD) rats which were sensitive to acetylcholine-calcium chloride mixture were randomly divided into four groups:control (CTL), control treated with DHA (DHA), atrial fibrillation (AF) and atrial fibrillation treated with DHA (DHA+AF). The duration of atrial fibrillation was measured. The atrial myocyte action potential duration (APD) and TWIK-related acid-sensitive K⁺ channels-1 (TASK-1) currents were recorded by whole-cell patch-clamp technique. The expression of TASK-1 at protein level in atrial tissue was detected by Western blot method. Results: Atrial fibrillation of the rats was induced by acetylcholine-calcium chloride mixture, and the duration time of atrial fibrillation was increased with the drug-induced time prolonged. Compared with control group, the time of atrial myocyte action potential duration at 50% repolarization (APD₅₀) and at 90% repolarization (APD₉₀) were significantly shorten in AF group, TASK-1 current density and TASK-1 protein expression were increased (P<0.05). Compared with AF group, the duration of atrial fibrillation was decreased,the time of atrial myocyte APD₅₀ and APD₉₀ were prolonged, TASK-1 current density and protein expression were significantly reduced in DHA+AF group (P<0.05). Conclusion: DHA can prolong the atrial myocyte APD in atrial fibrillation rats, which may be related to down-regulation of TASK-1 protein expression and decreasing TASK-1 current density in atrial tissue.