Abstract: 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.

Key words: atrial fibrillation, docosahexaenoic acid, atrial electrical remodeling, TASK-1