Effect of dexmedetomidine on action potential duration of rat ventricular myocytes and the role of α2 receptors

Abstract

Objective To evaluate the effect of dexmedetomidine on action potential duration(APD)of rat ventricular myocytes and the role of α2 receptors. Methods Eighteen ventricular myocytes acutely isolated from Sprague-Dawley rats by enzymatic hydrolysis were divided into 3 groups(n=6 each)using a random number table: dexmedetomidine group(D group), yohimbine group(Y group)and dexmedetomidine plus yohimbine group(DY group). Isolated ventricular myocytes were first perfused for 2 min with Tyrode′s solution alone, and APD at 90% repolarization(APD90)was recorded using whole-cell patch-clamp technique.D, Y and DY groups were subsequently perfused for 2 min with Tyrode′s solution containing dexmedetomidine 10-9 mol/L, yohimbine 10-6 mol/L, and dexmedetomidine 10-9 mol/L plus yohimbine 10-6 mol/L, respectively, and APD90 was recorded.The percentage of changes in APD90 was calculated. Results Compared with the isolated ventricular myocytes perfused with Tyrode′s solution alone, APD90 of ventricular myocytes was significantly prolonged in group D(P 0.05). The percentage of changes in APD90 of ventricular myocytes was significantly shortened in group DY and group Y when compared with group D(P<0.05). Conclusion Dexmedetomidine can prolong APD90 of rat ventricular myocytes, and the mechanism is related to activating α2 receptors. Key words: Dexmedetomidine; Myocytes, cardiac; Receptor adrenergic alpha- 2; Action potentials