Effects of dexmedetomidine on electrophysiological stability of ventricular myocardium and expression of gap junction connexin43 in rats: an in vitro experiment / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effects of dexmedetomidine on the electrophysiological stability of ventricular myocardium and the expression of gap junction connexin43 (Cx43) in rats in an in vitro experiment.Methods Healthy adult Sprague-Dawley rats of both sexes,weighing 270-330 g,were anesthetized with 3.0％ pentobarbital sodium 50 mg/kg.Their hearts were excised and retrogradely perfused in a Langendorff apparatus with K-H solution saturated with 95％ 02-5％ CO2 at 37 ℃.Twelve isolated rat hearts were divided into 2 groups (n =6 each) using a random number tablecontrol group (group C) and dexmedetomidine group (group D).After 15 min of perfusion with K-H solution,hearts were continuously perfused for 30 min with K-H solution in group C or with K-H solution containing dexmedetomidine 50 ng/ml in group D.The monophasic action potential (MAP) and ventricular effective refractory period (VERP) of the left ventricular myocardium were recorded.Myocardial MAP duration at 90％ repolarization (MAPD90) and the ratio of VERP to MAPD9.(VERP/MAPD90) were calculated.Repetitive regular stimuli (S1) were followed by a single extrastimulus (S2),and the longest pacing cycle length of ventricular fibrillation threshold and development of ventricular arrhythmia were recorded.Left ventricular myocardial tissues were obtained for detection of the expression of myocardial Cx43 by Western blot.Results Compared with group C,the MAPD90 and VERP were significantly prolonged,VERP/MAPD90 ratio was decreased,the longest pacing cycle length of ventricular fibrillation threshold was prolonged,the incidence of ventricular arrhythmia was increased,and the expression of myocardial Cx43 was down-regulated in group D (P＜ 0.05).Conclusion Dexmedetomidine can decrease the electruphysiological stability of ventricular myocardium and down-regulate the expression uf Cx43,thus increasing the risk of arrhythmia in rats in an in vitro experiment.