Effects of dexmedetomidine on myocardial electrical conduction velocity and expression and distribution of connexin 43 in rats: an in vitro experiment / 中华麻醉学杂志

ABSTRACT

Objective:To investigate the effects of dexmedetomidine on the myocardial electrical conduction velocity and the expression and distribution of connexin 43 (Cx43) in rats.Methods:Healthy adult Sprague-Dawley rats of both sexes, weighing 270-330 g, were used.Twelve isolated rat hearts successfully perfused in the Langendorff apparatus were divided into 2 groups ( n=6 each) using a random number table method: control group (group C) and dexmedetomidine group (group D). The hearts were perfused for 15 min with K-H solution, and then the hearts were continuously perfused for 30 min with 37 ℃ K-H solution in group C and with K-H solution containing dexmedetomidine 50 ng/ml in group D. Programmed electrical stimulation was performed after the end of perfusion, the activation latency was recorded, and the electrical conduction velocity of myocardial tissues was calculated, and then the left ventricular myocardial tissues were obtained for determination of the expression and distribution of myocardial Cx43 protein by immunohistochemistry method. Results:Compared with group C, the activation latency was significantly prolonged, the electrical conduction velocity was reduced, and the expression of Cx43 was down-regulated in group D ( P<0.05). Cx43 protein was mostly distributed in intercalated discs at both ends of cells in group C, and there was a tendency for the proteins localized at end-to-end contact sites of ventricular cardiomyocytes to localize at side-to-side contact sites, and the distribution was messy in group D. Conclusions:Dexmedetomidine causes arrhythmia probably through down-regulating the expression of Cx43 protein, changing its distribution, and reducing myocardial electrical conduction velocity in rats.