Abstract

Objective To investigate the role of potassium channel in remifentanil-induced prolongation of monophasic action potential duration (MAPD) in the myocardium of rabbits. Methods Eighteen adult rabbit hearts successfully perfused in a Langendorff apparatus were randomly divided into 3 groups (n=6 each) using a random number table: control group (group C), remifentanil group (group R), and K+ channel blocker tetraethylammonium group (group T). After 15 min stabilization with K-H solution, group C was continuously perfused with K-H solution for 60 min, and R and T groups were perfused with K-H solution containing 12 ng/ml remifentanil and 10 ng/ml tetraethylammonium, respectively, for 60 min.At 15 min of stabilization, and 15, 30 and 60 min of perfusion, heart rate, MAPD of all the three layers of the myocardium in the anterior wall of the left ventricular was recorded.MAPD at 50% and 90% repolarization (MAPD50, MAPD90) were calculated. Results Compared with group C, heart rate was significantly decreased, MAPD50 and MAPD90 were prolonged in R and T groups (P <0.05). Conclusion The mechanism by which remifentanil prolongs MAPD in the myocardium of rabbits is associated with blockade of the potassium channels. Key words: Piperidines; Potassium channels; Action potentials; Bradycardia

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