Abstract

Abstract Background Many clinical studies suggest an impact of propofol on the occurrence of atrial arrhythmias. Purpose Since experimental data is sparse, purpose of this study was to investigate the influence of propofol on atrial electrophysiology and the vulnerability to atrial fibrillation in a sensitive whole-heart model of atrial fibrillation. Methods 11 hearts of New Zealand white rabbits were isolated and Langendorff-perfused. Two catheters were placed on both atria to record atrial monophasic action potentials. Hearts were stimulated at three different cycle lengths (350ms, 250ms, 150ms), thereby obtaining cycle-length dependent atrial action potential durations (aAPD90) and effective refractory periods (aERP). Atrial post-repolarization (aPRR) refractoriness was defined as the difference between aERP and aAPD90. To increase the occurrence of atrial fibrillation, hearts were perfused with a combination of acetylcholine (ACh, 1μM) and isoproterenol (Iso, 1μM) after obtaining baseline data. Vulnerability to atrial fibrillation was tested by a standardized protocol consisting of several trains of burst pacing. Results Acetylcholine/isoproterenol infusion reduced aAPD90 (−3ms), aERP (−16ms) and aPRR (−14ms). Additional treatment with propofol prolonged aAPD90 (+5ms), aERP (+24ms) and aPRR (+20ms). Under baseline conditions, 13 episodes of atrial fibrillation lasting longer than 1s occurred. Additional treatment with acetylcholine/isoproterenol provoked more episodes of atrial fibrillation (33 episodes, p<0.05). Infusion of propofol on top of acetylcholine/isoproterenol significantly suppressed atrial fibrillation (2 episodes, p<0.05). Conclusion In this study, propofol prolonged aAPD90 and significantly reduced the occurrence of atrial fibrillation. Prolongation of effective refractory periods and especially of post-repolarization refractoriness protects the atrial myocardium against premature excitation and thereby prevents arrhythmias.

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