Electrophysiologic Effect of Desflurane on the Prolongation of Action Potential Duration in Ventricular Myocytes

Abstract

Background: Desflurane has been reported to prolong the QTc. Several ionic currents that contribute to the prolongation of the action potential (AP) duration were investigated using guinea pig (GP) and rat ventricular myocytes. Methods: The normal APs were measured in isolated GP papillary muscles at 37. Ventricular myocytes were obtained from GP and rat hearts. Both the delayed outward current () and the inward rectifier current () were assessed using a voltage ramp protocol. A more detailed study on the was performed. The was measured. In the rat ventricular myocytes, the transient outward current () was obtained. All the patch clamp experiments were carried out at room temperature. The values are presented as mean SD. Results: 0.91 mM desflurane significantly prolonged the APD in the GP ventricular myocytes. Using a linear voltage ramp protocol, the at -130 mV and the peak outward at -60 to -50 mV were not found to be significantly reduced by 0.78 and 1.23 mM desflurane, respectively. However, the peak outward at +60 mV was significantly reduced to 63 19% and 58 12% of the baseline by 0.78 and 1.23 mM desflurane, respectively. At a membrane potential of +60 mV, 0.78 and 1.23 mM desflurane reduced the to 80 8% and 68 7%, respectively. A concentration-dependent reduction in the was observed. Conclusions: The prolongation of the APD induced by clinically relevant concentrations of desflurane in GP and rat ventricular myocytes is most likely the result of and suppression.