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 K⁺ current (I_K) and the inward rectifier K⁺ current (I_KI) were assessed using a voltage ramp protocol. A more detailed study on the I_K was performed. The I_{Ca, L} was measured. In the rat ventricular myocytes, the transient outward K⁺ current (I_to) 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 I_KI at -130 mV and the peak outward I_KI) 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 I_K 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 I_to to 80 ± 8% and 68 ± 7%, respectively. A concentration-dependent reduction in the I_{Ca, L} 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 I_K and I_to suppression.