Han J, Kim E, Ho W K, Earm Y E
Department of Physiology and Biophysics, Inje University, Pusan, Korea.
Biochem Biophys Res Commun. 1996 Dec 24;229(3):852-6. doi: 10.1006/bbrc.1996.1891.
It has been suggested that volatile anesthetic, isoflurane mediates cardioprotective effects via activation of the ATP-sensitive K+ (KATP) channels. However, no direct evidence has been provided to define whether isoflurane activates cardiac KATP channels using patch-clamp technique. We examined the effects of isoflurane on the KATP channels in rabbit ventricular myocytes by use of patch-clamp technique. Contrary to the results of the in vivo experiments, isoflurane inhibited the channel activity without a change in the single-channel conductance. Isoflurane decreased the channel activity by a decrease in burst duration and an increase in the inter-burst duration. On the other hand, isoflurane diminished the ATP sensitivity of KATP channels, indicating an increased probability of KATP channel opening for a given concentration of ATP after isoflurane anesthesia. The result supports, at least in part, the hypothesis that isoflurane mediates cardioprotective effects via KATP channel activation.
有人提出挥发性麻醉剂异氟烷通过激活ATP敏感性钾离子（KATP）通道介导心脏保护作用。然而，尚未提供直接证据来确定异氟烷是否使用膜片钳技术激活心脏KATP通道。我们通过膜片钳技术研究了异氟烷对兔心室肌细胞中KATP通道的影响。与体内实验结果相反，异氟烷抑制通道活性，而单通道电导没有变化。异氟烷通过减少爆发持续时间和增加爆发间期持续时间来降低通道活性。另一方面，异氟烷降低了KATP通道的ATP敏感性，表明异氟烷麻醉后在给定ATP浓度下KATP通道开放的概率增加。该结果至少部分支持了异氟烷通过KATP通道激活介导心脏保护作用的假说。
