Wilde D W
Department of Anesthesiology, University of Michigan Medical Center, Ann Arbor 48109-0615, USA.
Anesth Analg. 1996 Dec;83(6):1307-13. doi: 10.1097/00000539-199612000-00030.
Volatile anesthetics vasodilate in part by direct action on vascular smooth muscle. Isoflurane-induced relaxation of portal vein smooth muscle involves alteration of membrane ionic currents that control cell excitability and contraction. Whole cell voltage clamp technique was used to examine outward Ca(2+)-activated K+ current (IK,Ca) in guinea pig portal vein cells. Isoflurane caused a concentration-dependent reduction in IK,Ca at steady-state conditions but had no significant effect on resting potential. Isoflurane transiently potentiated IK,Ca by a mechanism that may partly involve Ca2+ release from intracellular storage sites. The depression of IK,Ca by isoflurane may occur by direct action on the channel protein or on the lipid environment of the channel to alter conductance or kinetic properties. Since isoflurane reduces IK,Ca coincident with suppression of Ca2+ channel current, it was concluded that the depression of IK,Ca by isoflurane is of secondary importance to reduction in inward Ca2+ channel current. Potentiation of IK,Ca may preclude significant membrane activation during the onset of isoflurane's action.
挥发性麻醉剂部分通过对血管平滑肌的直接作用而产生血管舒张作用。异氟烷诱导的门静脉平滑肌松弛涉及控制细胞兴奋性和收缩的膜离子电流的改变。采用全细胞电压钳技术检测豚鼠门静脉细胞外向钙激活钾电流（IK,Ca）。在稳态条件下，异氟烷使IK,Ca呈浓度依赖性降低，但对静息电位无显著影响。异氟烷通过一种可能部分涉及细胞内储存部位钙释放的机制短暂增强IK,Ca。异氟烷对IK,Ca的抑制可能是通过对通道蛋白或通道的脂质环境的直接作用来改变电导或动力学特性。由于异氟烷在降低钙通道电流的同时降低IK,Ca，因此得出结论，异氟烷对IK,Ca的抑制相对于内向钙通道电流的降低而言是次要的。IK,Ca的增强可能会在异氟烷作用开始时阻止显著的膜激活。
