Effects of halothane, an inhalational anesthetics, on endothelium-dependent hyperpolarization in canine coronary arteries

本研究旨在探讨吸入麻醉剂氟烷是否能通过缝隙连接抑制血管内皮细胞与平滑肌之间的电偶联，从而抑制犬冠状动脉血管内皮细胞依赖性超极化。用玻璃毛细管微电极测定细胞膜电位。在吲哚美辛和N^G-硝基-L-精氨酸(NLA)存在下，静息膜电位约为-50 mV，不受血管紧张素转换酶抑制剂培哚普利拉的影响。在多美辛和NLA同时存在的情况下，缓激肽只在有内皮的组织中引起短暂的和浓度依赖的超极化，培哚普利拉增强了这种超极化。氟烷对缓激肽的膜超极化无抑制作用。在较高浓度(10℃~(-4)M)时，氟烷和庚醇(另一种吸入麻醉剂)可引起膜的去极化，但不能抑制缓激肽的超极化。本研究结果表明，血管内皮细胞的超极化不是内皮细胞与内皮细胞之间电通讯的结果，提示内皮源性超极化因子EDHF的存在。

The present study was designed to determine whether or not halothane, an inhalation al anesthetic, which could inhibit electrical coupling between endothelium and smooth muscle through gap junction, could inhibit endothelium-dependent hyperpolarization of vascular smooth muscle in caninecoronary arteries. The membrane potential of smooth muscle cells was measured by glass capillary microelectrodes. In the presence of in domethacin and N^G-nitro-L-arginine (NLA), the resting membrane potential wasabout-50 mV,and was not affected by treatment with perindoprilat, an angiotensin converting enzyme in hibitor. In the presence of both in domethacin and NLA,bradykinin evoked transient and concentration-dependent hyperpolarizations only in tissues with endothelium, which were augmented by perindoprilat. Halothane did not inhibit membrane hyperpolarization to bradykinin. In higher concentration (10^<-4> M), halothane and heptanol (another inhalational an esthetic) caused depolarization of the membrane, but did not inhibit hyperpolarization to bradykinin. The present findings indicate that endothelium-dependent hyperpolarization in smooth muscle cells does not result from an electrical communication between the endothelium and the underlying smooth muscles, and suggest the existence of endothelium-derived hyperpolarizing factor EDHF.