Rorie D K, Tyce G M, Mackenzie R A
Anesth Analg. 1984 Dec;63(12):1059-64.
Studies were done to determine the mechanism whereby halothane inhibits the release of norepinephrine from postganglionic sympathetic nerve endings. Helical strips of dog saphenous vein were mounted for superfusion and measurement of isometric contractile tension in the presence or absence of halothane (1.2 or 2.5%). Endogenous norepinephrine overflowing in response to electrical stimulation (10 V, 2 Hz for 15 min), and the content of norepinephrine remaining in the veins after stimulation, were measured by liquid chromatography with electrochemical detection. The data indicate that halothane decreased the stimulation-evoked release of norepinephrine by stimulation of prejunctional inhibitory muscarinic receptors. Evidence was also obtained that halothane may impair clearance of norepinephrine from the synaptic cleft.
开展了多项研究以确定氟烷抑制节后交感神经末梢去甲肾上腺素释放的机制。将犬隐静脉螺旋条安装好用于在有或没有氟烷(1.2%或2.5%)存在的情况下进行灌注和等长收缩张力测量。通过液相色谱电化学检测法测量响应电刺激(10伏,2赫兹,持续15分钟)而溢出的内源性去甲肾上腺素,以及刺激后静脉中剩余的去甲肾上腺素含量。数据表明,氟烷通过刺激节前抑制性毒蕈碱受体减少了刺激诱发的去甲肾上腺素释放。还获得了证据表明氟烷可能损害去甲肾上腺素从突触间隙的清除。