Muldoon S M, Vanhoutte P M, Lorenz R R, Van Dyke R A
Anesthesiology. 1975 Jul;43(1):41-8. doi: 10.1097/00000542-197507000-00006.
Experiments were performed to determine whether depression of venomotor responses with halothane results from interference with sympathetic activation or from an effect on venous smooth muscle cells. Changes in isometric tension of isolated canine saphenous-vein strips were recorded. Adrenergic activation was achieved by transmural electrical stimulation, by addition of tyramine, and by addition of morepinephrine. Halothane (0.5 to 3 per cent) did not significantly alter basal tension. It lessened the reaction of the veins to electrical stimulation but not their response to norepinephrine; it increased the response to tyramine. Since the responses to norepinephrine and tyramine were not decreased, halothane appears to act on the nerve terminal to prevent release of neurotransmitter associated with nerve-terminal depolarization. Thus, halothane causes inhibition of electrically induced venoconstriction in cutaneous veins, probably by interfering with the release of norepinephrine from nerve terminals rather than by an inhibitory effect on the smooth muscle cells.
进行实验以确定氟烷对静脉运动反应的抑制是源于对交感神经激活的干扰还是对静脉平滑肌细胞的影响。记录了分离的犬隐静脉条的等长张力变化。通过透壁电刺激、添加酪胺和添加去甲肾上腺素来实现肾上腺素能激活。氟烷（0.5%至3%）并未显著改变基础张力。它减弱了静脉对电刺激的反应，但未减弱其对去甲肾上腺素的反应；它增强了对酪胺的反应。由于对去甲肾上腺素和酪胺的反应未降低，氟烷似乎作用于神经末梢以阻止与神经末梢去极化相关的神经递质释放。因此，氟烷可能通过干扰神经末梢去甲肾上腺素的释放而非对平滑肌细胞的抑制作用来抑制皮肤静脉中电诱导的静脉收缩。
