Kobayashi Y, Freas W, Muldoon S M
Department of Anesthesiology, Kanagawa Dental College, Japan.
Anesth Analg. 1995 Aug;81(2):265-71. doi: 10.1097/00000539-199508000-00010.
We examined the pre- and postsynaptic effects of enflurane on the superior mesenteric artery and vein. We measured the release of norepinephrine (NE) from sympathetic nerve terminals caused by electrical stimulation (ES) or potassium and changes in vascular smooth muscle tension. The effect of enflurane was also examined in the presence of alpha 1- and alpha 2-adrenoceptor antagonists. Enflurane (1.4 to 1.6 minimum alveolar anesthetic concentration [MAC] in the dog) did not alter basal tension, but it significantly inhibited tension development caused by 40 mM KCl and ES in the canine mesenteric artery and vein. Enflurane inhibited the KCl- and ES-induced release of NE from sympathetic nerve terminals in the canine mesenteric vein. The alpha 1- and alpha 2-adrenoceptor antagonists, corynanthine or yohimbine, did not modify the effect of enflurane on the ES-induced frequency response curve of the mesenteric artery and vein. These data suggest that enflurane has at least two sites of action in mesenteric vascular beds. One site is presynaptic where it inhibits NE release, and the other is a postsynaptic site distal to the adrenergic receptor where it inhibits the smooth muscle contraction process.
我们研究了恩氟烷对肠系膜上动脉和静脉的突触前和突触后效应。我们测量了由电刺激(ES)或钾引起的交感神经末梢去甲肾上腺素(NE)的释放以及血管平滑肌张力的变化。还在存在α1和α2肾上腺素能受体拮抗剂的情况下研究了恩氟烷的作用。恩氟烷(犬体内1.4至1.6最低肺泡麻醉浓度[MAC])并未改变基础张力,但它显著抑制了犬肠系膜动脉和静脉中由40 mM氯化钾和电刺激引起的张力发展。恩氟烷抑制了犬肠系膜静脉中由氯化钾和电刺激诱导的交感神经末梢NE释放。α1和α2肾上腺素能受体拮抗剂,育亨宾碱或育亨宾,并未改变恩氟烷对肠系膜动脉和静脉电刺激诱导的频率反应曲线的作用。这些数据表明恩氟烷在肠系膜血管床中至少有两个作用位点。一个位点是突触前的,它抑制NE释放,另一个是肾上腺素能受体远端的突触后位点,它抑制平滑肌收缩过程。