Stacher G, Berner P, Naske R, Schuster P, Stärker H, Schulze D
Int J Clin Pharmacol Biopharm. 1976 Sep;14(2):126-31.
The effects of bromazepam (0.1 mg/kg b.w. i.v.) and of placebo on gastric acid secretion related to hypnotically induced anxiety were evaluated in a double blind study, 22 experiments were carried out on 4 healthy volunteers. Drugs were injected after one basal hour. Hypnosis was induced immediately thereafter, and a sequence of anxiety-charged situations out of the subjects past was recalled. After one hour, posthypnotic amnesia was suggested, the subjects awakened and observation continued for another hour. Acid output was measured by means of intragastric titration and a telemetering capsule. During hypnosis and recalling of anxiety in both series, acid output decreased. In the posthypnotic hour there was a significant increase of secretion in the placebo-series, while there was virtually no change in the the bromazepam-series. The pattern of acid output in the placebo-series seems to result from an activation of the sympathetic system under anxiety and a rebound vagal activation in the posthypnotic hour. By contrast, under the sedating effect of bromazepam, no anxiety could be evoked and no rebound vagal activation and thereby no increase of acid secretion resulted.
在一项双盲研究中,评估了溴西泮(0.1毫克/千克体重,静脉注射)和安慰剂对与催眠诱导焦虑相关的胃酸分泌的影响,对4名健康志愿者进行了22次实验。在一个基础小时后注射药物。此后立即诱导催眠,并回忆起受试者过去一系列充满焦虑的情境。一小时后,暗示催眠后遗忘,受试者醒来并继续观察一小时。通过胃内滴定法和遥测胶囊测量胃酸分泌量。在两个系列的催眠和焦虑回忆期间,胃酸分泌量下降。在催眠后一小时,安慰剂组的分泌量显著增加,而溴西泮组几乎没有变化。安慰剂组胃酸分泌模式似乎是由于焦虑状态下交感神经系统的激活以及催眠后一小时迷走神经的反跳性激活所致。相比之下,在溴西泮的镇静作用下,无法诱发焦虑,也没有迷走神经的反跳性激活,因此不会导致胃酸分泌增加。