Stacher G, Stärker D
Am J Dig Dis. 1975 Feb;20(2):156-61. doi: 10.1007/BF01072342.
The action of bromazepam on insulin-stimulated gastric acid secretion was examined in 5 healthy volunteers in a randomized study. To measure acid output, the intragastric titration technique and a pH-sensitive telemetering capsule were used. Three series of experiments were performed: (1) insulin (0.2 U/kg body weight), stimulation alone; (2) simultaneous injection of insulin and bromazepam (0.1 mg/kg body weight), subjects kept awake; (3) synchronous injection of insulin and bromazepam but with subjects allowed to fall asleep after drug administration. In all three series after insulin administration a significant initial inhibition of gastric secretion occurred. There were no significant differences between the three series regarding the intensity of hypoglycemia. Blood glucose levels lower than 25 mg/100 ml were reached in all experiments. Bromazepam in subjects kept awake caused drowsiness and a lower gastric acid response to hypoglycemia as compared to insulin alone, but the difference was not significant. In subjects allowed to sleep, this reduction was marked and gastric acid output was significantly lower than in both other series. These findings suggest that sleep and drowsiness, rather than bromazepam itself, cause inhibition of insulin-induced gastric secretion.
在一项随机研究中，对5名健康志愿者检测了溴西泮对胰岛素刺激胃酸分泌的作用。为测量胃酸排出量，采用了胃内滴定技术和一种对pH敏感的遥测胶囊。进行了三组实验：(1)单独注射胰岛素(0.2 U/kg体重)；(2)同时注射胰岛素和溴西泮(0.1 mg/kg体重)，受试者保持清醒；(3)同步注射胰岛素和溴西泮，但给药后让受试者入睡。在所有三组中，注射胰岛素后最初均出现胃酸分泌的显著抑制。三组之间低血糖的严重程度无显著差异。所有实验中血糖水平均降至低于25 mg/100 ml。与单独注射胰岛素相比，保持清醒的受试者注射溴西泮后出现嗜睡，且对低血糖的胃酸反应较低，但差异不显著。在允许入睡的受试者中，这种降低很明显，胃酸排出量显著低于其他两组。这些发现表明，是睡眠和嗜睡，而非溴西泮本身，导致胰岛素诱导的胃酸分泌受到抑制。
