Baron J H
Gut. 1970 Oct;11(10):826-36. doi: 10.1136/gut.11.10.826.
Fourteen studies of gastric acid secretion in a basal hour and in the two hours after a single intravenous injection of soluble insulin (0.01 to 0.40 units/kg) were performed in a healthy man. The peak acid output after insulin (measured as the two consecutive 15-minute samples giving the highest acid output) was significantly correlated with the lowest concentration of blood glucose, the fall in blood glucose, the rate of fall of blood glucose, and the maximum fall of blood glucose in any 15 minutes. Peak acid outputs after insulin were similar over the range 0.1 to 0.2 units/kg, and greater than at lower or higher doses. These results are contrary to the accepted assumption that insulin-stimulated acid secretion is an ;all-or-none' phenomenon. They support instead the hypothesis that insulin hypoglycaemia provides a quantitative glycopenic stimulus producing quantitative vagal acid response. Extreme hypoglycaemia, below about 15 mg/100 ml of blood glucose, inhibits insulin-stimulated acid secretion.
在一名健康男性身上进行了14项关于基础状态下胃酸分泌以及单次静脉注射可溶性胰岛素(0.01至0.40单位/千克)后两小时胃酸分泌的研究。胰岛素注射后的胃酸分泌峰值(以连续两个15分钟内胃酸分泌量最高的样本计算)与血糖最低浓度、血糖下降值、血糖下降速率以及任何15分钟内血糖的最大下降值显著相关。胰岛素剂量在0.1至0.2单位/千克范围内时,注射后胃酸分泌峰值相似,且高于较低或较高剂量时的峰值。这些结果与公认的假设相反,即胰岛素刺激胃酸分泌是一种“全或无”现象。相反,它们支持了这样一种假说,即胰岛素低血糖提供了一种定量的低血糖刺激,从而产生定量的迷走神经介导的胃酸反应。血糖低于约15毫克/100毫升的极端低血糖会抑制胰岛素刺激的胃酸分泌。