Stenquist B, Knutson U, Rehnberg O, Olbe L
Scand J Gastroenterol. 1977;12(2):169-75.
The gastric acid response to i.v. injection of 0.15 U of soluble insulin/kg b.w. was determined in healthy subjects and duodenal ulcer patients during intragastric perfusion with water, 0.1 M HC1, and alkaline buffer (pH 8.3). Perfusion with hydrochloric acid significantly reduced the peak gastric acid output following insulin in 6 healthy subjects (reduction 45%, p less than 0.05) but had no significant effect on the peak gastric acid response to insulin in 7 DU patients (reduction 16%, p greater than 0.05). The 2.5-hour gastric acid response to insulin was, however, significantly reduced in both groups (56% and 35%, respectively) by exogenous acidification of the stomach. The gastric acid response to insulin hypoglycaemia in 3 DU patients was the same with intragastric water and alkaline buffer perfusion. The reduction of the gastric acid response to insulin hypoglycaemia by intragastric acidification corresponded to a reduced volume secretion and could not be ascribed to increased back diffusion of hydrogen ions or duodenal inhibition. These findings suggest that the gastric acid response to insulin hypoglycaemia is inhibited by a low intragastric pH in man, and that DU patients are less sensitive to the inhibitory mechanism than healthy subjects.
在健康受试者和十二指肠溃疡患者中,于胃内灌注水、0.1M盐酸和碱性缓冲液(pH 8.3)期间,测定静脉注射0.15U可溶性胰岛素/千克体重后胃酸的反应。用盐酸灌注可使6名健康受试者胰岛素注射后胃酸分泌峰值显著降低(降低45%,p<0.05),但对7名十二指肠溃疡患者胰岛素注射后胃酸分泌峰值无显著影响(降低16%,p>0.05)。然而,通过胃的外源性酸化,两组患者胰岛素注射后2.5小时的胃酸反应均显著降低(分别为56%和35%)。3名十二指肠溃疡患者在胃内灌注水和碱性缓冲液时,对胰岛素低血糖的胃酸反应相同。胃内酸化导致胰岛素低血糖时胃酸反应降低,这与分泌量减少有关,不能归因于氢离子反向扩散增加或十二指肠抑制。这些发现表明,人体胃内低pH可抑制对胰岛素低血糖的胃酸反应,且十二指肠溃疡患者对这种抑制机制的敏感性低于健康受试者。