Athow A C, Sewerniak A T, Barton T P, Clark C G, Lewin M R
Clin Sci (Lond). 1985 Jul;69(1):37-40. doi: 10.1042/cs0690037.
The blood cortisol and gastric acid responses to insulin hypoglycaemia were investigated in 18 healthy control subjects and 14 patients with endoscopically proven duodenal ulceration. In both controls and patients, insulin hypoglycaemia caused blood cortisol and acid output to rise and peak simultaneously, the rises being significantly greater in patients with duodenal ulcer than in control subjects. The peak acid output and the base to peak cortisol increments were also found to be significantly greater in patients with duodenal ulcer than in control subjects (P less than 0.001 and P less than 0.005 respectively). We conclude that insulin hypoglycaemia causes stimulation of the sympathetic and parasympathetic nervous systems and of the hypothalamo-pituitary-adrenal axis, resulting in the simultaneous elevation of gastric juice acidity and blood cortisol levels. We have shown that synchronous rises in gastric acid and blood cortisol occur during insulin hypoglycaemia and that these rises are greater in patients with duodenal ulcer.
对18名健康对照者和14名经内镜证实患有十二指肠溃疡的患者，研究了其对胰岛素低血糖的血皮质醇和胃酸反应。在对照者和患者中，胰岛素低血糖均导致血皮质醇和胃酸分泌量同时升高并达到峰值，十二指肠溃疡患者的升高幅度显著大于对照者。十二指肠溃疡患者的胃酸分泌峰值以及皮质醇从基础值到峰值的增量也显著大于对照者（分别为P<0.001和P<0.005）。我们得出结论，胰岛素低血糖会刺激交感神经系统、副交感神经系统以及下丘脑-垂体-肾上腺轴，导致胃液酸度和血皮质醇水平同时升高。我们已经表明，胰岛素低血糖期间胃酸和血皮质醇会同步升高，且十二指肠溃疡患者的升高幅度更大。
