Hansky J, Korman M G, Cowley D J, Baron J H
Gut. 1971 Dec;12(12):959-62. doi: 10.1136/gut.12.12.959.
Serum gastrin has been measured by radioimmunoassay in normal subjects and patients with proven duodenal ulcer in response to insulin hypoglycaemia in conjunction with manoeuvres to decrease the intragastric acidity. Insulin hypoglycaemia alone caused a rise in the serum gastrin level from 5 +/- 1.0 to 49 +/- 2.9 pg/ml in duodenal ulcer and from 17 +/- 5.6 to 42 +/- 7.7 pg/ml in normals. With complete intragastric neutralization of acid and the same stimulus, the rise in duodenal ulcer was from 5 +/- 1.3 to 128 +/- 13.6 pg/ml and in normals from 13 +/- 2.6 to 84 +/- 2.6 pg/ml. These studies suggest an increased production rate of gastrin in response to vagal stimulation in duodenal ulcer, and indicate the precise role of acid inhibition in the control of gastrin release and support the concept of both an increased ;G cell' mass and parietal cell mass in duodenal ulcer. They have also offered an explanation of the variable vagal stimulation of gastrin release in normal subjects.
采用放射免疫分析法测定了正常受试者和确诊为十二指肠溃疡患者在胰岛素低血糖反应并结合降低胃内酸度操作时的血清胃泌素水平。仅胰岛素低血糖就导致十二指肠溃疡患者的血清胃泌素水平从5±1.0 pg/ml升至49±2.9 pg/ml，正常受试者从17±5.6 pg/ml升至42±7.7 pg/ml。在胃内酸完全中和且刺激相同的情况下，十二指肠溃疡患者的胃泌素水平从5±1.3 pg/ml升至128±13.6 pg/ml，正常受试者从13±2.6 pg/ml升至84±2.6 pg/ml。这些研究表明，十二指肠溃疡患者对迷走神经刺激的胃泌素产生率增加，表明酸抑制在胃泌素释放控制中的精确作用，并支持十二指肠溃疡中“G细胞”和壁细胞数量均增加的概念。它们还解释了正常受试者中胃泌素释放的迷走神经刺激变化情况。
