Nakajima S, Magee D F
Ann Surg. 1974 Aug;180(2):243-6. doi: 10.1097/00000658-197408000-00020.
In unanesthetized dogs with Heidenhain pouches and separated duodenal pouches, intravenous infusion of commercial cholecystokinin (1.0 IDU per min) produced a significant depression of pouch acid and pepsin secretion stimulated by pentagastrin (1.0 microg per min) or by methacholine (2.0 microg per min). Acid response to methacholine was temporarily augmented. Irrigation of the duodenal pouches with emulsified fat produced similar patterns of depression of acid secretion in response to pentagastrin and pepsin secretion in response to pentagastrin or methacholine. Acid secretion stimulated by methacholine was temporarily augmented after the irrigation. It is concluded that fat releases endogenous cholecystokinin from the duodenal mucosa and that cholecystokinin, or duodenal fat, powerfully depresses Heidenhain pouch pepsin secretion in dogs. The involvment of the gastric inhibitory polypeptide (GIP) cannot be assessed from the present experiments.
在具有海登海因小胃和分离十二指肠小胃的未麻醉犬中，静脉输注商用缩胆囊素（每分钟1.0国际单位）可显著抑制由五肽胃泌素（每分钟1.0微克）或乙酰甲胆碱（每分钟2.0微克）刺激引起的小胃酸和胃蛋白酶分泌。对乙酰甲胆碱的酸反应暂时增强。用乳化脂肪灌洗十二指肠小胃，可产生类似的对五肽胃泌素刺激的酸分泌抑制模式，以及对五肽胃泌素或乙酰甲胆碱刺激的胃蛋白酶分泌抑制模式。灌洗后，乙酰甲胆碱刺激的酸分泌暂时增强。得出的结论是，脂肪从十二指肠黏膜释放内源性缩胆囊素，并且缩胆囊素或十二指肠脂肪可强烈抑制犬海登海因小胃的胃蛋白酶分泌。本实验无法评估胃抑制性多肽（GIP）的参与情况。
