Richardson C T, Walsh J H, Hicks M I, Fordtran J S
J Clin Invest. 1976 Sep;58(3):623-31. doi: 10.1172/JCI108509.
Liquid test meals were infused into the stomach and acid secretion was measured by intragastric titration at pH 5.0 Acid secretion after 500 or 750-ml sodium chloride meals was two to three times higher than basal secretion rates and was equivalent to 25-30% of the peak acid output in response to histamine. Since these meals did not cause a rise in serum gastrin concentration, it is assumed that they stimulate acid secretion by causing distention of the body and fundus of the stomach. Compared with this distention stimulus, glucose meals had no effect on acid secretion and fat-inhibited acid secretion; however, both glucose and fat caused an increase in serum gastrin concentration. Amino acids caused a much greater increase in serum gastrin concentration and enhanced acid secretion above that noted with distention alone. In contrast, albumin did not enhance the serum gastrin concentration or stimulate acid secretion to a statistically significant extent. There was a close correlation between the rise in serum gastrin concentration and rate of acid secretion after different test meals when average results for each test meal were plotted. However, there was a poor correlation between acid secretion and serum gastrin concentration when the responses of the individual subjects with a given test meal were compared. Our interpretations are: (a) Distention is an important stimulant of the acid-secretory response to a meal, and this is not mediated by gastrin release. (b) Gastrin is one but probably not the only mediator of the chemical phase of acid secretion, i.e., acid secretion noted with amino acids that cannot be explained by distention. (c) Glucose and fat also release gastrin; however, with glucose the rise in serum gastrin is too small and too transient to enhance acid secretion, and fat probably releases unmeasured inhibitors that overwhelm the effect of gastrin on acid secretion. (d) Albumin is not a stimulant of acid secretion.
将液体测试餐注入胃内，并通过胃内滴定法在pH 5.0时测量胃酸分泌。500毫升或750毫升氯化钠餐食后的胃酸分泌比基础分泌率高两到三倍，相当于组胺刺激下最大胃酸分泌量的25%-30%。由于这些餐食不会导致血清胃泌素浓度升高，因此推测它们通过引起胃体和胃底扩张来刺激胃酸分泌。与这种扩张刺激相比，葡萄糖餐对胃酸分泌没有影响，脂肪则抑制胃酸分泌；然而，葡萄糖和脂肪都会导致血清胃泌素浓度升高。氨基酸导致血清胃泌素浓度升高幅度更大，并使胃酸分泌比仅由扩张引起的分泌量进一步增加。相比之下，白蛋白在统计学上并没有显著提高血清胃泌素浓度或刺激胃酸分泌。当绘制每种测试餐的平均结果时，不同测试餐后血清胃泌素浓度的升高与胃酸分泌速率之间存在密切相关性。然而，当比较个体受试者对给定测试餐的反应时，胃酸分泌与血清胃泌素浓度之间的相关性较差。我们的解释是：(a)扩张是餐食引起胃酸分泌反应的重要刺激因素，且这一过程不是由胃泌素释放介导的。(b)胃泌素是胃酸分泌化学阶段的一种介质，但可能不是唯一的介质，即氨基酸引起的胃酸分泌无法用扩张来解释。(c)葡萄糖和脂肪也会释放胃泌素；然而，葡萄糖引起的血清胃泌素升高幅度太小且过于短暂，无法增强胃酸分泌，脂肪可能释放了未检测到的抑制剂，从而抵消了胃泌素对胃酸分泌的作用。(d)白蛋白不是胃酸分泌的刺激物。
