pH dependence of acid secretion and gastrin release in normal and ulcer subjects.

pH dependence of acid secretion and gastrin release in normal and ulcer subjects.
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正常和溃疡受试者中酸分泌和胃泌素释放的 pH 依赖性。

DOI:
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发表时间:
1975
影响因子:
15.9
通讯作者:
J. Fordtran
J. Fordtran
中科院分区:
医学1区
文献类型:
--
作者:
J. Walsh;C. T. Richardson;J. Fordtran

文献摘要

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使用最近描述的一种方法,通过测量碳酸氢钠的输注速率来估计胃酸分泌率,以保持胃内pH恒定,在5名正常受试者中测量胃酸分泌率和血清胃泌素的变化,同时将胃pH保持在5.5、4.0、3.0和2.5。初步实验表明,该方法不能准确测量pH值低于2.5时的酸分泌。通过在胃中灌注氨基酸和玉米淀粉的溶液来刺激胃酸分泌。氨基酸粕的分泌率在pH为5.5时最高,是相同pH下牛排粕分泌率的60%。随着氨基酸粕的pH降低,酸分泌量逐步减少,因此在pH为2.5时,酸分泌率仅为pH为5.5时的一半。氨基酸餐产生的血清胃泌素的增加也没有牛排餐产生的明显。在氨基酸刺激下,血清胃泌素在pH为5.5、4.0和3.0时的反应相似,但当膳食保持在pH为2.5时,胃泌素没有增加。将6名十二指肠溃疡患者与7名正常受试者在pH值5.5和2.5下进行比较。在两个pH值下,溃疡患者在每个时间段释放更多的胃泌素,分泌更多的酸。更重要的是,在pH为2.5时,溃疡患者的抑制程度明显较低。例如,在刺激后的第2小时,溃疡患者只有30%的胃酸分泌受到抑制,而正常人则有70%。这些发现提示,在低pH条件下,溃疡患者胃泌素释放和胃酸分泌的自我调节存在缺陷,这可能在该疾病的发病机制中起作用。
By use of a recently described method, which estimates the rate of gastric acid secretion by measuring the rate of sodium bicarbonate infusion needed to keep intragastric pH constant, gastric acid secretion rates and changes in serum gastrin were measured in five normal subjects while gastric pH was kept at 5.5, 4.0, 3.0, or 2.5. Preliminary experiments revealed that the method did not accurately measure acid secretion at a pH lower than 2.5. Stimulation of acid secretion was produced by gastric instillation of a solution of amino acids and cornstarch. The secretion rate with the amino acid meal was highest at pH 5.5 and was 60% of that produced by a steak meal at the same pH. As the pH of the amino acid meal was decreased, there was a stepwise reduction in acid secretion so that at pH 2.5 the rate was only half as great as at pH 5.5. The amino acid meal produced increases in serum gastrin that were also less marked than those produced by a steak meal. With amino acid stimulation, serum gastrin responses were similar at pH 5.5, 4.0, and 3.0, but no increase in gastrin could be measured when the meal was maintained at pH 2.5. A group of six patients with duodenal ulcers was compared with seven normal subjects at pH 5.5 and 2.5. Ulcer patients released more gastrin and secreted more acid at each time period at both pH values. More important, the degree of inhibition at pH 2.5 was significantly less in ulcer patients. For example, during the 2nd h after stimulation acid secretion was inhibited by only 30% in ulcer patients compared with 70% in normal subjects. These findings suggest a defect in autoregulation of gastrin release and gastric acid secretion at low pH in ulcer patients which may play a role in pathogenesis of this disease.