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在“健康”受试者中,胃窦扩张会抑制胃酸分泌还是刺激碳酸氢盐分泌?

Does antral distension inhibit gastric acid secretion or stimulate bicarbonate secretion in 'healthy' subjects?

作者信息

Hamlet A, Dalenbäck J, Olbe L, Fändriks L

机构信息

Dept. of Physiology, University of Gothenburg, Sweden.

出版信息

Scand J Gastroenterol. 1993 Nov;28(11):999-1004. doi: 10.3109/00365529309098299.

Abstract

The effects of a 150-ml antral balloon distension on pentagastrin-stimulated gastric acid secretion and bicarbonate secretion were studied in nine healthy subjects and eight duodenal ulcer (DU) patients. The gastric secretions were simultaneously measured, using a luminal perfusion and pH/PCO2 measurements. Two of the healthy subjects and six of the DU patients were positive for Helicobacter pylori. When H. pylori-positive and -negative subjects were compared, basal gastric acid and bicarbonate outputs did not differ significantly. In H. pylori-infected subjects the bicarbonate transport increased by about 70% on pentagastrin stimulation. In the H. pylori-negative group pentagastrin had no effect on the bicarbonate secretion. Antral distension elicited a 30-35% inhibition of pentagastrin-stimulated gastric acid secretion in the group of H. pylori-negative subjects, whereas the acid secretory level remained essentially unchanged in the positive group. Bicarbonate secretion decreased transiently by the distension in the negative subjects, whereas a slight increase was observed in the infected group. We conclude that antral distension inhibits pentagastrin-stimulated gastric acid output in healthy H. pylori-negative subjects. Our results strongly suggest that the underlying mechanism is a direct inhibition of gastric parietal cell function and not an increased gastric bicarbonate secretion. Furthermore, the results indicate that this defective distension-induced acid inhibition may be correlated to H. pylori infection rather than to duodenal ulcer disease.

摘要

在9名健康受试者和8名十二指肠溃疡(DU)患者中,研究了150毫升胃窦球囊扩张对五肽胃泌素刺激的胃酸分泌和碳酸氢盐分泌的影响。采用腔内灌注和pH/PCO2测量法同时测定胃分泌物。9名健康受试者中有2名、8名DU患者中有6名幽门螺杆菌检测呈阳性。比较幽门螺杆菌阳性和阴性受试者时,基础胃酸和碳酸氢盐分泌量无显著差异。在幽门螺杆菌感染的受试者中,五肽胃泌素刺激后碳酸氢盐转运增加约70%。在幽门螺杆菌阴性组中,五肽胃泌素对碳酸氢盐分泌无影响。胃窦扩张使幽门螺杆菌阴性组中五肽胃泌素刺激的胃酸分泌受到30%-35%的抑制,而在阳性组中胃酸分泌水平基本保持不变。在阴性受试者中,扩张使碳酸氢盐分泌短暂减少,而在感染组中观察到略有增加。我们得出结论,胃窦扩张抑制幽门螺杆菌阴性健康受试者中五肽胃泌素刺激的胃酸分泌。我们的结果强烈表明,其潜在机制是直接抑制胃壁细胞功能,而非胃碳酸氢盐分泌增加。此外,结果表明这种扩张诱导的胃酸抑制缺陷可能与幽门螺杆菌感染有关,而非与十二指肠溃疡病有关。

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