十二指肠酸化和促胰液素可通过前列腺素抑制人胃酸分泌，但十二指肠内脂肪则无此作用。

Duodenal acidification and secretin, but not intraduodenal fat, inhibit human gastric acid secretion via prostaglandins.

作者信息

Taylor S D, Soudah H C, Chey W Y, Scheiman J M

机构信息

Division of Gastroenterology, University of Michigan, Ann Arbor.

出版信息

Gastroenterology. 1994 Dec;107(6):1680-5. doi: 10.1016/0016-5085(94)90808-7.

DOI:10.1016/0016-5085(94)90808-7

PMID:7958679

Abstract

BACKGROUND/AIMS: Acid and fat in the duodenum inhibit gastric acid secretion and increase plasma secretin. The role of prostaglandins and secretin in the inhibition of gastric acid secretion by duodenal infusion of hydrochloric acid and fat in healthy human volunteers was studied.

METHODS

Gastric acid secretion was submaximally stimulated with intravenous pentagastrin followed by duodenal infusion of 0.1N hydrochloric acid, oleic acid, or intravenous secretin. To inhibit endogenous prostaglandins, the protocol was then repeated after indomethacin treatment.

RESULTS

Duodenal fat infusion inhibited acid secretion 80% +/- 5% and was unaffected by indomethacin treatment. Intraduodenal acidification inhibited acid secretion by 43% +/- 8% and was reduced by indomethacin treatment to 15% +/- 4% (P < 0.01). Similarly, intravenous secretin inhibited acid secretion by 34% +/- 3%, which was decreased to 13% +/- 6% by indomethacin treatment (P < 0.01). The increase in plasma secretin levels after intraduodenal hydrochloric acid treatment was significantly greater than that observed with intravenous secretin or introduodenal oleic acid treatment; all were within the physiological range. Acid in the duodenum releases secretin, which inhibits gastric acid secretion at least in part via prostaglandins. In contrast, fat in the duodenum strongly inhibits gastric acid secretion via a nonprostaglandin pathway.

CONCLUSIONS

Secretin is the predominant mediator for the inhibition of human gastric acid secretion induced by the presence of acid, but not fat, in the duodenum.

摘要

背景/目的：十二指肠中的酸和脂肪可抑制胃酸分泌并增加血浆促胰液素水平。本研究旨在探讨前列腺素和促胰液素在健康人类志愿者中十二指肠灌注盐酸和脂肪对胃酸分泌抑制作用中的角色。

方法

静脉注射五肽胃泌素使胃酸分泌达到亚最大刺激水平，随后十二指肠灌注0.1N盐酸、油酸或静脉注射促胰液素。为抑制内源性前列腺素，在吲哚美辛治疗后重复该方案。

结果

十二指肠灌注脂肪使胃酸分泌抑制80%±5%，且不受吲哚美辛治疗影响。十二指肠酸化使胃酸分泌抑制43%±8%，吲哚美辛治疗后降至15%±4%（P<0.01）。同样，静脉注射促胰液素使胃酸分泌抑制34%±3%，吲哚美辛治疗后降至13%±6%（P<0.01）。十二指肠内盐酸治疗后血浆促胰液素水平的升高显著大于静脉注射促胰液素或十二指肠内油酸治疗；所有均在生理范围内。十二指肠中的酸释放促胰液素，其至少部分通过前列腺素抑制胃酸分泌。相比之下，十二指肠中的脂肪通过非前列腺素途径强烈抑制胃酸分泌。