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吲哚美辛对人体胃酸和碳酸氢盐分泌的影响。

Effect of indomethacin on gastric acid and bicarbonate secretion in humans.

作者信息

Feldman M, Colturi T J

出版信息

Gastroenterology. 1984 Dec;87(6):1339-43.

PMID:6149164
Abstract

The role of endogenous prostaglandins in the physiologic regulation of gastric secretion is unclear. We evaluated the effect of indomethacin, an inhibitor of endogenous prostaglandin synthesis, on basal gastric secretion in humans using a two-component model for calculating gastric acid and bicarbonate secretion. After a control, gastric secretory study, 11 healthy volunteers were given 50 mg of indomethacin orally every 8 h for a total of 10 doses, after which the gastric secretory experiment was repeated. Indomethacin significantly (p less than 0.05) increased basal gastric juice volume, hydrogen ion concentration, osmolality, and acid output. Indomethacin increased acid secretion significantly (from 4.9 +/- 1.2 to 7.4 +/- 1.7 mmol/75 min, p less than 0.02) without affecting gastric bicarbonate secretion (control 2.7 +/- 0.8, indomethacin 3.0 +/- 0.7 mmol/75 min; p greater than 0.05). The increase in basal acid secretion after indomethacin administration was quite variable from subject to subject and was unaccompanied by significant changes in basal serum gastrin concentrations. Unlike basal acid secretion, indomethacin had no significant effect on acid secretion stimulated by intragastric infusion of homogenized food. Moreover, indomethacin did not prevent intravenous somatostatin 14 from inhibiting food-stimulated acid secretion, in contrast to a previous study in rats in which indomethacin blocked the inhibitory effect of somatostatin on acid secretion. Assuming the effect of indomethacin is due to reduced endogenous prostaglandin synthesis, we conclude that (a) in some individuals endogenous prostaglandins suppress basal acid secretion by a mechanism independent of the hormone gastrin; (b) endogenous prostaglandins play little, if any, role in the regulation of basal bicarbonate secretion by the stomach; and (c) endogenous prostaglandins do not regulate food-stimulated acid secretion, nor do they mediate the inhibitory effect of somatostatin on gastric acid secretion in humans.

摘要

内源性前列腺素在胃分泌的生理调节中的作用尚不清楚。我们使用一种计算胃酸和碳酸氢盐分泌的双组分模型,评估了内源性前列腺素合成抑制剂吲哚美辛对人体基础胃分泌的影响。在进行对照性胃分泌研究后,11名健康志愿者每8小时口服50毫克吲哚美辛,共服用10剂,之后重复胃分泌实验。吲哚美辛显著(p小于0.05)增加了基础胃液量、氢离子浓度、渗透压和酸分泌量。吲哚美辛显著增加了酸分泌(从4.9±1.2增至7.4±1.7毫摩尔/75分钟,p小于0.02),而不影响胃碳酸氢盐分泌(对照为2.7±0.8,吲哚美辛为3.0±0.7毫摩尔/75分钟;p大于0.05)。服用吲哚美辛后基础酸分泌的增加在个体间差异很大,且基础血清胃泌素浓度无显著变化。与基础酸分泌不同,吲哚美辛对胃内输注匀浆食物刺激的酸分泌无显著影响。此外,与之前在大鼠中的研究不同,在大鼠研究中吲哚美辛阻断了生长抑素对酸分泌的抑制作用,而在人体中吲哚美辛并未阻止静脉注射的生长抑素14抑制食物刺激的酸分泌。假设吲哚美辛的作用是由于内源性前列腺素合成减少,我们得出以下结论:(a) 在某些个体中,内源性前列腺素通过一种独立于胃泌素激素的机制抑制基础酸分泌;(b) 内源性前列腺素在胃基础碳酸氢盐分泌的调节中作用甚微(如果有作用的话);(c) 内源性前列腺素不调节食物刺激的酸分泌,也不介导生长抑素对人体胃酸分泌的抑制作用。

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