反对前列腺素介导生长抑素抑制胃酸分泌的证据。

Evidence against prostaglandin-mediation of somatostatin-inhibition of gastric secretions.

作者信息

Albinus M, Gomez-Pan A, Hirst B H, Shaw B

出版信息

Regul Pept. 1985 Mar;10(2-3):259-66. doi: 10.1016/0167-0115(85)90020-5.

Abstract

The inhibitory activities of somatostatin and PGE2 against pentagastrin-stimulated gastric acid and pepsin secretions were investigated, with and without pretreatment with the cyclooxygenase inhibitor indomethacin, in conscious cats prepared with gastric fistulae. Somatostatin was a potent inhibitor of acid secretion in both vagus intact and vagotomized animals, and its effect was not diminished by indomethacin pretreatment. Somatostatin inhibition of pepsin secretion was diminished after indomethacin, but a similar effect was noted with exogenous PGE2, suggesting a mechanism unrelated to inhibition of prostaglandin synthesis. It is concluded that there is no evidence to implicate endogenous prostaglandins in somatostatin inhibition of feline gastric exocrine secretions.

摘要

在有胃瘘的清醒猫中，研究了生长抑素和前列腺素E2（PGE2）对五肽胃泌素刺激的胃酸和胃蛋白酶分泌的抑制活性，有无环氧化酶抑制剂吲哚美辛预处理。生长抑素对迷走神经完整和迷走神经切断的动物都是胃酸分泌的有效抑制剂，吲哚美辛预处理不会减弱其作用。吲哚美辛处理后，生长抑素对胃蛋白酶分泌的抑制作用减弱，但外源性PGE2也有类似作用，提示这一机制与抑制前列腺素合成无关。结论是，没有证据表明内源性前列腺素参与生长抑素对猫胃外分泌的抑制作用。