Aliño S F, Marti-Bonmati E, Torregrosa A, Callaghan R, Morcillo E, Garcia D, Gallego J, Esplugues J
Horm Metab Res. 1985 Mar;17(3):123-6. doi: 10.1055/s-2007-1013470.
The inhibitory action on somatostatin (ST) on the spontaneous and stimulated (pentagastrin 18 micrograms/kg/h i.v. and histamine 5 mg/kg/h i.v.) gastric acid secretion and its modification after pretreatment with an inhibitor of endogenous prostaglandins biosynthesis (indomethacin 5 mg/kg i.v.) has been studied in the anaesthetized rat. ST 30 micrograms/kg/h i.v. inhibits basal and stimulated gastric acid secretion. In the presence of indomethacin the inhibition elicited by ST on basal and pentagastrin induced gastric acid secretion was partially attenuated, whereas in the histamine group the inhibitory action was totally abolished. The antagonism elicited by indomethacin was not surmounted by increasing (X 3.3) the dose of ST. These findings suggest that endogenous prostaglandins may be involved in the mechanism by which ST exerts its antisecretory effect in this model.
在麻醉大鼠中，研究了生长抑素（ST）对胃酸自发分泌及刺激分泌（静脉注射五肽胃泌素18微克/千克/小时和组胺5毫克/千克/小时）的抑制作用，以及在用内源性前列腺素生物合成抑制剂（静脉注射消炎痛5毫克/千克）预处理后其作用的改变。静脉注射ST 30微克/千克/小时可抑制基础胃酸分泌和刺激胃酸分泌。在消炎痛存在的情况下，ST对基础胃酸分泌和五肽胃泌素诱导的胃酸分泌的抑制作用部分减弱，而在组胺组中，抑制作用完全消失。增加（X 3.3）ST剂量并不能克服消炎痛引起的拮抗作用。这些发现表明，内源性前列腺素可能参与了ST在该模型中发挥抗分泌作用的机制。
