Cho C H, Chen S W, Chen S M, Ho L T
Pharmacol Biochem Behav. 1983 Dec;19(6):925-7. doi: 10.1016/0091-3057(83)90392-1.
The effects of somatostatin on ulcer formation, gastric acid secretion and histamine release were assessed during vagus nerve stimulation in rats. Direct electrical vagal stimulation significantly increased histamine release and acid output in gastric secretion but decreased mast cell counts in gastric glandular mucosa. Hemorrhagic ulceration on the gastric glandular mucosa was also observed. Somatostatin pretreatment (10 micrograms/kg) did not inhibit gastric ulcer formation, gastric acid secretion or histamine release induced by vagal stimulation. Cimetidine (an H2 blocker) pretreatment, however, significantly decreased gastric acid secretion as well as ulcer formation. The present study indicates the direct vagal stimulation increases gastric acid secretion and ulcer formation. These effects are partially histamine dependent. Somatostatin did not inhibit histamine release induced by vagal stimulation and reflects the inability of the drug to prevent ulcer formation and gastric output under these conditions in rats. However, the inhibition of basal gastric acid secretion produced by somatostatin might be useful clinically in humans.
在大鼠迷走神经刺激过程中，评估了生长抑素对溃疡形成、胃酸分泌和组胺释放的影响。直接电刺激迷走神经可显著增加组胺释放和胃酸分泌，但会降低胃腺黏膜中的肥大细胞计数。还观察到胃腺黏膜出现出血性溃疡。生长抑素预处理（10微克/千克）并未抑制迷走神经刺激诱导的胃溃疡形成、胃酸分泌或组胺释放。然而，西咪替丁（一种H2受体阻滞剂）预处理可显著减少胃酸分泌以及溃疡形成。本研究表明，直接迷走神经刺激会增加胃酸分泌和溃疡形成。这些作用部分依赖于组胺。生长抑素并未抑制迷走神经刺激诱导的组胺释放，这反映出该药物在这些条件下无法预防大鼠的溃疡形成和胃酸分泌。然而，生长抑素对基础胃酸分泌的抑制作用在临床上可能对人类有用。
