Blandizzi C, Bernardini M C, Natale G, del Tacca M
Institute of Medical Pharmacology, University of Pisa, Italy.
J Pharm Pharmacol. 1990 Oct;42(10):685-8. doi: 10.1111/j.2042-7158.1990.tb06559.x.
The effects of the selective alpha 2-adrenoceptor agonist detomidine on gastric acid secretion from pylorus-ligated and stomach-perfused rats have been investigated. In pylorus-ligated rats i.p. injection of detomidine markedly inhibited acid secretion, this effect being prevented by yohimbine or idazoxan. Under the same conditions, idazoxan significantly increased secretion in a dose-independent fashion. In non-vagotomized and vagotomized stomach-perfused rats i.p. detomidine stimulated acid secretion: this excitatory effect was antagonized by idazoxan. The present results suggest that both inhibitory and excitatory gastric secretory effects of detomidine are mediated by alpha 2-adrenoceptors on cholinergic and adrenergic nerves, respectively. The stimulant activity of idazoxan on gastric secretion from pylorus-ligated rats may be interpreted in terms of increased excitatory vagal tone following the blockade of inhibitory alpha 2-adrenoceptors.
研究了选择性α2-肾上腺素能受体激动剂右美托咪定对幽门结扎和胃灌注大鼠胃酸分泌的影响。在幽门结扎的大鼠中，腹腔注射右美托咪定可显著抑制胃酸分泌，育亨宾或咪唑克生可阻止这种作用。在相同条件下，咪唑克生以剂量非依赖性方式显著增加胃酸分泌。在未切断迷走神经和切断迷走神经的胃灌注大鼠中，腹腔注射右美托咪定可刺激胃酸分泌：这种兴奋作用可被咪唑克生拮抗。目前的结果表明，右美托咪定的抑制性和兴奋性胃分泌作用分别由胆碱能神经和肾上腺素能神经上的α2-肾上腺素能受体介导。咪唑克生对幽门结扎大鼠胃分泌的刺激活性可通过抑制性α2-肾上腺素能受体被阻断后迷走神经兴奋性增加来解释。
