Maeda-Hagiwara M, Watanabe H, Watanabe K
Br J Pharmacol. 1983 Dec;80(4):735-9. doi: 10.1111/j.1476-5381.1983.tb10065.x.
Effects of the intracerebroventricular thyrotropin-releasing hormone (TRH) on gastric mucosa were studied in rats. TRH (3 and 10 micrograms rat-1 i.c.v.) produced slight gastric lesions and also aggravated indomethacin-, aspirin- or 5-hydroxytryptamine (5-HT)-induced gastric lesions, while restraint and cold stress-induced lesions were not influenced by TRH. Bethanechol used at a dose sufficient to produce acid secretion did not influence the gastric mucosa in intact or indomethacin-treated rats. Enhancement of indomethacin-induced gastric lesions by TRH was not inhibited to any significant degree by atropine 0.1 mg kg-1 s.c., which prevented TRH-induced gastric acid secretion, but tended to be inhibited by phentolamine, 2.5 mg kg-1 i.p. It is concluded that the enhancement by TRH of indomethacin-induced gastric lesions is due to a combination of the central and peripheral actions of the ulcerogenic agents.
研究了大鼠脑室内注射促甲状腺激素释放激素(TRH)对胃黏膜的影响。TRH(3和10微克/大鼠,脑室内注射)可产生轻微的胃损伤,还会加重吲哚美辛、阿司匹林或5-羟色胺(5-HT)诱导的胃损伤,而束缚和冷应激诱导的损伤不受TRH影响。以足以产生胃酸分泌的剂量使用的氨甲酰甲胆碱对完整或吲哚美辛处理的大鼠的胃黏膜没有影响。0.1毫克/千克皮下注射阿托品可阻止TRH诱导的胃酸分泌,但对TRH增强吲哚美辛诱导的胃损伤没有显著抑制作用,而2.5毫克/千克腹腔注射酚妥拉明则有抑制趋势。得出结论,TRH增强吲哚美辛诱导的胃损伤是由于致溃疡剂的中枢和外周作用共同所致。