Goto Y, Debas H T
Dig Dis Sci. 1983 Jan;28(1):56-9. doi: 10.1007/BF01393361.
Parenteral administration of beta-(p-chlorophenyl)-gamma-aminobutyric acid (PCP-GABA), a lipophilic GABA mimetic, has been shown to aggravate stress-induced ulcerations in the rat. Since acid hypersecretion may be a possible mechanism for this, we studied the effect of graded doses of PCP-GABA on rat gastric acid secretion. The stimulatory effect of PCP-GABA was found to be dose-dependent, long-acting, and massive, exceeding the maximal effects of histamine and bethanechol. The acid stimulant effect of PCP-GABA was completely abolished not only by atropine but also by truncal vagotomy. Vagotomized, PCP-GABA-treated animals responded to bethanechol, suggesting that a peripheral (cellular) mechanism is not involved. We conclude that PCP-GABA acts centrally to activate vagal centers and to cause acid hypersecretion. Although hypersecretion of acid caused by PCP-GABA may be involved in the observed aggravation of stress-induced ulceration in the rat stomach, evidence for this has yet to be provided.
亲脂性γ-氨基丁酸模拟物β-（对氯苯基）-γ-氨基丁酸（PCP-GABA）的肠胃外给药已显示会加重大鼠应激诱导的溃疡。由于胃酸分泌过多可能是其一种潜在机制，我们研究了不同剂量的PCP-GABA对大鼠胃酸分泌的影响。发现PCP-GABA的刺激作用具有剂量依赖性、长效性且作用强烈，超过了组胺和氨甲酰甲胆碱的最大作用效果。PCP-GABA的酸刺激作用不仅被阿托品完全消除，也被迷走神经干切断术消除。经迷走神经切断术处理并给予PCP-GABA的动物对氨甲酰甲胆碱有反应，这表明不涉及外周（细胞）机制。我们得出结论，PCP-GABA通过中枢作用激活迷走神经中枢并导致胃酸分泌过多。尽管PCP-GABA引起的胃酸分泌过多可能与观察到的大鼠胃应激诱导溃疡加重有关，但尚未有证据支持这一点。
