【摘要】 小白鼠脑室注射ＧＡＢＡ（２、 ４、 ６ ｍｏｌ）对盐酸诱导型胃溃疡产生一种明显的剂量－效应依赖的抑制效应。腹腔注射ＧＡＢＡ（１００ ｍｏｌ）对盐酸诱导型胃溃疡无影响。荷包牡丹碱（ｉ．ｃ.ｖ．０．２ｍｅｏｌ）、β－氯苯氨丁酸（ｉ．ｃ．ｖ．４ｍｏｌ）或荷包牡丹碱（ｉ．ｃ．ｖ．０.２ｍｏｌ）加β－氯苯氯丁酸（ｉｃ．ｖ．４ ｍｏｌ）对盐酸诱导型胃溃疡均无影响。但荷包牡丹碱（ｉ．ｃ．ｖ．０．２ ｍｏｌ）可以消除ＧＡＢＡ对盐酸诱导型用溃疡的抑制效应。阿托品（ｓ．ｃ．０·２ ｍｇ·ｋｇ～－１）和酚妥拉明（ｉ．ｍ．２５ｍｇ·Ｋｇ～－１）也不影响盐酸诱导胃溃疡，但两者都能使ＧＡＢＡ对盐酸诱导型胃溃疡的抑制效应消失。盐酸（ｉ．ｇ．０·２Ｎ，０．２ｍｌ）使胃壁粘液量显著减少，若预先脑室注射ＧＡＢＡ可使胃壁粘液量恢复到正常水平。这些结果表明，盐田诱导胃溃疡与减弱胃出－ＨＣＯ～－３屏障有关。外源性ＧＡＢＡ通过对中枢而非外周的特异性作用抑制盐酸诱导型胃溃疡。其主要机制可能是ＧＡＢＡ通过激活脑中ＧＡＢＡ受体后，改变了迷走神经和交感神经两者的输出活动，增强了胃粘液－ＨＣＯ～－３屏障，提高了胃粘膜对盐酸的防御能力。更多还原

【Abstract】 Intracerebroventricular injection （i. c. v. ） of GABA （2, 4, 6 mol ） in mice significantly evoked a suppressive effect of gastric ulcer induced by HCI （i. g. ） in a dosage response, whereas peripherally applied GABA （i. p. 100mol） could not modify the development of HCI-induced gastric ulcer. All of bicuculline （i. c. v. 0. 2mol）, baclofen （i. c. v. 4mlo） and bicuculline （i. c. v. 0.2mol） +baclofen （i. c. v. 4mol） did not affect the HCI-induced gastric ulcer, but bicuculline completely blocked the inhibition of i. c. v. and administrated GABA on HCI-induced gastric ulcer. Atropine （s. c. 0.2mg. kg～-1 ）and regetine （i. m. 2.5ing. kg～-1） also did not affect the development of HCI-induced gastric ulcer, but both of them abolished the suppression of GABA on HCI-induced ulcer. The HCI （i. g. 0.2N, 0.2ml） markedly decreased the mucus secretion of stomach wall, whereas pretreatment with GABA （i. c. v. ） recovered the mucus of stomach wall to normal level. Above results indicated that the HCI-induced gastric ulcer was closely related to the weakening of gastric mucus-HCO-₃ barrier. The exogenous GABA inhibited HCI-induced gastric ulcer through a certain central GABA-ergic mechanism and thereby modified the excitability of vagus and sympathetic nerve and stressed gastric mucus-HCO-₃, barrier and inhibited the HCl-induced gastric ulcer.更多还原