γ-氨基丁酸对小白鼠离体胃标本胃酸分泌的促进效应

为了探索γ-氨基丁酸(GABA)对小白鼠离体胃标本胃酸分泌(GAS)的影响及机制，在体外37℃缓冲液中培育离体、胃腔灌流并维持胃内12 cm水柱压力的全胃标本，用pHS-3型精密酸度计测定灌流液的pH。结果表明：γ-氨基丁酸(GABA)(1～10×10-7mol/L)和巴氯芬(Bac, 0.6～9.6×10-7mol/L)以一种浓度依赖的方式显著地促进胃酸分泌(GAS)，而西咪替丁(Cim, 2～20×10-7mol/L)以一种浓度依赖的方式有力地抑制GAS。印防已毒素(Pic, 3×10-7mol/L)不影响基础胃酸分泌(BGAS)和GABA促进GAS的效应，而番氯芬(Phac, 0.6×10-7mol/L)能完全阻断GABA的促进效应。Cim不能完全消除GABA和Bac对GAS的促进效应。以上结果提示，在小鼠中GABA可以通过激活胃中GABAB受体促进离体胃标本的GAS，可能胃壁胆碱能神经元和非神经细胞，如壁细胞及某些内分泌细胞上都存在GABAB受体，GABA可直接或简接地剌激胃壁细胞分泌酸。

PROMOTIVE EFFECTS OF GABA ON ACID SECRETION FROM ISOLATED MOUSE STOMACH IN VITRO

To explore the effects and the mechanism of γ-aminobutyric acid (GABA) on gastric acid secretion (GAS) of isolated mouse stomach with perfused lumen, 12 cm H2O column intragastric pressure-provided. Whole stomach preparations from mice were incubated in buffer at 37℃ in vitro, and perfusate was measured for pH with a pHS-3 type pH meter. The results shown that GABA (1～10×10-7mol/L) and baclofen (Bac) (0.6～9.6×10-7mol/L) significantly promoted GAS in a concentration-dependent manner, whereas cimetidine (Cim) (2～20×10-7mol/L) potently inhibited GAS in the same manner. Picrotoxin (Pic) (3×10-7mol/L) did not affect basal gastric acid secretion (BGAS) and the promotive effect of GABA on GAS. Phaclofen (Phac) (0.6×10-7mol/L) completely inhibited the promotive effect of GABA on GAS. Cim did not completely eliminate the promotive effects of GABA and Bac on GAS in isolated mouse stomach. Above results suggest that in mouse, GABA may promote GAS in isolated stomach, possibly by affecting GABAB receptors on both cholinergic neurons and non-neuronal cells, such as parietal cells and some endocrine cells. GABA may stimulate parietal cells to secrete acid directly or indirectly.