Yonehara T
Second Department of Internal Medicine, Osaka Medical College.
Nihon Shokakibyo Gakkai Zasshi. 1992 Sep;89(9):1996-2006.
To investigate the effect of the acid-base imbalance on the gastric mucosal defense mechanism, the intracellular pH of gastric surface epithelial cells were measured with double-barreled H+ selective microelectrodes in the isolated antral mucosa of bullfrog stomach. By knowing the intracellular pH and the PCO2 of the serosal perfusate, the intracellular HCO3- concentration was estimated, and the rate of HCO3- secretion was directly measured with the pH-stat method in mounted preparations on a Ussing's chamber. Both the calculated intracellular HCO3- concentration and the rate of HCO3- secretion were dependent on the exogenous HCO3- supplied from the serosal perfusate. The alkaline tide raised the intracellular HCO3- concentration, thus increasing the mucosal buffering power against acid. Under mild respiratory acidosis, the production of endogenous HCO3- from the serosal CO2 was enhanced, and both the intracellular HCO3- concentration and the rate of HCO3- secretion were increased. As a result, the intracellular pH was maintained at a physiologically optimal level, and the ability of gastric mucosal protection was strengthened by enrichment of cellular bicarbonate supply. It is confirmed in this study that the maintenance of acid-base status in the cell is indispensable in the protection of gastric mucosa against acid invasion.
为研究酸碱失衡对胃黏膜防御机制的影响,采用双管H⁺选择性微电极在牛蛙胃分离的胃窦黏膜中测量胃表面上皮细胞的细胞内pH。通过测定细胞内pH和浆膜灌流液的PCO₂,估算细胞内HCO₃⁻浓度,并采用pH计法在尤斯灌流小室的固定标本中直接测量HCO₃⁻分泌速率。计算得到的细胞内HCO₃⁻浓度和HCO₃⁻分泌速率均依赖于浆膜灌流液提供的外源性HCO₃⁻。碱潮提高了细胞内HCO₃⁻浓度,从而增强了黏膜对酸的缓冲能力。在轻度呼吸性酸中毒时,浆膜CO₂产生内源性HCO₃⁻增加,细胞内HCO₃⁻浓度和HCO₃⁻分泌速率均升高。结果,细胞内pH维持在生理最佳水平,细胞内碳酸氢盐供应增加增强了胃黏膜保护能力。本研究证实,细胞内酸碱状态的维持对于保护胃黏膜免受酸侵袭是必不可少的。