Ohe K, Hayashi K, Shirakawa T, Yamada K, Kawasaki T, Miyoshi A
Am J Physiol. 1980 Dec;239(6):G457-62. doi: 10.1152/ajpgi.1980.239.6.G457.
To clarify the mechanism of initiation of the hydrogen ion backdiffusion, the effects of aspirin and taurocholate, two representative gastric mucosal barrier breakers, on the potential difference, secretory activity, energy metabolism, and the hydrogen ion permeability of guinea pig gastric mucosa was studied in vitro. 1) The ATP content and energy charge of the gastric mucosa showed a statistically significant reduction when the potential difference decreased to one-half of that before addition. 2) The mucosal acid secretion was reduced by addition of the barrier breaker. 3) However, the hydrogen ion backdiffusion, as measured by titrating the acid appearing in the serosal solution, became detectable when the potential difference decreased to one-fourth of that before addition. It has been concluded, therefore, that the primary action of gastric mucosal barrier breakers is to damage the energy metabolism of the mucosal cells, and that the hydrogen ion backdiffusion takes place as the result of cellular death caused by the impairment of energy metabolism.
为阐明氢离子反向扩散的起始机制，在体外研究了两种典型的胃黏膜屏障破坏剂阿司匹林和牛磺胆酸盐对豚鼠胃黏膜电位差、分泌活性、能量代谢及氢离子通透性的影响。1）当电位差降至添加前的一半时，胃黏膜的三磷酸腺苷（ATP）含量和能荷在统计学上有显著降低。2）添加屏障破坏剂后，黏膜酸分泌减少。3）然而，当电位差降至添加前的四分之一时，通过滴定浆膜溶液中出现的酸来测定的氢离子反向扩散变得可检测到。因此得出结论，胃黏膜屏障破坏剂的主要作用是损害黏膜细胞的能量代谢，且氢离子反向扩散是能量代谢受损导致细胞死亡的结果。
