Durbin R P
Am J Physiol. 1984 Feb;246(2 Pt 1):G114-9. doi: 10.1152/ajpgi.1984.246.2.G114.
Backdiffusion of H+ was studied in isolated bullfrog gastric mucosa using direct titration to evaluate changes in luminal H+ level. In resting mucosae, the resulting permeability coefficient for H+ (uncorrected for electrical effects) was 0.4 X 10(-5) cm X S-1, which is of the same order of magnitude as that estimated from data in the literature for dog and rabbit gastric mucosa in vivo. With maximal stimulation of acid secretion, backdiffusion of H+ was considerably increased. In both resting and stimulated mucosae, an increase in Cl- flux from lumen to serosa was observed to accompany H+ backdiffusion. In experiments in which electrical activity of resting mucosae was monitored, instilled H+ lowered gastric potential difference but had little effect on the normal resistance. Sudden drops in resistance and potential were observed, independent of luminal acid; after such events instilled H+ had no effect on mucosal resistance. It appears that a substantial part of H+ backdiffusion occurs as the ion pair HCl.
利用直接滴定法研究了离体牛蛙胃黏膜中H⁺的反向扩散，以评估管腔内H⁺水平的变化。在静息黏膜中，所得到的H⁺通透系数（未校正电效应）为0.4×10⁻⁵cm×s⁻¹，这与根据文献中狗和兔体内胃黏膜数据估算的值处于同一数量级。在酸分泌受到最大刺激时，H⁺的反向扩散显著增加。在静息和受刺激的黏膜中，均观察到从管腔到浆膜的Cl⁻通量增加伴随着H⁺的反向扩散。在监测静息黏膜电活动的实验中，注入的H⁺降低了胃电位差，但对正常电阻影响很小。观察到电阻和电位突然下降，与管腔内酸无关；在这些事件之后，注入的H⁺对黏膜电阻没有影响。似乎H⁺的大量反向扩散是以离子对HCl的形式发生的。
