Kivilaakso E, Fromm D, Silen W
Gastroenterology. 1978 Oct;75(4):641-8.
Intramural pH of the gastric mucosa was measured using a microelectrode technique in rabbit gastric pouches under different secretory conditions and luminal acidity. Exposure of spontaneously secreting or metiamide-treated fundic pouches to a relatively high concentration of luminal acid. HCl 120 mM, for 60 min, led to a marked net loss of luminal H+ which was associated with a significant decrease in the intramural pH (7.28 +/- 0.09 to 6.88 +/- 0.10 and 7.23 +/- 0.07 to 6.99 +/- 0.09, respectively). A linear relationship was observed between the rates of net disappearance of luminal acid and the intramural pH. All 10 spontaneously secreting and five metiamide-treated pouches had superficial mucosal erosions. In contrast, when fundic pouches were exposed to luminal acid in histamine-treated animals, the net loss of luminal H+ was negligible and the intramural pH remained at its base-line level (7.25 +/- 0.07). Histamine stimulation without acid in the lumen caused a small but insignificant increase in the intramural pH (7.27 +/- 0.03 to 7.39 +/- 0.05). Only three of the eight histamine-treated fundic pouches had lesions. In the antral pouches the intramural pH changes in response to exposure to luminal acid were smaller and histamine treatment did not influence the intramural pH. None of the antral pouches had lesions. The results suggest that acidification of the tissue by the diffusion of luminal acid may be an important factor in the pathogenesis of acute gastric ulceration. The acid secretory state of the gastric mucosa can significantly influence the acid-base balance in the mucosa and thus modify its response to acid diffusing from the lumen. Histamine stimulation protected the gastric mucosa by improving its buffering capacity and/or otherwise decreasing the diffusion of H+ from the lumen into the mucosa.
采用微电极技术,在不同分泌状态和管腔酸度条件下,对兔胃小囊胃黏膜的壁内pH值进行了测量。将自发分泌或用甲硫咪胺处理过的胃底小囊暴露于相对高浓度的管腔酸(120 mM盐酸)中60分钟,导致管腔H⁺明显净损失,这与壁内pH值显著降低相关(分别从7.28±0.09降至6.88±0.10以及从7.23±0.07降至6.99±0.09)。观察到管腔酸净消失速率与壁内pH值之间呈线性关系。所有10个自发分泌的小囊和5个用甲硫咪胺处理过的小囊均出现浅表黏膜糜烂。相比之下,当在组胺处理的动物中胃底小囊暴露于管腔酸时,管腔H⁺的净损失可忽略不计,壁内pH值保持在基线水平(7.25±0.07)。管腔内无酸时组胺刺激使壁内pH值有小幅但不显著的升高(从7.27±0.03升至7.39±0.05)。8个用组胺处理的胃底小囊中只有3个有病变。在胃窦小囊中,暴露于管腔酸时壁内pH值变化较小,组胺处理不影响壁内pH值。所有胃窦小囊均无病变。结果表明,管腔酸扩散导致组织酸化可能是急性胃溃疡发病机制中的一个重要因素。胃黏膜的酸分泌状态可显著影响黏膜中的酸碱平衡,从而改变其对从管腔扩散而来的酸的反应。组胺刺激通过提高胃黏膜的缓冲能力和/或以其他方式减少H⁺从管腔向黏膜的扩散来保护胃黏膜。