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胃酸分泌状态对胃黏膜耐受氢离子反向弥散的影响。

Influence of acid secretory state on the gastric mucosal tolerance to back diffusion of H+.

作者信息

O'Brine P, Silen W

出版信息

Gastroenterology. 1976 Nov;71(5):760-5.

PMID:9331
Abstract

The effect of back diffusion of H+ PON THE POTENTIAL DIFFERence (PD), electrical resistance (R), and short circuit current (Isc) of spontaneously secreting and burimamide-inhibited amphibian gastric mucosae were studied in vitro. When back diffusion of H+ was induced by the passage of an electrical current of 510 mua per cm2 from the secretory (S) side of pH 2.25 to the nutrient side (N) for 30 min, the spontaneously secreting mucosae showed small decreases in PD (23.6 leads to 16.2 mv) and Isc (80 leads to 61 mua per cm2) but no significant change in R. In the burimamide-inhibited mucosae there were marked and significantly greater decreases of PD (26.8 leads to 3.4 mv), R (473 leads to 170 ohms cm2) and Isc (50 leads to 13 mua per cm2). When back diffusion of H+ was induced by establishing a concentration gradient of H+ from S leads to N or by exposing the secretory surface to sodium taurocholate with secretory pH 2.25, the burimamide-inhibited tissue demonstrated significantly greater depression of the electrical parameters than the secreting mucosae. Intracellular pH, measured by the 5,5-dimethoxyazolidine-2,4-dione method, was significantly higher in the histamine-stimulated tissues (7.28) than in the metiamide-inhibited tissues (7.11). These studies strongly suggest that the secretory status of the mucosa and hence its acid-base status are important determinants in the tolerance of the tissue to exogenous back diffusion of H+. The measure of absolute loss of H+ From the mucosal solution alone may not be an adequate assessment of the gastric mucosal barrier.

摘要

研究了H⁺反向扩散对体外自发分泌及被甲氰咪胍抑制的两栖类胃黏膜电位差(PD)、电阻(R)和短路电流(Isc)的影响。当通过每平方厘米510微安的电流,从pH 2.25的分泌(S)侧向营养侧(N)通电30分钟诱导H⁺反向扩散时,自发分泌的黏膜PD(从23.6毫伏降至16.2毫伏)和Isc(从每平方厘米80微安降至61微安)略有下降,但R无显著变化。在被甲氰咪胍抑制的黏膜中,PD(从26.8毫伏降至3.4毫伏)、R(从473欧姆·平方厘米降至170欧姆·平方厘米)和Isc(从每平方厘米50微安降至13微安)有明显且显著更大幅度的下降。当通过建立从S到N的H⁺浓度梯度或通过将分泌表面暴露于分泌pH 2.25的牛磺胆酸钠来诱导H⁺反向扩散时,被甲氰咪胍抑制的组织的电参数下降幅度明显大于分泌性黏膜。用5,5 - 二甲氧基唑烷 - 2,4 - 二酮法测量的细胞内pH,在组胺刺激的组织(7.28)中显著高于甲硫咪特抑制的组织(7.11)。这些研究强烈表明,黏膜的分泌状态及其酸碱状态是组织对外源性H⁺反向扩散耐受性的重要决定因素。仅从黏膜溶液中H⁺的绝对损失量来衡量,可能不足以评估胃黏膜屏障。

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