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胃溃疡发病机制的当前概念(作者译)

[Current concepts in gastric ulcer pathogenesis (author's transl)].

作者信息

Schiessel R, Starlinger M

出版信息

Wien Klin Wochenschr. 1982 Feb 19;94(4):95-100.

PMID:7043902
Abstract

Recent research has opened up new aspects in the pathogenesis of gastric ulcers. The central role of luminal acid remains unchallenged, although hypersecretion of acid is not necessarily a prerequisite factor in acute or chronic ulceration. A delicate balance is now known to exist between several protective mechanisms and this is essential in enabling the gastric mucosa to withstand the high H-ion gradient between lumen and surface cells. Apart from the role played by other protective mechanisms like mucosal permeability, alkaline secretion and secretory status, blood flow and intracellular buffering of influxing H+ seem to be the most important factors in maintaining the integrity of the gastric mucosa, because their absence always leads to ulceration. Chronic ulcer disease may, however, be dependent on a defect in the regeneration of the gastric mucosa, in addition to the lack of one or more protective mechanisms.

摘要

最近的研究为胃溃疡的发病机制开辟了新的方向。尽管胃酸分泌过多不一定是急性或慢性溃疡形成的必要前提因素,但腔内酸的核心作用仍然无可争议。目前已知在几种保护机制之间存在微妙的平衡,这对于胃黏膜耐受管腔与表面细胞之间的高氢离子梯度至关重要。除了黏膜通透性、碱性分泌和分泌状态等其他保护机制所起的作用外,血流和进入的氢离子的细胞内缓冲似乎是维持胃黏膜完整性的最重要因素,因为它们的缺失总会导致溃疡形成。然而,慢性溃疡病可能除了缺乏一种或多种保护机制外,还依赖于胃黏膜再生的缺陷。

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