Shorrock C J, Rees W D
Department of Gastroenterology, Hope Hospital (University of Manchester School of Medicine), Salford, United Kingdom.
Am J Med. 1988 Feb 22;84(2A):25-34. doi: 10.1016/0002-9343(88)90251-3.
The ability of the gastric mucosa to resist autodigestion has been recognized for over 200 years. Since these early observations, several components of gastroduodenal defense against injury from damaging luminal contents have been identified. The first line of defense is the thick layer of mucus gel into which bicarbonate is secreted by the underlying epithelial cells. The "mucus-bicarbonate" barrier sustains a pH gradient between the lumen and cell surface such that epithelial cells are maintained at pH 7 to 8, despite the presence of intraluminal acid. The epithelial cells form a second line of defense; since the pH gradient may be overwhelmed by physiologic concentrations of intraluminal acid, this mechanism may be important in maintaining mucosal integrity. The physical properties of the apical cell membrane and intercellular junctions and the presence of surface-active phospholipids on the membrane may be responsible for preventing hydrogen ions (H+) from diffusing into the mucosa by providing a physical barrier to their movement. Furthermore, epithelial cells are capable of rapid turnover and migration and may breach a defect in the epithelium within hours. The aftermath of mucosal damage may generate a further defense mechanism: a thick layer of mucus containing sloughed epithelial cells together with passive movement of bicarbonate-rich fluid from the damaged mucosa. This may prevent exposure of undamaged cell nests to acid and thus aid re-epithelialization. Finally, mucosal blood flow plays a vital role in maintaining epithelial integrity. Studies have shown that increasing or decreasing mucosal blood flow will, respectively, reduce or enhance susceptibility to damage. Although the precise physiologic control mechanisms for mucosal protection have not been defined, there is evidence that local endogenous prostaglandin metabolism may play an important role [4]. The release of neurotransmitters and hormones may also contribute to or modulate the defense mechanisms.
胃黏膜抵抗自身消化的能力已被认识超过200年。自这些早期观察以来，已确定了胃十二指肠抵御来自损伤性腔内内容物损伤的几个组成部分。第一道防线是厚厚的黏液凝胶层，其下的上皮细胞会向其中分泌碳酸氢盐。“黏液 - 碳酸氢盐”屏障在管腔和细胞表面之间维持pH梯度，使得尽管腔内存在酸，上皮细胞仍能保持在pH 7至8。上皮细胞构成第二道防线；由于pH梯度可能会被腔内酸的生理浓度所抵消，这种机制在维持黏膜完整性方面可能很重要。顶端细胞膜和细胞间连接的物理特性以及膜上表面活性磷脂的存在，可能通过为氢离子（H +）的移动提供物理屏障来防止其扩散到黏膜中。此外，上皮细胞能够快速更新和迁移，并且可能在数小时内修复上皮中的缺陷。黏膜损伤的后果可能会产生进一步的防御机制：一层厚厚的黏液，其中含有脱落的上皮细胞以及富含碳酸氢盐的液体从受损黏膜的被动移动。这可以防止未受损的细胞巢暴露于酸中，从而有助于重新上皮化。最后，黏膜血流在维持上皮完整性方面起着至关重要的作用。研究表明，增加或减少黏膜血流将分别降低或增强对损伤的易感性。尽管尚未确定黏膜保护的确切生理控制机制，但有证据表明局部内源性前列腺素代谢可能起重要作用[4]。神经递质和激素的释放也可能有助于或调节防御机制。
