Slomiany B L, Slomiany A
Research Center, University of Medicine and Dentistry of New Jersey, Newark 07103-2400.
J Physiol Pharmacol. 1991 Jun;42(2):147-61.
Even though there is no general agreement as to the mechanism of gastric mucosal protection, the consensus is that the initial brunt of luminal insults falls on the mucus layer which constitutes the only identifiable physical barrier between the gastric lumen and the mucosal surface. The continuous renewal and resilient nature of this layer efficiently counters peptic erosion of the gel, assures its viscoelastic and permselective properties, and provides a milieu for containment of the diffusing luminal acid by mucosal bicarbonate. Disturbances in this delicate balance lead to the impairment of the protective function of mucus resulting in gastric disease. Indeed, the weakening of gastric mucosal defense is intimately associated with the diminished viscoelastic qualities of mucus, decrease in hydrogen ion retardation capacity, and the extensive proteolysis of its mucin component. Although until recently the disintegration of the mucus coat was attributed exclusively to the enhanced activity of intragastric pepsin, our studies provided strong argument that a bacterial factor, namely infection by Helicobacter pylori, through the action of its protease and lipase enzymes also is highly detrimental to the integrity of gastric mucus. Hence, agents capable of interfering with the pathogenic activity of this bacteria are becoming the drugs of choice in peptic ulcer therapy.
尽管对于胃黏膜保护机制尚无普遍共识，但一致的看法是，管腔损伤的最初冲击落在黏液层上，黏液层是胃腔与黏膜表面之间唯一可识别的物理屏障。该层的持续更新和弹性特性有效地对抗了凝胶的消化性侵蚀，确保了其粘弹性和选择渗透性，并为黏膜碳酸氢盐抑制扩散的管腔酸提供了环境。这种微妙平衡的紊乱会导致黏液保护功能受损，从而引发胃部疾病。事实上，胃黏膜防御功能的减弱与黏液粘弹性质量的降低、氢离子阻滞能力的下降以及其黏蛋白成分的广泛蛋白水解密切相关。尽管直到最近，黏液层的崩解一直被认为完全是由于胃内胃蛋白酶活性增强所致，但我们的研究有力地证明，一种细菌因素，即幽门螺杆菌感染，通过其蛋白酶和脂肪酶的作用，也对胃黏液的完整性极为有害。因此，能够干扰这种细菌致病活性的药物正成为消化性溃疡治疗的首选药物。
