Gyires K
Department of Pharmacology, Semmelweis University of Medicine, Budapest, Hungary.
Agents Actions. 1994 Mar;41(1-2):73-9. doi: 10.1007/BF01986397.
Numerous factors are involved in the gastrointestinal mucosal damage induced by non-steroidal anti-inflammatory drugs. The physico-chemical-acidic-property of the drugs is responsible partly for the rapid absorption, mucosal accumulation and barrier breaking effect, partly for the topical irritant action. The drugs decrease the defensive mechanisms of the stomach at different level, destroy the mucosal barrier, decrease the surface hydrophobicity, the mucosal blood flow, and inhibit the prostaglandin synthesis. Exogenous sulfhydryls and interleukin-1 inhibit the NSAID-induced mucosal damage, whether they are also involved in the ulcerogenic action has not been clearly determined. On the other hand, injurious factors are also stimulated; enhanced gastric acid secretion, increased pepsin activity, enhanced formation of free radicals and leukotrienes, as well as activation of leukocyte can also contribute to the mucosal lesions induced by NSAIDs. Prior Campylobacter pylori infection may make the mucosa more susceptible to NSAID-associated injury.
非甾体抗炎药引起的胃肠道黏膜损伤涉及多种因素。药物的物理化学酸性特性部分导致了其快速吸收、黏膜蓄积和屏障破坏作用,部分导致了局部刺激作用。这些药物在不同水平上降低胃的防御机制,破坏黏膜屏障,降低表面疏水性、黏膜血流量,并抑制前列腺素合成。外源性巯基和白细胞介素-1可抑制非甾体抗炎药引起的黏膜损伤,但它们是否也参与致溃疡作用尚未明确确定。另一方面,损伤因素也会被刺激;胃酸分泌增加、胃蛋白酶活性增强、自由基和白三烯形成增加,以及白细胞活化也会导致非甾体抗炎药引起的黏膜损伤。先前的幽门螺杆菌感染可能会使黏膜更容易受到与非甾体抗炎药相关的损伤。