[Gastro-protection in vivo and in vitro]
- PMID: 1296166
[Gastro-protection in vivo and in vitro]
Abstract
Experimental evidence coming from Andre Robert studies indicates that prostaglandins (PG) administered exogenously or released endogenously by mild irritants prevent the formation of gross mucosal lesions induced by various ulcerogens such as absolute ethanol, bile salts, hypertonic solution and acidified aspirin. This action appears to be independent of their gastric inhibitory effects. Mild irritants such as 5 mM NaCl, 20% ethanol and 20 mM taurocholate prevent gastric necrosis through adaptive cytoprotection involving an increase in the generation of endogenous PG. In addition, PG have been shown to increase gastric mucosal blood flow and to stimulate mucosal bicarbonate as well as mucus secretion and these effect may contribute to their gastro-protective action. As demonstrated recently, PG prevented the damage of isolated gastric glands in vitro condition, where systemic, neural and hormonal factors are excluded. Gastro-protection is not the unique property of PG, however the mucosal generation of protective PG is essential for gastro-protective effects of solcoseryl. This paper reviews not only protective factors but also the mechanism and possible pathogenic implications of three related compounds thromboxanes, leukotrienes and platelet activating factor (PAF) in acute mucosal injury by topical irritants. The release of these mediators have been thought to be involved in the mechanism of mucosal injury, especially damage to the microvascular endothelium. Whether gastro-protection plays crucial role in the mechanism of ulcer healing remain unknown, however in chronic studies, PG failed to affect the speed of ulcer healing. On the other hand, epidermal growth factor (EGF) exhibits both gastro-protective and ulcer healing properties due to the potent trophic action and to the stimulation of polyamine biosynthesis. The accumulation of EGF in a large quantities in the ulcer area by the antiulcer drugs such as sucralfate and De-Nol may explain their well-known enhancing effects on ulcer healing.
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