{"title":"[体内和体外胃保护]。","authors":"T Brzozowski","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":76310,"journal":{"name":"Patologia polska","volume":"43 1","pages":"1-9"},"PeriodicalIF":0.0000,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"[Gastro-protection in vivo and in vitro].\",\"authors\":\"T Brzozowski\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":76310,\"journal\":{\"name\":\"Patologia polska\",\"volume\":\"43 1\",\"pages\":\"1-9\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1992-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Patologia polska\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Patologia polska","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
来自Andre Robert研究的实验证据表明,前列腺素(PG)外源性给药或通过轻度刺激物内源性释放,可防止各种溃疡原(如无水乙醇、胆盐、高渗溶液和酸化阿司匹林)诱导的粘膜损伤的形成。这种作用似乎独立于它们的胃抑制作用。5 mM NaCl、20%乙醇和20 mM牛磺胆酸盐等轻度刺激物通过增加内源性PG生成的适应性细胞保护来预防胃坏死。此外,PG已被证明可以增加胃粘膜血流量,刺激粘膜碳酸氢盐和粘液分泌,这些作用可能有助于其胃保护作用。正如最近所证明的,PG在体外条件下可以防止离体胃腺的损伤,其中排除了系统、神经和激素因素。胃保护并不是PG的独特特性,但保护性PG的粘膜生成对茄沙莱的胃保护作用至关重要。本文综述了三种相关化合物血栓烷、白三烯和血小板活化因子(PAF)在局部刺激物急性粘膜损伤中的作用机制及可能的致病意义。这些介质的释放被认为参与了粘膜损伤的机制,特别是对微血管内皮的损伤。胃保护是否在溃疡愈合机制中起关键作用尚不清楚,但在慢性研究中,PG未能影响溃疡愈合的速度。另一方面,表皮生长因子(EGF)由于其强大的营养作用和对多胺生物合成的刺激,表现出胃保护和溃疡愈合的特性。抗溃疡药物如硫硫钠和De-Nol在溃疡区域大量积累EGF,这可能解释了它们众所周知的促进溃疡愈合的作用。
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.