Dousa T P, Dozois R R
Gastroenterology. 1977 Oct;73(4 Pt 2):904-12.
Based on the current experimental evidence, a model is proposed for mutual interactions of histamine, prostaglandins, and cyclic AMP in regulation of gastric secretion and pathogenesis of peptic ulcer. Histamine acting on H2-receptor-associated adenylate cyclase stimulates cyclic AMP formation and consequently secretion of hydrochloric acid in oxyntic cells. Prostaglandins (mainly E type) in another cell population stimulate cyclic AMP formation which may lead to formation of glycosaminoglycans and glycoproteins. Glycosaminoglycans and glycoproteins may have antisecretory and cytoprotective properties. In addition to this effect, prostaglandin endoperoxides may inhibit histamine-stimulated cyclic AMP formation in oxyntic cells.
基于目前的实验证据,提出了一个关于组胺、前列腺素和环磷酸腺苷在胃分泌调节和消化性溃疡发病机制中相互作用的模型。组胺作用于与H2受体相关的腺苷酸环化酶,刺激环磷酸腺苷的形成,从而导致壁细胞分泌盐酸。另一类细胞中的前列腺素(主要是E型)刺激环磷酸腺苷的形成,这可能导致糖胺聚糖和糖蛋白的形成。糖胺聚糖和糖蛋白可能具有抗分泌和细胞保护特性。除了这种作用外,前列腺素内过氧化物可能抑制壁细胞中组胺刺激的环磷酸腺苷的形成。