Odonkor P, Mowat C, Himal H S
Am J Gastroenterol. 1980 Jun;73(6):496-9.
The role of gastric mucus in the pathogenesis of septic erosions and as an explanation for prostaglandin cytoprotection is unclear. In a reproducible canine septic model bacterial peritonitis was induced in three groups of dogs. One group served as a control and each of the remaining groups received 16,16 dimethyl PGE2 either 0.2 microgram/kg. or 0.4 microgram/kg. I.M. q6h beginning 24 hours prior to peritonitis and continued during the septic period. Gastroscopy was performed and basal gastric juice collected prior to peritonitis and during the septic period. All animals in the control group developed acute gastric erosions and gastric juice protein significantly decreased while sialic acid and fucose significantly increased during the septic period. In the animals receiving 16,16 dimethyl PGE2 acute gastric erosions did not develop; sialic acid and fucose were significantly elevated compared to control dogs during sepsis. We conclude that prostaglandin cytoprotection may be related to increases in gastric glycoprotein secretion.
胃黏液在感染性糜烂发病机制中的作用以及作为前列腺素细胞保护作用的一种解释尚不清楚。在一个可重复的犬类感染模型中，对三组犬诱发细菌性腹膜炎。一组作为对照，其余每组分别接受16,16 - 二甲基前列腺素E2，剂量为0.2微克/千克或0.4微克/千克，肌肉注射，每6小时一次，在腹膜炎发生前24小时开始给药，并在感染期持续给药。在腹膜炎发生前和感染期进行胃镜检查并收集基础胃液。对照组所有动物均发生急性胃糜烂，感染期胃液蛋白显著降低，而唾液酸和岩藻糖显著增加。在接受16,16 - 二甲基前列腺素E2的动物中未发生急性胃糜烂；与感染期的对照犬相比，唾液酸和岩藻糖显著升高。我们得出结论，前列腺素的细胞保护作用可能与胃糖蛋白分泌增加有关。
