Weissenborn U, Maedge S, Sewing K F
Pharmacology. 1984;28(5):275-80. doi: 10.1159/000137974.
The effect of 16,16-dimethyl prostaglandin E2 (DmPGE2), in doses subthreshold for antisecretory activity, were examined in female rats. The aims were to determine if DmPGE2 alters the disposition of acetylsalicylic acid (ASA) within the gastric mucosa and if DmPGE2 could attenuate the ulcerogenic effect of oral ASA. Gastric lesions occurred after an oral, but not an intravenous dose of 150 mg/kg ASA. Lesions could be prevented by pretreatment with 5 micrograms/kg DmPGE2 orally 30 min prior to ASA. DmPGE2 elevated fundic concentrations of both ASA and salicylic acid (SA) within the first hour when ASA was given orally. The ratio of the concentration of ASA/SA in fundus was not changed, indicating that DmPGE2 did not depress the fundic esterase activity. It is concluded that the cytoprotective effect of DmPGE2 is not related to a change in mucosal concentration or elimination of ASA or SA.
在雌性大鼠中研究了16,16 - 二甲基前列腺素E2(DmPGE2)在低于抗分泌活性阈值剂量时的作用。目的是确定DmPGE2是否会改变胃黏膜内乙酰水杨酸(ASA)的分布,以及DmPGE2是否能减轻口服ASA的致溃疡作用。口服150mg/kg ASA后会出现胃损伤,但静脉注射该剂量则不会。在给予ASA前30分钟口服5μg/kg DmPGE2可预防损伤。口服ASA后,DmPGE2在第一小时内会提高胃底中ASA和水杨酸(SA)的浓度。胃底中ASA/SA的浓度比没有变化,表明DmPGE2不会抑制胃底酯酶活性。得出的结论是,DmPGE2的细胞保护作用与黏膜中ASA或SA的浓度变化或消除无关。