前列腺素E2及其16,16-二甲基类似物未能预防血小板活化因子诱导的胃黏膜损伤。
Failure of prostaglandin E2 and its 16,16-dimethyl analogue to prevent the gastric mucosal damage induced by Paf.
作者信息
Steel G, Wallace J L, Whittle B J
出版信息
Br J Pharmacol. 1987 Feb;90(2):365-71. doi: 10.1111/j.1476-5381.1987.tb08966.x.
Intravenous and orally administered prostaglandin E2 (PGE2) and 16,16-dimethyl PGE2 (dmPGE2) protect the rat gastric mucosa from injury induced by oral administration of acidified 40% ethanol. The effects of pretreatment with these prostaglandins on platelet activating factor (Paf)-induced gastric damage has now been investigated in the rat. A 10 min infusion of Paf (50 or 100 ng kg-1 min-1, i.v.) resulted in dose-related vasocongestion of the gastric mucosa. Intravenous pretreatment with dmPGE2 (20 micrograms kg-1) failed to prevent the gastric damage induced by the higher dose of Paf. Pretreatment with PGE2 (10-100 micrograms kg-1) or dmPGE2 (1-20 micrograms kg-1), either orally or intravenously, also failed to prevent the gastric vasocongestion induced by the lower dose of Paf. On the contrary, significant augmentation of Paf-induced damage was observed with several of the doses of PGE2 and dmPGE2. These studies demonstrate that the protective properties of PGE2 and dmPGE2 in the gastric mucosa do not extend to damage induced by Paf.
静脉注射和口服前列腺素E2（PGE2）以及16,16 - 二甲基PGE2（dmPGE2）可保护大鼠胃黏膜免受口服酸化40%乙醇所致的损伤。现已在大鼠中研究了用这些前列腺素预处理对血小板活化因子（Paf）诱导的胃损伤的影响。静脉输注Paf（50或100 ng kg-1 min-1，静脉注射）10分钟会导致胃黏膜出现剂量相关的血管充血。用dmPGE2（20微克 kg-1）进行静脉预处理未能预防高剂量Paf诱导的胃损伤。口服或静脉注射PGE2（10 - 100微克 kg-1）或dmPGE2（1 - 20微克 kg-1）预处理也未能预防低剂量Paf诱导的胃血管充血现象。相反，观察到几种剂量的PGE2和dmPGE2会显著增强Paf诱导的损伤。这些研究表明，PGE2和dmPGE2在胃黏膜中的保护特性并不适用于Paf诱导的损伤。
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