Fujii E, Irie K, Uchida Y, Ohba K, Muraki T
Department of Pharmacology, Tokyo Women's Medical College, Japan.
Eur J Pharmacol. 1995 Feb 6;273(3):267-72. doi: 10.1016/0014-2999(94)00697-6.
We investigated the role of endogenous eicosanoids and nitric oxide (NO) in the platelet-activating factor (PAF)-induced increase in vascular permeability in mouse skin. Subcutaneous injection of PAF (45-180 pmol/site) induced a dose-related increase in vascular permeability at the injection site. The vascular permeability induced by PAF (180 pmol/site) was significantly inhibited by pretreatment with an intraperitoneal injection of 1-O-hexadecyl-2-acetyl-sn-glycero-3-phospho (N,N,N-trimethyl) hexanolamine (PAF receptor antagonist) (5 and 25 mg/kg) and indomethacin (cyclooxygenase inhibitor) (10 mg/kg), whereas it was not affected by concurrent intravenous administration of NO synthase inhibitors NG-nitro-L-arginine methyl ester (10 mg/kg) or methylene blue (100 micrograms/kg) nor by topical injection of NG-nitro-L-arginine methyl ester. The inhibitory effect of indomethacin was partially reversed by topical administration of prostaglandin E2. These results suggest that PAF increases venular permeability by activating PAF receptors and that plasma extravasation is potentiated by the release of prostanoids which cause arteriolar dilatation. However, NO is not involved in the effect of PAF in mouse skin.
我们研究了内源性类花生酸和一氧化氮（NO）在血小板活化因子（PAF）诱导的小鼠皮肤血管通透性增加中的作用。皮下注射PAF（45 - 180 pmol/部位）可在注射部位诱导剂量相关的血管通透性增加。腹腔注射1 - O - 十六烷基 - 2 - 乙酰 - sn - 甘油 - 3 - 磷酸（N，N，N - 三甲基）己醇胺（PAF受体拮抗剂）（5和25 mg/kg）和吲哚美辛（环氧化酶抑制剂）（10 mg/kg）预处理可显著抑制PAF（180 pmol/部位）诱导的血管通透性，而同时静脉注射NO合酶抑制剂NG - 硝基 - L - 精氨酸甲酯（10 mg/kg）或亚甲蓝（100微克/千克）以及局部注射NG - 硝基 - L - 精氨酸甲酯对此没有影响。吲哚美辛的抑制作用可通过局部应用前列腺素E2部分逆转。这些结果表明，PAF通过激活PAF受体增加小静脉通透性，并且前列腺素的释放增强了血浆外渗，前列腺素可导致小动脉扩张。然而，NO不参与PAF对小鼠皮肤的作用。
