Kusner E J, Knee C D, Krell R D
Agents Actions. 1987 Feb;20(1-2):61-8. doi: 10.1007/BF01965626.
1-0-Alkyl-2-Acetyl-sn-Glycero-3-Phosphocholine (AGEPC) produced dose-dependent (75-500 ng/site) increases in cutaneous vascular permeability (CVP) in rats as measured by extravasation of Evans blue dye. In contrast, lyso-AGEPC, at 1000 ng/site, was without effect. Pyrilamine, methysergide, and phenoxybenzamine, antagonists of mast-cell derived mediators, did not affect the AGEPC-induced increase in CVP. Likewise, agents capable of inhibiting mast cell mediator release, such as disodium cromoglycate, PRD-92-EA, theophylline, or nifedipine, had no effect. The cyclooxygenase inhibitor indomethacin produced significant inhibition of the response to AGEPC, whereas the lipoxygenase inhibitor nordihydroguiaretic acid (NDGA) and the peptide leukotriene antagonist FPL 55712 were without effect. The response to AGEPC was enhanced by the vasodilator PGE2 and inhibited by the vasoconstrictor phenylephrine. The selective AGEPC antagonist CV-3988 provided marked inhibition of the response. Unaccountably, the combination of indomethacin and CV-3988 provided no greater inhibition of the responses than either agent alone. These observations indicate that the AGEPC-induced increase in CVP in rats is mediated in part by products of the cyclooxygenase pathway and in part by activation of an AGEPC receptor.
通过伊文思蓝染料外渗测定，1-0-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱（AGEPC）在大鼠中产生剂量依赖性（75 - 500 ng/部位）的皮肤血管通透性（CVP）增加。相比之下，溶血AGEPC在1000 ng/部位时无作用。组胺受体拮抗剂吡苄明、麦角新碱和酚苄明并不影响AGEPC诱导的CVP增加。同样，能够抑制肥大细胞介质释放的药物，如色甘酸钠、PRD - 92 - EA、茶碱或硝苯地平，也没有作用。环氧合酶抑制剂吲哚美辛对AGEPC的反应产生显著抑制，而脂氧合酶抑制剂去甲二氢愈创木酸（NDGA）和肽白三烯拮抗剂FPL 55712则无作用。血管舒张剂PGE2增强了对AGEPC的反应，血管收缩剂去氧肾上腺素则抑制了该反应。选择性AGEPC拮抗剂CV - 3988对该反应有显著抑制作用。令人费解的是，吲哚美辛和CV - 3988联合使用对反应的抑制作用并不比单独使用任何一种药物更强。这些观察结果表明，AGEPC诱导的大鼠CVP增加部分由环氧合酶途径的产物介导，部分由AGEPC受体的激活介导。
