Tissot M, Bonne C, Martin B, Solier M, Giroud J P
Agents Actions. 1984 Jan;14(1):76-81. doi: 10.1007/BF01966837.
The cellular origin and kinetics of TXB2 and 6-keto PGF1 alpha in carrageenan-induced pleurisy has been studied. Maximum levels of these prostanoids occurred 1 hour after induction of pleurisy. Mononuclear cells initially present in the pleural cavity synthesized TXB2 and 6-keto PGF1 alpha from (14C) arachidonic acid. By contrast, PMN cells harvested 6 hours after the induction of inflammation did not produce 6-keto-PGF1 alpha. Selective inhibition of thromboxane synthetase with drugs in vitro and in vivo increased the formation of 6-keto-PGF1 alpha, the stable breakdown product of PGI2. This metabolic effect was parallel to an increase in the volume of exudate and in PMN migration. These results suggest that TXA2 seems to be implicated not only as a chemotactic agent but also as an antagonist of PGI2 vasodilator effects.
已对角叉菜胶诱导的胸膜炎中TXB2和6-酮基PGF1α的细胞起源及动力学进行了研究。这些前列腺素的最高水平出现在胸膜炎诱导后1小时。最初存在于胸腔中的单核细胞可从(14C)花生四烯酸合成TXB2和6-酮基PGF1α。相比之下,炎症诱导6小时后收获的PMN细胞不产生6-酮基-PGF1α。在体外和体内用药物选择性抑制血栓素合成酶可增加6-酮基-PGF1α的形成,6-酮基-PGF1α是PGI2的稳定分解产物。这种代谢效应与渗出液体积增加和PMN迁移增加平行。这些结果表明,TXA2似乎不仅作为趋化剂起作用,而且作为PGI2血管舒张作用的拮抗剂起作用。