Cristol J P, Sirois P
Department of Pharmacology, Faculty of Medicine, University of Sherbrooke, P.Q., Canada.
Res Commun Chem Pathol Pharmacol. 1988 Mar;59(3):423-6.
Various compounds derived from the 5-lipoxygenase pathway of arachidonic acid (Leukotriene D4 [LTD4], 5S,6R-dihydroxy-7,9,11,14- eicosatetraenoic acid [5S,6R-DiHETE], 5S,6S-DiHETE, 5S,6R-Lipoxin A [5S,6R-Lx A], 5S,6S-Lx A) were tested on guinea-pig lung parenchyma strips (G.P.L.P.S.) and ileum smooth muscles (G.P.I.S.M.) mounted in a cascade superfusion system. These products induced contractile responses on G.P.L.P.S., whereas only the LTD4 was active on G.P.I.S.M. FPL-55712 inhibited almost totally their myotropic activity. The 5S,6R compounds were more active than the 5S,6S ones, with an order of potency of LTD4 greater than 5,6-DiHETE greater than Lx A. It is suggested that 5,6-DiHETE and Lx A isomers may act via the lung LTD4 receptors which appear less specific than ileum LTD4 receptors.
从花生四烯酸的5-脂氧合酶途径衍生出的各种化合物（白三烯D4 [LTD4]、5S,6R-二羟基-7,9,11,14-二十碳四烯酸 [5S,6R-DiHETE]、5S,6S-DiHETE、5S,6R-脂氧素A [5S,6R-Lx A]、5S,6S-Lx A）在安装于级联超灌注系统中的豚鼠肺实质条（G.P.L.P.S.）和回肠平滑肌（G.P.I.S.M.）上进行了测试。这些产物在G.P.L.P.S.上诱导收缩反应，而只有LTD4在G.P.I.S.M.上有活性。FPL-55712几乎完全抑制了它们的肌otropic活性。5S,6R化合物比5S,6S化合物更具活性，效力顺序为LTD4大于5,6-DiHETE大于Lx A。有人提出，5,6-DiHETE和Lx A异构体可能通过肺LTD4受体起作用，这些受体似乎比回肠LTD4受体特异性更低。
