Hwang D H, Chanmugam P, Hymel G, Boudreau M
Prostaglandins Leukot Med. 1987 Mar;26(3):299-305. doi: 10.1016/0262-1746(87)90039-4.
Effects of chronic ethanol ingestion (3 weeks) on the capacity of peritoneal macrophages, lung and heart tissues, to metabolize endogenous arachidonic acid (AA) in rats, and the in vitro effect of ethanol on 3'-5' cyclic adenosine monophosphate (cAMP) levels in rat platelets were studied. Peritoneal resident macrophages were stimulated by calcium ionophore (A23187) and levels of 5-hydroxyeicosatetraenoic acid (5-HETE), leukotriene B4 (LTB4) and PGE2 were measured by radioimmunoassay. There were no differences in levels of the eicosanoids synthesized by macrophages between the ethanol treated and the control group. There were also no differences found in levels of the eicosanoids synthesized by heart or lung homogenate between the two groups. These results suggest that chronic ethanol ingestion does not alter the capacity to synthesize the eicosanoids from the endogenous precursor in tissues studied here. Preincubation of ethanol with platelet rich plasma resulted in a dose dependent increase in cAMP levels. The well documented inhibitory effects of ethanol in vitro on aggregation and AA metabolism in platelets may be due to the enhanced cAMP levels.
研究了慢性乙醇摄入(3周)对大鼠腹膜巨噬细胞、肺和心脏组织代谢内源性花生四烯酸(AA)能力的影响,以及乙醇对大鼠血小板中3'-5'环磷酸腺苷(cAMP)水平的体外作用。用钙离子载体(A23187)刺激腹膜常驻巨噬细胞,并用放射免疫分析法测定5-羟基二十碳四烯酸(5-HETE)、白三烯B4(LTB4)和前列腺素E2的水平。乙醇处理组和对照组巨噬细胞合成的类花生酸水平没有差异。两组心脏或肺匀浆合成的类花生酸水平也没有差异。这些结果表明,慢性乙醇摄入不会改变此处研究组织中从内源性前体合成类花生酸的能力。乙醇与富血小板血浆预孵育导致cAMP水平呈剂量依赖性升高。乙醇在体外对血小板聚集和AA代谢的抑制作用已有充分记录,这可能是由于cAMP水平升高所致。