Hatake K, Wakabayashi I
Department of Legal Medicine, Nara Medical University, Japan.
Nihon Arukoru Yakubutsu Igakkai Zasshi. 2000 Apr;35(2):61-8.
Using isolated rat aortic strips without endothelium, we investigated the effect of ethanol on L-arginine-induced relaxation. L-Arginine (10(-5)-10(-3) M) produced a relaxation response in vascular strips incubated for 6 hr with bacterial lipopolysaccharide (1 microgram/ml). The relaxation was either abolished by cycloheximide (10(-5) M) and actinomycin D (10(-5) M) or diminished by polymyxin B (10 micrograms/ml), dexamethasone (10(-5) M) and nitro-L-arginine (10(-4) M) under conditions in which these inhibitors were coincubated with lipopolysaccharide. Also, L-arginine-induced relaxation was significantly inhibited when ethanol (200, 400 mM) was present together with lipopolysaccharide during the 6-hr incubation. However, when ethanol was added to the organ bath after 6-hr incubation with lipopolysaccharide, it did not inhibit the relaxation. These results suggest that the relaxation response to L-arginine is mediated by an inducible type of nitric oxide synthase, which can be induced by lipopolysaccharide, and that ethanol may attenuate this nitric oxide-mediated relaxation by inhibiting expression of inducible nitric oxide synthase.
我们使用无内皮的离体大鼠主动脉条，研究了乙醇对L-精氨酸诱导的舒张作用的影响。L-精氨酸（10⁻⁵ - 10⁻³ M）在与细菌脂多糖（1微克/毫升）孵育6小时的血管条中产生舒张反应。在这些抑制剂与脂多糖共同孵育的条件下，该舒张反应要么被放线菌酮（10⁻⁵ M）和放线菌素D（10⁻⁵ M）消除，要么被多粘菌素B（10微克/毫升）、地塞米松（10⁻⁵ M）和硝基-L-精氨酸（10⁻⁴ M）减弱。此外，在6小时孵育期间，当乙醇（200、400 mM）与脂多糖同时存在时，L-精氨酸诱导的舒张被显著抑制。然而，在用脂多糖孵育6小时后将乙醇加入器官浴中时，它并未抑制舒张。这些结果表明，对L-精氨酸的舒张反应是由一种可诱导型一氧化氮合酶介导的，该酶可由脂多糖诱导，并且乙醇可能通过抑制诱导型一氧化氮合酶的表达来减弱这种一氧化氮介导的舒张。
