Loegering D J, Richard C A, Leahy K P, Davison C B
Department of Physiology & Cell Biology, Albany Medical College, NY, USA.
Life Sci. 1995;57(20):PL321-6. doi: 10.1016/0024-3205(95)02172-f.
There is growing evidence that an oxidant stress contributes to the deleterious effects of bacterial lipopolysaccharide (LPS). The present study evaluated the ability of the antioxidant, U74389, to prevent the depression of vascular reactivity caused by LPS. Aortic rings taken from rats given LPS showed a depression of maximum force in response to phenylephrine that was reversed by an inhibitor of nitric oxide synthase. Pretreatment of animals with U74389 attenuated this depression of vascular reactivity. U74389 did not limit the increase in serum tumor necrosis factor levels caused by LPS. These results show that U74389 can ameliorate the depression of vascular reactivity caused by LPS possibly by interfering with the induction of nitric oxide synthase.
越来越多的证据表明，氧化应激会导致细菌脂多糖（LPS）产生有害影响。本研究评估了抗氧化剂U74389预防LPS引起的血管反应性降低的能力。取自给予LPS大鼠的主动脉环对去氧肾上腺素的最大反应力降低，一氧化氮合酶抑制剂可逆转这种降低。用U74389预处理动物可减轻这种血管反应性降低。U74389并未限制LPS引起的血清肿瘤坏死因子水平升高。这些结果表明，U74389可能通过干扰一氧化氮合酶的诱导来改善LPS引起的血管反应性降低。
