Berisha H, Pakbaz H, Absood A, Foda H D, Said S I
SUNY at Stony Brook.
Ann N Y Acad Sci. 1994 Jun 17;723:422-5.
In both paraquat and X/XO models of lung injury, the injury, previously attributed to the generation of reactive oxygen species, was related to the induction of NO. synthesis, and was totally preventable by inhibition of this synthesis. The results support the view that the NO. radical itself is an essential intermediary in the pathogenesis of at least some forms of oxidant tissue damage. Another form of oxidant injury, caused by prolonged perfusion of the lung ex vivo, is not mediated by NO. however.
在百草枯和黄嘌呤/黄嘌呤氧化酶诱导的肺损伤模型中，先前认为由活性氧生成导致的损伤，实际上与一氧化氮（NO）合成的诱导有关，并且通过抑制这种合成可完全预防。这些结果支持了以下观点：即NO自由基本身是至少某些形式的氧化组织损伤发病机制中的关键中介物。然而，另一种由离体肺长时间灌注引起的氧化损伤形式并非由NO介导。
