Torkunov P A, Shabanov P D
Eksp Klin Farmakol. 2009 Mar-Apr;72(2):44-6.
The preventive and curative action of NO-synthase inhibitors derived from L-arginine was investigated on the model of toxic lung edema induced by phosgene (LCt50 - 84) in mice. The most pronounced decrease in the phosgene-induced lung edema was observed for aminoguanidine, NG-nitro-L-arginine (L-NNA), and L-nitroarginine methyl ester (L-NAME). Aminoguanidine was effective in cases of both preventive and curative administration. L-NNA, an inhibitor of the constitutive isoform of NO-synthase, was effective only after preventive injection, while L-NAME, an inhibitor of both inducible and constitutive isoforms of NO-synthase, was effective only after curative use. Therefore, the NO-synthase inhibitors are a promising group of pharmacological agents for the treatment of toxic lung edema induced by phosgene.
在小鼠光气(LCt50 - 84)诱导的中毒性肺水肿模型上,研究了源自L-精氨酸的一氧化氮合酶抑制剂的预防和治疗作用。观察到氨基胍、NG-硝基-L-精氨酸(L-NNA)和L-硝基精氨酸甲酯(L-NAME)对光气诱导的肺水肿有最显著的减轻作用。氨基胍在预防和治疗给药的情况下均有效。L-NNA是一氧化氮合酶组成型同工型的抑制剂,仅在预防性注射后有效,而L-NAME是一氧化氮合酶诱导型和组成型同工型的抑制剂,仅在治疗使用后有效。因此,一氧化氮合酶抑制剂是治疗光气诱导的中毒性肺水肿的一组有前景的药物。