Wegener T, Wallin R, Saldeen T
Ups J Med Sci. 1986;91(1):45-52. doi: 10.3109/03009738609178490.
Intravascular coagulation was induced in rats by i.p. injection of a fibrinolysis inhibitor, tranexamic acid (AMCA, 200 mg/kg B.W.), and i.v. injection of bovine thrombin (500 NIH units/kg B.W.) and the fibrin deposition in the lungs was assessed with 125I-labelled fibrinogen. Treatment with N-acetylcysteine (NAC) partly prevented the deposition of fibrin in the lungs, and the disappearance of fibrinogen from the blood, but did not seem to influence the elimination of fibrin in the lungs. The results indicate that NAC may counteract pulmonary damage in this experimental model, by inhibiting intravascular fibrin formation.
通过腹腔注射纤溶抑制剂氨甲环酸(AMCA,200毫克/千克体重)和静脉注射牛凝血酶(500美国国立卫生研究院单位/千克体重)诱导大鼠血管内凝血,并用125I标记的纤维蛋白原评估肺内纤维蛋白沉积。用N-乙酰半胱氨酸(NAC)治疗可部分预防肺内纤维蛋白沉积和血液中纤维蛋白原的消失,但似乎不影响肺内纤维蛋白的清除。结果表明,NAC可能通过抑制血管内纤维蛋白形成来对抗该实验模型中的肺损伤。