Effect of N-acetylcysteine on fibrin deposition in the rat lung due to intravascular coagulation.
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.
D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D004211:Disseminated Intravascular Coagulation / Q000139:chemically induced / Q000378:metabolism*; D005337:Fibrin / Q000378:metabolism*; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D007457:Iodine Radioisotopes; D007700:Kinetics; D008168:Lung / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D014148:Tranexamic Acid
D007457:Iodine Radioisotopes; D014148:Tranexamic Acid; D005337:Fibrin; D005340:Fibrinogen; D000111:Acetylcysteine