title: Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats.
abstract: OBJECTIVE
  Tissue factor and lipopolysaccharide frequently have been used to induce disseminated intravascular coagulation in experimental animal models. Although the pathophysiology of disseminated intravascular coagulation may differ according to the agents used to induce it, these previous models have not distinguished between the use of different disseminated intravascular coagulation-inducing agents. In this study, we attempted to evaluate the characteristic features of these agents in two types of disseminated intravascular coagulation models, with special reference to selected hemostatic parameters and pathologic findings in the kidney.
  
  
  METHODS
  Prospective, comparative, experimental study.
  
  
  METHODS
  Laboratory at a university hospital.
  
  
  METHODS
  Twenty-seven male Wistar rats, age 6-7 wks, weighing 160-170 g.
  
  
  METHODS
  Three groups of animals were studied: a control group (n = 8) receiving physiologic saline, a tissue factor-treated group (n = 11) receiving tissue factor 3.75 units/kg, and a lipopolysaccharide-treated group (n = 8) receiving lipopolysaccharide 30 mg/kg; each group sustained infusion for 4 hrs via the tail vein.
  
  
  RESULTS
  The degree of hemostatic activation in both types of experimental disseminated intravascular coagulation was identical, based on the results of thrombin-antithrombin III complex levels. Markedly elevated D-dimer concentrations were observed without organ dysfunction or fibrin deposition in the kidney on administration of tissue factor, whereas markedly elevated plasminogen activator inhibitor activity, decreased antithrombin III activity, severe organ failure, and marked fibrin deposition in the kidney were observed for lipopolysaccharide administration.
  
  
  CONCLUSIONS
  Because pathophysiology differed remarkably between the tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats, we recommend that they be assessed carefully as distinct entities to determine implications of their experimental and clinical use.
authors.affiliation: Department of Internal Medicine (III), Kanazawa University, School of Medicine, Ishikawa, Japan. hasakura@med3.m.kanazawa-u.ac.jp
authors.forename: Hidesaku
authors.initials: H
authors.lastname: Asakura
authors.forename: Yukio
authors.initials: Y
authors.lastname: Suga
authors.forename: Keiji
authors.initials: K
authors.lastname: Aoshima
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Ontachi
authors.forename: Tomoe
authors.initials: T
authors.lastname: Mizutani
authors.forename: Minori
authors.initials: M
authors.lastname: Kato
authors.forename: Masanori
authors.initials: M
authors.lastname: Saito
authors.forename: Eriko
authors.initials: E
authors.lastname: Morishita
authors.forename: Masahide
authors.initials: M
authors.lastname: Yamazaki
authors.forename: Akiyoshi
authors.initials: A
authors.lastname: Takami
authors.forename: Ken-ichi
authors.initials: K
authors.lastname: Miyamoto
authors.forename: Shinji
authors.initials: S
authors.lastname: Nakao
mesh_terms: D000818:Animals; D000990:Antithrombin III; D004195:Disease Models, Animal; D004211:Disseminated Intravascular Coagulation / Q000209:etiology* / Q000503:physiopathology*; D005337:Fibrin / Q000032:analysis; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D006487:Hemostasis / Q000502:physiology*; D007668:Kidney / Q000473:pathology; D008070:Lipopolysaccharides; D008297:Male; D010447:Peptide Hydrolases / Q000097:blood; D011446:Prospective Studies; D051381:Rats; D017208:Rats, Wistar; D013925:Thromboplastin
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D008070:Lipopolysaccharides; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; D000990:Antithrombin III; D005337:Fibrin; D013925:Thromboplastin; D010447:Peptide Hydrolases