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Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats.

AbstractOBJECTIVE:
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.
DESIGN:
Prospective, comparative, experimental study.
SETTING:
Laboratory at a university hospital.
SUBJECTS:
Twenty-seven male Wistar rats, age 6-7 wks, weighing 160-170 g.
INTERVENTIONS:
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.
MEASUREMENTS AND MAIN 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.
CONCLUSION:
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.
AuthorsHidesaku Asakura, Yukio Suga, Keiji Aoshima, Yasuo Ontachi, Tomoe Mizutani, Minori Kato, Masanori Saito, Eriko Morishita, Masahide Yamazaki, Akiyoshi Takami, Ken-ichi Miyamoto, Shinji Nakao
JournalCritical care medicine (Crit Care Med) Vol. 30 Issue 1 Pg. 161-4 (Jan 2002) ISSN: 0090-3493 [Print] United States
PMID11902257 (Publication Type: Comparative Study, Journal Article)
Chemical References
  • Fibrin Fibrinogen Degradation Products
  • Lipopolysaccharides
  • antithrombin III-protease complex
  • fibrin fragment D
  • Antithrombin III
  • Fibrin
  • Thromboplastin
  • Peptide Hydrolases
Topics
  • Animals
  • Antithrombin III
  • Disease Models, Animal
  • Disseminated Intravascular Coagulation (etiology, physiopathology)
  • Fibrin (analysis)
  • Fibrin Fibrinogen Degradation Products (analysis)
  • Hemostasis (physiology)
  • Kidney (pathology)
  • Lipopolysaccharides
  • Male
  • Peptide Hydrolases (blood)
  • Prospective Studies
  • Rats
  • Rats, Wistar
  • Thromboplastin

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