Marked difference in pathophysiology between tissue factor- and lipopolysaccharide-induced disseminated intravascular coagulation models in rats.
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.
Asakura
Hidesaku
H
Department of Internal Medicine (III), Kanazawa University, School of Medicine, Ishikawa, Japan. hasakura@med3.m.kanazawa-u.ac.jp
Suga
Yukio
Y
Aoshima
Keiji
K
Ontachi
Yasuo
Y
Mizutani
Tomoe
T
Kato
Minori
M
Saito
Masanori
M
Morishita
Eriko
E
Yamazaki
Masahide
M
Takami
Akiyoshi
A
Miyamoto
Ken-ichi
K
Nakao
Shinji
S
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
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