Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation

Blood ◽  
1976 ◽  
Vol 47 (2) ◽  
pp. 287-296 ◽  
Author(s):  
DH Wigton ◽  
GJ Kociba ◽  
EA Hoover

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin- fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.

Blood ◽  
1976 ◽  
Vol 47 (2) ◽  
pp. 287-296 ◽  
Author(s):  
DH Wigton ◽  
GJ Kociba ◽  
EA Hoover

Abstract The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin- fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.


2013 ◽  
Vol 58 (No. 11) ◽  
pp. 587-590 ◽  
Author(s):  
I. Uhrikova ◽  
K. Machackova ◽  
L. Rauserova-Lexmaulova ◽  
K. Rehakova ◽  
J. Doubek

Gastric dilatation and volvulus syndrome is associated with changes in haemostatic profiles. The aims of this study were to compare selected haemostatic and fibrinolytic parameters between healthy dogs and dogs with gastric dilatation and volvulus syndrome, estimate the incidence of disseminated intravascular coagulation (DIC), and determine the most sensitive test for detection of DIC in these patients. Blood was collected from 22 dogs with gastric dilatation and volvulus syndrome, and nine healthy control dogs. Platelet counts, prothrombin time, activated partial thromboplastin time, fibrinogen concentrations and fibrin/fibrinogen degradation products were measured in all control dogs and patients with gastric dilatation and volvulus syndrome, before and after surgery. Significant differences between control dogs and patients were seen in activated partial thromboplastin time and fibrin/fibrinogen degradation products before surgery and all measured parameters after surgery. The incidence of DIC was 59%. The most sensitive tests for detection of DIC before surgery were those for activated partial thromboplastin time and fibrin/fibrinogen degradation products.


1983 ◽  
Vol 49 (03) ◽  
pp. 190-192 ◽  
Author(s):  
T Yoshikawa ◽  
M Murakami ◽  
Y Furukawa ◽  
S Takemura ◽  
M Kondo

SummaryThe effects of ticlopidine and aspirin on endotoxin-induced experimental disseminated intravascular coagulation (DIC) were studied in rats. Experimental DIC was induced by a 4 hr sustained infusion of endotoxin at a dose of 100 mg/kg. The rats were intraperitoneally injected with ticlopidine at 2.0, 20.0, 50.0, 100.0 or 200.0 mg/kg, or aspirin at 0.03, 0.3, 3.0 or 30.0 mg/kg, followed by the continuous infusion of 100 mg/kg/4 hr of endotoxin. A preventive effect against DIC was noted in all the parameters, such as fibrinogen and fibrin degradation products (FDP), fibrinogen level, prothrombin time, partial thromboplastin time (PTT), platelet count and the number of renal glomeruli with fibrin thrombi, in the rats treated with 20.0, 50.0, 100.0 or mg/kg of ticlopidine. Although a preventive effect was also noted in FDP, PTT, platelet count and the number of glomeruli with thrombi in rats treated with 0.03 or 0.3 mg/kg of aspirin, this agent was less effective than ticlopidine.


2000 ◽  
Vol 2 (2) ◽  
pp. 115-119 ◽  
Author(s):  
A E Ridyard ◽  
E A Welsh ◽  
D A Gunn-Moore

A peri-parturient fifteen-month-old female Maine Coon cat was presented with extreme weakness and depression, profound hypovolaemia and hypothermia. Severe hyperkalaemia, hyponatraemia and anaemia were detected. Disseminated intravascular coagulation was suspected due to marked prolongation of activated partial thromboplastin time. Uterine torsion was diagnosed at exploratory laparotomy. The cat made a full recovery following ovariohysterectomy and intensive supportive therapy.


Author(s):  
N. V. Galeeva ◽  
I. E. Kravchenko

Goal of the study is to reveal the particular features of hemostasis in patients with chronic hepatitis C in dynamics of natural course of disease. Materials and methods. The indices of hemostasis in 535 patients with chronic hepatitis C were assessed by the number of platelets, degree of their aggregation with the use of inductor of adenosine triphosphate and without it (spontaneous aggregation of platelets). Coagulative hemostasis was analyzed by the activated partial thromboplastin time, antitrombin III, prothrombin ratio, prothrombin time, fibrinogen concentration in plasma and international normalized ratio. Based on the number of Tr, typical for the disseminated intravascular coagulation syndrome, conditionally the patients were divided into 3 groups: I group - hypercoagulability; II - transient phase between hyper and hypocoagulation and III- hypocoagulation, which also included patients with liver cirrhosis. Results and discussion. Independent on the phase of disseminated intravascular coagulation syndrome, increase of aggregation of Tr with the growth of maximal amplitude was observed. The main part of studied indices of coagulative hemostasis indicated at the condition of hypocoagulation in patients with chronic hepatitis C - this is significant increase of activated partial thromboplastin time, prothrombin time, international normalized ratio and decrease of fibrinogen concentration in the studied groups by the phases of disseminated intravascular coagulation syndrome. Value of antitrombin III changed oppositely, it decreased, so that plasma hemostasis tends to the hypercoagulation. Conclusion. Under the chronic hepatitis C all phases of disseminated intravascular coagulation syndrome were observed with the disorder of thrombocytic coagulative hemostasis. There was followed up multidirectional change of hemostasis which obtained in the most cases character of delitescent course of disseminated intravascular coagulation syndrome.


2000 ◽  
Vol 84 (07) ◽  
pp. 54-58 ◽  
Author(s):  
Wakako Izutani ◽  
Yoshikazu Komurasaki ◽  
Mitsugu Fujita

SummaryThe effect of urinary protein C inhibitor (uPCI) on disseminated intravascular coagulation (DIC) was investigated using an experimental DIC in rats. uPCI (0.5 and 1.0 mg/kg) was continuously administrated into the left femoral vein of the rats with lipopolysaccharide (50 mg/kg)-induced DIC. In all doses, uPCI significantly prevented the drastic changes in the parameters such as fibrinogen concentration, activated partial thromboplastin time (APTT), prothrombin time (PT), fibrin/fibrinogen degradation products (FDP) level, aspartate aminotransferase (AST) level and alanine aminotransferase (ALT) level. Furthermore, uPCI significantly inhibited the increase in the levels of plasma kallikrein and thrombin which act not only as the procoagulant proteases but also as the chemotactic factors to neutrophils and monocytes. These results show that uPCI may prevent hypercoagulation, the induction of secondary fibrinolysis and organ failure in the DIC model. Therefore, uPCI may be a useful agent for the clinical treatment of DIC.


Author(s):  
N. V. Galeeva ◽  
I. E. Kravchenko

Goal of the study is to reveal the particular features of hemostasis in patients with chronic hepatitis C in dynamics of natural course of disease. Materials and methods. The indices of hemostasis in 535 patients with chronic hepatitis C were assessed by the number of platelets, degree of their aggregation with the use of inductor of adenosine triphosphate and without it (spontaneous aggregation of platelets). Coagulative hemostasis was analyzed by the activated partial thromboplastin time, antitrombin III, prothrombin ratio, prothrombin time, fibrinogen concentration in plasma and international normalized ratio. Based on the number of Tr, typical for the disseminated intravascular coagulation syndrome, conditionally the patients were divided into 3 groups: I group - hypercoagulability; II - transient phase between hyper and hypocoagulation and III- hypocoagulation, which also included patients with liver cirrhosis. Results and discussion. Independent on the phase of disseminated intravascular coagulation syndrome, increase of aggregation of Tr with the growth of maximal amplitude was observed. The main part of studied indices of coagulative hemostasis indicated at the condition of hypocoagulation in patients with chronic hepatitis C - this is significant increase of activated partial thromboplastin time, prothrombin time, international normalized ratio and decrease of fibrinogen concentration in the studied groups by the phases of disseminated intravascular coagulation syndrome. Value of antitrombin III changed oppositely, it decreased, so that plasma hemostasis tends to the hypercoagulation. Conclusion. Under the chronic hepatitis C all phases of disseminated intravascular coagulation syndrome were observed with the disorder of thrombocytic coagulative hemostasis. There was followed up multidirectional change of hemostasis which obtained in the most cases character of delitescent course of disseminated intravascular coagulation syndrome.


Sign in / Sign up

Export Citation Format

Share Document