Skip to main content
Journal cover image

Hemostatic activation in a chemically induced rat model of severe hemolysis and thrombosis.

Publication ,  Journal Article
Lewis, DA; Nyska, A; Potti, A; Hoke, HA; Klemp, KF; Ward, SM; Peddada, SD; Wu, J; Ortel, TL
Published in: Thromb Res
2006

INTRODUCTION: In hemolytic diseases such as sickle cell disease and beta-thalassemia, the mechanisms of thrombosis are poorly understood, however erythrocyte/endothelium interactions are thought to play an important role. Appropriate animal models would increase our understanding of the pathophysiology of thrombosis and aid in the development of new therapeutic strategies. We previously reported that rats exposed to 2-butoxyethanol (2-BE) develop hemolysis and enhanced adherence of erythrocytes to the extracellular matrix, possibly secondary to the recruitment of cellular adhesion molecules at the erythrocyte/endothelium interface. METHODS: We exposed rats to 250 mg/kg/day of 2-BE for 4 days, and collected blood for coagulation markers on each day. RESULTS: As previously observed, erythrocytes dropped precipitously (8.0 to 1.8x10(6)/microl in 48 h), and diffuse microvascular thrombosis developed in the heart, lungs, liver, bones and eyes. Prothrombin times, activated partial thromboplastin times, fibrinogen, and antithrombin-III were unchanged between treated and control rats, indicating that hemostasis is largely unperturbed. However the thrombin-antithrombin III levels in the 2-BE treated rats for all days were 3-7 times greater than the control rats. The plasma intercellular adhesion molecule-1 (ICAM-1) levels of 2-BE treated animals were approximately twice that of the controls on days 2 and 3 and 1.5 times the controls on day 4 (P<0.05). CONCLUSION: Our findings are consistent with the observations of increased erythrocyte aggregation, increased erythrocyte/endothelium interaction, and increased plasma ICAM-1 levels observed in sickle cell disease and beta-thalassemia patients. This model may be useful for studying therapeutic agents that disrupt erythrocyte/endothelium interactions.

Duke Scholars

Published In

Thromb Res

DOI

ISSN

0049-3848

Publication Date

2006

Volume

118

Issue

6

Start / End Page

747 / 753

Location

United States

Related Subject Headings

  • beta-Thalassemia
  • Thrombosis
  • Rats, Inbred F344
  • Rats
  • Peptide Hydrolases
  • Intercellular Adhesion Molecule-1
  • Hemostasis
  • Hemolysis
  • Female
  • Ethylene Glycols
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Lewis, D. A., Nyska, A., Potti, A., Hoke, H. A., Klemp, K. F., Ward, S. M., … Ortel, T. L. (2006). Hemostatic activation in a chemically induced rat model of severe hemolysis and thrombosis. Thromb Res, 118(6), 747–753. https://doi.org/10.1016/j.thromres.2005.11.010
Lewis, Deborah A., Abraham Nyska, Anil Potti, Heather A. Hoke, Keith F. Klemp, Sandra M. Ward, Shyamal D. Peddada, Jogin Wu, and Thomas L. Ortel. “Hemostatic activation in a chemically induced rat model of severe hemolysis and thrombosis.Thromb Res 118, no. 6 (2006): 747–53. https://doi.org/10.1016/j.thromres.2005.11.010.
Lewis DA, Nyska A, Potti A, Hoke HA, Klemp KF, Ward SM, et al. Hemostatic activation in a chemically induced rat model of severe hemolysis and thrombosis. Thromb Res. 2006;118(6):747–53.
Lewis, Deborah A., et al. “Hemostatic activation in a chemically induced rat model of severe hemolysis and thrombosis.Thromb Res, vol. 118, no. 6, 2006, pp. 747–53. Pubmed, doi:10.1016/j.thromres.2005.11.010.
Lewis DA, Nyska A, Potti A, Hoke HA, Klemp KF, Ward SM, Peddada SD, Wu J, Ortel TL. Hemostatic activation in a chemically induced rat model of severe hemolysis and thrombosis. Thromb Res. 2006;118(6):747–753.
Journal cover image

Published In

Thromb Res

DOI

ISSN

0049-3848

Publication Date

2006

Volume

118

Issue

6

Start / End Page

747 / 753

Location

United States

Related Subject Headings

  • beta-Thalassemia
  • Thrombosis
  • Rats, Inbred F344
  • Rats
  • Peptide Hydrolases
  • Intercellular Adhesion Molecule-1
  • Hemostasis
  • Hemolysis
  • Female
  • Ethylene Glycols