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Immune complex-induced disseminated intravascular coagulation (DIC). An experimental study.
S Nakamura1, T Shimokama, Y Yoshikawa
1Department of Pathology, Saga Medical School, Japan.
Acta Pathologica Japonica
|July 1, 1990
Summary
Researchers developed a rabbit model to study immune complex-induced disseminated intravascular coagulation (DIC). This model helps understand how antigen-antibody complexes trigger DIC, affecting blood cells and fibrinogen levels.
Area of Science:
- Immunology
- Hematology
- Pathology
Background:
- Disseminated intravascular coagulation (DIC) is a complex hematological disorder.
- Immune complex formation is implicated in the pathogenesis of DIC.
Purpose of the Study:
- To establish a reliable rabbit model for studying immune complex-induced DIC.
- To investigate the mechanisms underlying DIC triggered by antigen-antibody complexes.
Main Methods:
- Rabbits were passively sensitized with antiferritin antiserum and challenged with ferritin.
- Blood cell counts, fibrinogen levels, and tissue morphology were analyzed.
- Immune complex deposition and phagocytosis were examined.
Main Results:
- Induced DIC characterized by rapid drops in white blood cells, platelets, and fibrinogen.
- Fibrin thrombi formation observed in multiple organs, peaking between 5-7 hours.
- Kupffer cell saturation correlated with widespread fibrin thrombosis.
Conclusions:
- Antigen-antibody complexes in microcirculation likely initiate DIC by activating platelets and neutrophils.
- Complement activation and reticuloendothelial system blockade may exacerbate DIC.
- This model provides a valuable tool for further research into immune complex-induced DIC.