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Endotoxin-induced intravascular coagulation (DIC) and its therapy.
Advances in Shock Research
|January 1, 1979
Summary
This study investigated anticoagulants' effects on endotoxin-induced disseminated intravascular coagulation (DIC) in dogs. Heparin and antithrombin III (AT III) reduced fibrinogen consumption but not platelet loss, suggesting direct endotoxin effects on platelets.
Area of Science:
- Veterinary Medicine
- Pharmacology
- Hematology
Background:
- Endotoxin infusion in dogs consistently triggers disseminated intravascular coagulation (DIC).
- Understanding the efficacy of various anticoagulants in mitigating DIC is crucial for clinical management.
Purpose of the Study:
- To evaluate the effects of heparin, dipyridimole, steroids, prostaglandin E1, Macrodex, and antithrombin III (AT III) on endotoxin-induced DIC in a canine model.
- To elucidate the mechanism of endotoxin-induced thrombocytopenia and hypofibrinogenemia.
Main Methods:
- Dogs received endotoxin infusion, with various anticoagulants administered beforehand in separate experiments.
- Platelet counts and fibrinogen levels were monitored to assess the coagulopathy.
- Dosages of heparin and AT III were specifically designed to assess their impact on DIC markers.
Main Results:
- Heparin (1-10 mg/kg) and AT III (doubling circulating levels) significantly reduced fibrinogen utilization but did not prevent thrombocytopenia.
- Dipyridimole, steroids, Macrodex, and prostaglandin E1 showed minimal impact on the development of thrombocytopenia or hypofibrinogenemia.
- Endotoxin's effect on dog platelets appears to be direct, not mediated by thrombin.
Conclusions:
- Heparin and AT III are effective in preventing fibrinogen consumption during endotoxin-induced DIC but do not protect platelets.
- The findings suggest that the endotoxin's impact on platelets is direct.
- The clinical use of heparin in DIC management may be most beneficial when renal complications are present.