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Platelet dysfunction during Bothrops jararaca snake envenomation in rabbits.
Marcelo Larami Santoro1, Ida Sigueko Sano-Martins
1Laboratory of Pathophysiology, Institute Butantan, São Paulo, Brazil. santoro@butantan.gov.br
Thrombosis and Haemostasis
|July 23, 2004
Summary
Snake venom from Bothrops jararaca causes platelet dysfunction and activation in rabbits, suggesting plasma inhibitors interfere with aggregation. This study investigates platelet disorders following envenomation.
Area of Science:
- Toxicology
- Hematology
- Biochemistry
Background:
- Snake envenomation is known to disrupt blood coagulation and fibrinolysis.
- Limited data exists on the specific effects of snake venom on blood platelet function.
Purpose of the Study:
- To investigate the impact of Bothrops jararaca envenomation on platelet disorders in an experimental rabbit model.
- To elucidate the mechanisms underlying venom-induced platelet dysfunction and activation.
Main Methods:
- Experimental envenomation of rabbits with Bothrops jararaca venom.
- Analysis of platelet count, fibrinogen levels, von Willebrand factor, platelet aggregation, ATP secretion, serotonin levels, and P-selectin expression.
- Flow cytometry to assess GPIIb-IIIa and LIBS-1 expression on platelets.
Main Results:
- Envenomed rabbits exhibited thrombocytopenia, hypofibrinogenemia, and elevated von Willebrand factor.
- Platelet hypoaggregation was observed in platelet-rich plasma and whole blood, but not in washed platelets.
- Decreased platelet ATP secretion and increased P-selectin expression indicated platelet activation, while GPIIb-IIIa expression showed altered epitopes.
- Intraplatelet serotonin and plasma platelet factor 4 levels remained normal.
Conclusions:
- Thrombin generated by Bothrops jararaca venom likely contributes to platelet and coagulation disorders.
- Platelet activation, evidenced by P-selectin elevation, occurs in circulating platelets.
- The findings suggest a plasma inhibitor interfering with platelet aggregation in Bothrops envenomation.