Thrombocytopenia and platelet hypoaggregation induced by Bothrops asper snake venom. Toxins involved and their contribution to metalloproteinase-induced pulmonary hemorrhage
Research article published in Thrombosis and haemostasis (2005)
Abstract
Thrombocytopenia and platelet dysfunction occur in patients bitten by Bothrops sp snakes in Latin America. An experimental model was developed in mice to study the effects of B. asper venom in platelet numbers and function. Intravenous administration of this venom induces rapid and prominent thrombocytopenia and ex vivo platelet hypoaggregation. The drop in platelet numbers was primarily due to aspercetin, a protein of the C-type lectin family which induces von Willebrand factor-mediated platelet aggregation/agglutination. In addition, the effect of class P-III hemorrhagic metalloproteinases on the microvessel wall also contributes to thrombocytopenia since jararhagin, a P-III metalloproteinase, reduced platelet counts. Hypoaggregation was associated with the action of procoagulant and defibrin(ogen)ating proteinases jararacussin-I (a thrombin-like serine proteinase) and basparin A (a prothrombin activating metalloproteinase). At the doses which induced hypoaggregation, these enzymes caused defibrin(ogen)ation, increments in fibrin(ogen) degradation products and D-dimer and prolongation of the bleeding time. Incubation of B. asper venom with batimastat and alpha2-macroglobulin abrogated the hypoaggregating activity, confirming the role of venom proteinases in this effect. Neither aspercetin nor the defibrin(ogen)ating and hypoaggregating components induced hemorrhage upon intravenous injection. However, aspercetin, but not the thrombin-like or the prothrombin-activating proteinases, potentiated the hemorrhagic activity of two hemorrhagic metalloproteinases in the lungs.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Резюме
Thrombocytopenia and platelet hypoaggregation induced by Bothrops asper snake venom. Toxins involved and their contribution to metalloproteinase-induced pulmonary hemorrhage.
Почему это важно для гирудотерапии
This study examined the specific mechanisms by which Bothrops asper snake venom induces thrombocytopenia and platelet hypoaggregation using an experimental mouse model. The abstract identifies specific venom toxins, including C-type lectins and class P-III hemorrhagic metalloproteinases, that collectively contribute to rapid platelet drops, defibrination, and potentiation of pulmonary hemorrhage. While the research provides detailed insights into venom-induced hemostatic dysregulation and metalloproteinase activity, it is fundamentally a study of snake venom pathology. It contains no data regarding leeches and holds no relevance to the therapeutic use of the leech secretome in hirudotherapy.
Цитирование
Thrombocytopenia and platelet hypoaggregation induced by Bothrops asper snake venom. Toxins involved and their contribution to metalloproteinase-induced pulmonary hemorrhage
Rucavado A et al. · Thrombosis and haemostasis, 2005
Связанный клинический контекст
Узнайте, как это исследование связано с клинической практикой
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