Biochimica et Biophysica Acta (BBA) - Biomembranes
Volume 1146, Issue 2, 14 March 1993, Pages 282-293
Regular paperThe mode of action of primary bile salts on human platelets
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The proteomic and metabolomic signatures of isolated and polytrauma traumatic brain injury
2023, American Journal of SurgeryViscoelastic measurements of platelet function, not fibrinogen function, predicts sensitivity to tissue-type plasminogen activator in trauma patients
2015, Journal of Thrombosis and HaemostasisFibrinolysis shutdown phenotype masks changes in rodent coagulation in tissue injury versus hemorrhagic shock
2015, Surgery (United States)Citation Excerpt :Nevertheless, rats are markedly resistant to tPA at baseline, and it is likely that other unmeasured regulators of fibrinolysis are present. TUCA has been shown to augment tPA-mediated fibrinolysis,11 but also has been shown to impair platelet function.21 Platelets have been proposed to provide a protective shell to a central fibrin clot, and support the clot by release of procoagulants and antifibrinolytics during degranulation.22
Shock releases bile acidinducing platelet inhibition and fibrinolysis
2015, Journal of Surgical ResearchCitation Excerpt :An animal model of shock and resuscitation supports that TUCA levels can increase within 30 min of low blood pressure and remain elevated after resuscitation. Bile acids have previously been associated with platelet dysfunction [11]. The proposed mechanism was through membrane deformity.
Vesiculation induced by amphiphiles and ionophore A23187 in porcine platelets: A transmission electron microscopic study
1996, Chemico-Biological InteractionsIn vivo effect of bile salts on platelet aggregation in rats
1995, Thrombosis Research
Copyright © 1993 Published by Elsevier B.V.