Hypothermia and Platelet Dysfunction
Abstract
Platelets are essential for normal hemostasis. The main functions of platelets are adhesion to damaged blood vessel walls, aggregation to form a platelet plug, and promotion of fibrin clot formation. Platelet adhesion is primarily mediated by the adhesive molecule von Willebrand factor, which binds both to a specific platelet surface receptor (the glycoprotein GP ib-Ix complex) and to exposed subendothelial components. Platelet-to-platelet aggregation is primarily mediated by fibrinogen binding to its platelet surface receptor (the GPIIb-IIIa complex). Circulating platelets are normally in a resting state and, despite the presence of platelet surface GPIb-IX and GPIIb-IIIa complexes, they bind neither plasma von Willebrand factor nor plasma fibrinogen. In vitro, the cationic antibiotic ristocetin induces binding of von Willebrand factor to its receptor on GPIb, but the in vivo analogue of ristocetin remains uncertain. Thrombin and other physiological platelet agonists (e.g., thromboxane A sub 2, adenosine diphosphate, and epinephrine) induce exposure of the fibrinogen receptor on the platelet surface GPIIb-IIIa complex. Thromboxane A sub 2 is generated by platelets and is an important marker of platelet activation.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 06, 1994
- Accession Number
- ADA360346
Entities
People
- A. D. Michelson
- C. R. Valeri
Organizations
- Boston University