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 ((3P th-Ix complex) and to exposed subendothelial c9mponents.1'2 Platelet-to-platelet aggregation is primarily mediated by fibrinogen binding to its platelet surface receptor (the OPlib-Illa complex).3 Circulating platelets are normally in a resting state and, despite the presence of platelet surface GPTh-IX and OPlib-Illa 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 QPlb,' but the in vivo analogue of ristocetin remains uncertain. Thrombin and other physiological platelet agonists (e.g. thromboxane A2, adenosine diphosphate, and epinephrine) induce exposure of the fibrinogen receptor on the platelet surface GPIIb-IIIa complex.3 Thromboxane A2 is generated by platelets and is an important marker of
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 06, 1993
- Accession Number
- ADA360161
Entities
People
- Alan D. Michelson
- C. R. Valeri
Organizations
- Boston University