Hemostasis platelet aggregation

Hemostasis is the cessation of bleeding from a cut or severed vessel, whereas thrombosis occurs when the endothelium lining blood vessels is damaged or removed (eg, upon rupmre of an atherosclerotic plaque). These processes encompass blood clotting (coagulation) and involve blood vessels, platelet aggregation, and plasma proteins that cause formation or dissolution of platelet aggregates. 

Platelets are actively involved in the process of hemostasis, by which any break in the vascular endothelium is rapidly repaired without compromising the fluidity of the blood. In response to injury, platelets adhere to the subendothelial matrix of a damaged vessel, spread over the surface, and recruit additional platelets within a developing platelet aggregate or thrombus. Whereas hemostasis is a normal physiological response to endothelial wound repair, improper regulation or overreactivity of this system can lead to the pathological condition of thrombosis. 

One last important function of thrombosthenin remains to be mentioned in relation to hemostasis, namely its ATPase activity. ADP arising from this activity must be considered of importance for platelet aggregation, and its production by the platelets during VM is perhaps an essential step in the arrest of hemorrhage as well as thrombus formation (Kaser-Glanzmann and Liischer, 1962). 

In humans, dextran administration is associated with a decrease in factor VIII activity, decreased fibrin clot formation and dilutional coagulopathy (Roberts Bratton 1998). Dextran 70 inhibits equine platelet aggregation in vitro (Heath et al 1998) but other effects on hemostasis have not been investigated. Dextran 70 has been used for its presumed antithrombotic properties in horses with a clinical diagnosis of verminous aneurysm (Table 17.9) (Greatorex 1977). Dextran 70, when combined with hypertonic saline, resulted in a... 

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