In transfusion medicine, platelets cannot be replaced by blood substit
utes. Circulating platelets must respond quickly to changes in normal
blood flow and blood-vessel injury to promote normal hemostasis, Adhes
ion of platelets at the site of vessel endothelial rupture is mediated
through platelet membrane glycoprotein receptors. The integrity of th
ese surface adhesion receptors and the signal-transduction pathways of
activation will determine, in large part, how well a platelet functio
ns in hemostasis. The deterioration of these systems during storage le
ads to a compromise of function known as the 'platelet-storage lesion'
.