Platelet Interaction with Vessel Wall and Collagen in Pigs with Homozygous von Willebrand’s Disease Associated with Abnormal Collagen Aggregation

Abstract

SummaryA subgroup of pigs with von Willebrand’s disease from the Mayo Clinic stock shows abnormal platelet aggregation in response to collagen [vWD-Homo(-)], in contrast to the normal aggregation responses observed in the main colony of pigs with homozygous vWD [vWD-Homo(+)]. This subgroup has been characterized at Mayo as a storage pool deficiency due to the reduced levels of ADP and Serotonin in the platelet dense granules. In the present studies, an ex-vivo perfusion chamber was utilized to investigate the deposition of 111In-labeled platelets on aortic subendothelium and collagen type I exposed to blood from vWD-Homo(-), vWD-Homo(+) and normal animals. Both non-anticoagulated and heparinized blood were exposed for wall shear rates ranging from 212 sec-1 to 3380 sec-1 and exposure times as long as 30 min. An enhanced decrease in platelet deposition in the vWD-Homo(-) animals was observed compared to vWD-Homo(+) animals. The decrease was observed primarily at the higher shear rates and was more pronounced in the absence of heparin and on the collagenous substrate. Thus, the abnormality in collagen-induced aggregation, which has been characterized as a storage-pool type defect, results in a decreased platelet deposition compared with that produced by severe vWD alone.