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Title: Platelet interaction with vessel wall and collagen in pigs with homozygous von Willebrand's disease associated with abnormal collagen aggregation. Author: Badimon L, Badimon JJ, Galvez A, Turitto V, Fuster V. Journal: Thromb Haemost; 1989 Feb 28; 61(1):57-64. PubMed ID: 2665168. Abstract: A 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.[Abstract] [Full Text] [Related] [New Search]