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Thromb Haemost 1989; 61(01): 057-064
DOI: 10.1055/s-0038-1646527
Original Article
Schattauer GmbH Stuttgart

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

L Badimon
The Division of Cardiology, Mount Sinai School of Medicine, New York, N. Y., USA
,
J J Badimon
The Division of Cardiology, Mount Sinai School of Medicine, New York, N. Y., USA
,
A Galvez
The Division of Cardiology, Mount Sinai School of Medicine, New York, N. Y., USA
,
V Turitto
The Division of Cardiology, Mount Sinai School of Medicine, New York, N. Y., USA
,
V Fuster
The Division of Cardiology, Mount Sinai School of Medicine, New York, N. Y., USA
› Author Affiliations
Further Information

Publication History

Received 18 February 1988

Accepted after revision 02 September 1988

Publication Date:
24 July 2018 (online)

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Summary

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.

Key words

von Willebrand factor - Platelet-vessel wall interaction - von Willebrand’s disease - Platelet aggregation - Storage pool disease - Shear rate - Blood flow
 

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