Thromb Haemost 1988; 60(02): 280-288
DOI: 10.1055/s-0038-1647045
Original Article
Schattauer GmbH Stuttgart

Conditions Influencing the Interaction of Asialo von Willebrand Factor with Human Platelets – The Effects of External Ionized Calcium Concentration and the Role of Arachidonate Pathway

Marco Cattaneo
*   The A. Bianchi Bonomi Hemophilia and Thrombosis Centre and Institute of Internal Medicine University of Milano and Maggiore Hospital, Milano, Italy and
,
J Fraser Mustard
**   The Dept, of Pathology, McMaster University, Hamilton, Ontario, Canada
,
Maria T Canciani
*   The A. Bianchi Bonomi Hemophilia and Thrombosis Centre and Institute of Internal Medicine University of Milano and Maggiore Hospital, Milano, Italy and
,
Mary Richardson
**   The Dept, of Pathology, McMaster University, Hamilton, Ontario, Canada
,
Augusto B Federici
*   The A. Bianchi Bonomi Hemophilia and Thrombosis Centre and Institute of Internal Medicine University of Milano and Maggiore Hospital, Milano, Italy and
,
Pier Mannuccio Mannucci
*   The A. Bianchi Bonomi Hemophilia and Thrombosis Centre and Institute of Internal Medicine University of Milano and Maggiore Hospital, Milano, Italy and
› Author Affiliations
Further Information

Publication History

Received 11 March 1988

Accepted after revision 22 June 1988

Publication Date:
28 June 2018 (online)

Summary

We have studied the interaction of ASvWf with human platelets in PRP and in suspensions of washed platelets containing either physiological or low external ionized calcium concentration [Ca2+]0. In hirudin-PRP or in washed platelets in 1.5-2 mM CaCl2, ASvWf up to 50 μg/ml does not induce platelet aggregation or the release reaction. When [Ca2+]c is decreased by addition of citrate to hirudin-PRP or when no CaCl2 is added to washed platelet suspensions, ASvWf does induce platelet aggregation and the release reaction. In low [Ca2+]0, ASvWf interacts with platelet GPIb to cause primary aggregation of disc-shaped platelets to each other through GPIIb/IIIa, with or without added fibrinogen. This primary platelet aggregation leads to thromboxane A2 formation and secondary aggregation and the release reaction. With [Ca2+]0 in the physiological range, there is less ASvWf interaction with GPIb, no primary platelet aggregation and no thromboxane A2 formation. The ASvWf-platelet interaction at physiological [Ca2+]0, however, enhances the platelet response to collagen or epinephrine.

 
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