Thromb Haemost 2006; 96(01): 60-67
DOI: 10.1160/TH05-11-0759
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

Turnover and fate of fibrinogen and platelets at the rabbit aorta wall immediately after a balloon de-endothelializing injury in vivo

Mark W. C. Hatton
1   McMaster Univiversity Health Science Centre, Department of Pathology (HSC-4N67), Hamilton, Ontario, Canada
,
Bonnie Ross
1   McMaster Univiversity Health Science Centre, Department of Pathology (HSC-4N67), Hamilton, Ontario, Canada
,
Marnie Timleck
1   McMaster Univiversity Health Science Centre, Department of Pathology (HSC-4N67), Hamilton, Ontario, Canada
,
Suzanne M. R. Southward
1   McMaster Univiversity Health Science Centre, Department of Pathology (HSC-4N67), Hamilton, Ontario, Canada
,
Mary Richardson
2   Juravinsky Cancer Centre, Hamilton, Ontario, Canada
› Author Affiliations

Financial support: This study was supported by funds (grant # T-4968) from the Heart and Stroke Foundation of Ontario.
Further Information

Publication History

Received 23 November 2005

Accepted after resubmission 29 May 2006

Publication Date:
29 November 2017 (online)

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Summary

A de-endothelializing injury to the artery wall in vivo results in a rapid procoagulant response at the surface of the exposed subendothelium. Activated tissue factor (TF)-bearing cells and hemostasis factors located at the site of injury respond by producing thrombin, and within minutes the principal thrombus-forming, blood-borne components (platelets, fibrinogen) accumulate at the site.To compare their behaviors, the rates of uptake and turnover of rabbit 51Cr-platelets and rabbit 125I-fibrinogen were quantified simultaneously during the initial 100-min interval after a balloon catheter injury to the rabbit aorta in vivo.Platelets (∼70,000/mm2) and fibrin(ogen) (∼2.8 pmol/cm2) saturated the ballooned aorta surface within five minutes after injury.Whereas the adherent platelet and fibrinogen concentrations remained steady at the aorta surface, fibrin(ogen)-related products continued to accumulate slowly in the tunica media (TM) for at least 100 minutes. A relatively small proportion (3.7%/min) of adhered platelets turned over at the ballooned aorta surface at 10 minutes, decreasing to 1.2%/min at 100 minutes. By contrast, a larger proportion of fibrin(ogen) (∼ 20%/min) was turned over within the platelet layer at 10 minutes, decreasing to 6%/min at 100 minutes. As verified by immunostaining aorta sections and by protein analysis ofTM extracts,the uptakes of platelets and fibrinogen at the site of injury contributed to an accumulation of products of platelet releasate and fibrin(ogen) degradation (FDPs) within the TM.These observations improve our understanding of the hemostatic processes and subsequent events that occur after an arterial injury in vivo.