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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3829-3838
Fibrinogen Deposition at the Postischemic Vessel Wall Promotes Platelet
Adhesion During Ischemia-Reperfusion In Vivo
Steffen Massberg,
Georg Enders,
Francine Cláudia de Melo Matos,
Luciana Inês Domschke Tomic,
Rosmarie Leiderer,
Simone Eisenmenger,
Konrad Messmer, and
Fritz Krombach
From the Ludwig-Maximilians-University, Institute for Surgical
Research, Klinikum Grosshadern, Munich, Germany.
Following ischemia-reperfusion (I/R), platelet adhesion is thought
to represent the initial event leading to remodeling and reocclusion of
the vasculature. The mechanisms underlying platelet adhesion to the
endothelium have not been completely established. Endothelial cells
rendered ischemic acquire a procoagulant phenotype, characterized by
fibrinogen accumulation. Therefore, we evaluated whether fibrinogen
deposition during I/R mediates platelet adhesion. Using fluorescence
microscopy, fibrinogen deposition and the accumulation of platelets
were assessed in vivo in a model of intestinal I/R (1.5 hours/60
minutes). Fibrinogen accumulated in arterioles and venules early after
the onset of reperfusion. The deposition of fibrinogen colocalized with
large numbers of adherent platelets (520 ± 65 and 347 ± 81 platelets/mm2 in arterioles and venules). Pretreatment with
an antifibrinogen antibody attenuated platelet adhesion. Intracellular
adhesion molecule (ICAM)-1 served as a major receptor for fibrinogen,
since fibrinogen deposition and platelet adhesion to the endothelial cell surface were markedly decreased in ICAM-1-deficient mice. The
platelet  IIb/ 3 integrin plays a key role
in fibrinogen-dependent platelet accumulation, because (1) platelet
adhesion involved RGD-recognition sequences, and (2) platelets isolated
from a patient with Glanzmann's disease showed decreased interaction
with the postischemic endothelium. Since platelets are demonstrated
here to induce tyrosine phosphorylation in endothelial cells, platelet recruitment might contribute to the development of an inflammatory reaction during I/R.
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