Leukocyte adhesion, transendothelial migration, and stasis are important co
mponents in the pathogenesis of deep vein thrombosis. Anesthetized cats wer
e treated with saline, a recombinant soluble form of P-selectin glycoprotei
n ligand-1 (rPSGL-Ig), or an E- and L-selectin antibody (EL-246) before exp
osure and occlusion of a jugular vein. After 2 or 6 hours of occlusion, jug
ular veins were perfused with buffer, fixed, and prepared for scanning elec
tron microscopy. In cats receiving saline, 2 and 6 hours of occlusion produ
ced moderate levels of leukocyte and platelet adhesion and endothelial cell
injury. Treatment of cats with rPSGL-Ig or EL-246 had no apparent effect o
n the magnitude of cell adhesion and endothelial cell injury compared with
no treatment. After 6 hours of occlusion, the presence of a mural thrombus
in untreated veins was observed and confirmed by scanning electron microsco
py. Pretreatment of cats with rPSGL-Ig completely (4.0 mg/kg) or partially
(1.0 mg/kg) prevented the occurrence of thrombi in the jugular veins. The r
eduction in thrombosis by rPSGL-Ig treatment after 6 hours of venous stasis
, in the absence of any effect on leukocyte-mediated endothelial cell injur
y, suggests an antithrombotic mechanism of action for this protein.