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Abstract
Purpose. To evaluate the role of intercellular adhesion molecule 1 (ICAM-1) in cutaneous leukocyte
trapping in venous disease, we used our rodent model of venous hypertension (VH).
Materials and methods. VH was created in adult rats by ligation of the inferior vena cava, bilateral common
iliac veins, and bilateral common femoral veins. In the Phase I experimental (exptl)
group, anti-ICAM-1 monoclonal antibody (1A29) was given intravenously prior to venous
ligations. Acute venous pressures were measured in the exptl and control (ctrl) (ligation
only) groups. Bilateral forelimb and hindlimb skin specimens were harvested for myeloperoxidase
(MPO) assay. In Phase II, VH was created in a chronic group; in a sham-operated group,
ties were placed around the same vessels without ligations. Two weeks later, venous
pressures were measured and radiolabeled (125I and 131I) monoclonal antibody (mAb) to ICAM-1 was injected and allowed to circulate for 5
min before the level of radiolabeled antibody within forelimb and hindlimb specimens
was measured.
Results. In the acute study with 1A29, hindlimb pressures were significantly elevated in both
the ctrl (n = 4) and exptl (n = 4) hindlimbs (15.4 ± 0.239 and 13.8 ± 1.89 mm Hg, respectively) compared with ctrl
and exptl forelimbs (1.38 ± 0.554 and 1.50 ± 0.612 mm Hg, respectively). However,
MPO activity was significantly elevated in the hindlimbs of the ctrl group compared
with the hindlimbs of the exptl animals (19.8 ± 1.54 U vs 6.71 ± 2.46 U). In the chronic
VH rats (n = 5) given radiolabeled anti-ICAM-1 mAb, the hindlimb pressures (10.1 ± 4.52 mm Hg)
were significantly elevated (P < 0.05) compared with forelimb pressures (1 ± 0.447 mm Hg) and compared with the
forelimb and hindlimb pressures in the sham-operated animals (n = 4) (1.63 ± 0.813 and 4.25 ± 2.13 mm Hg, respectively). However, there was not a
significant difference in the quantity of ICAM-1—hindlimb versus forelimb or chronic
VH versus sham.
Conclusions. Anti-ICAM-1 mAb decreased MPO activity in hypertensive hindlimb skin, supporting
the instrumental role of ICAM-1 in cutaneous leukocyte trapping. However, the constituent
endothelial ICAM-1 is not elevated by VH.
Keywords
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Article info
Footnotes
☆Presented at the 23rd Annual Symposium of the Association of Veterans Administration Surgeons, St. Louis, MO, May 2–4, 1999.
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© 2000 Academic Press. Published by Elsevier Inc. All rights reserved.
