Arterial thrombosis induces early upregulation of intercellular adhesion molecule in the media

Purpose: Thrombosed peripheral vessels that are pharmacologically or mechanically recanalized have diminished long-term patency rates compared with vessels that are repaired before occlusion. We hypothesized that thrombosis induces proinflammatory changes in the arterial media that may contribute to postthrombotic vascular remodeling. Methods: We studied expression of intercellular adhesion molecule (ICAM), a mediator of leukocyte recruitment, in the arterial wall after thrombosis. Thrombosis was induced in rabbit superficial femoral arteries by embolizing polystyrene beads (Thr- emb) or by ligation (Thr-lig). Control vessels were dissected but not ligated (C-dis) or were subjected to bead embolization and immediate removal (C- emb). Arterial wall ICAM expression was measured by indirect immunohistochemical analysis at 6 hours, 24 hours, and 1 week. Staining intensity was graded from 0 (none) to 4 (intense) by observers who were blinded to the experimental conditions. Results: No increase in ICAM expression by thrombosed vessels was present at 6 hours. After 24 hours, ICAM expression in the media of thrombosed vessels was increased (Thr-emb, 2.3 ± 0.5; Thr-lig, 2.0 ± 0) compared with control vessels (C-dis, 0 ± 0; C-emb, 0.8 ± 0.5; p < 0.004). This difference became more marked at 1 week. ICAM staining localized to actin-staining regions of the media. Conclusions: Arterial thrombosis, but not surgical injury, induces pronounced early and sustained upregulation of ICAM expression in smooth muscle-containing regions of the arterial media. Upregulation of ICAM is likely to promote recruitment of inflammatory cells or mediate vascular remodeling after luminal thrombosis.