TIME-COURSE OF ICAM-1 EXPRESSION AND LEUKOCYTE SUBSET INFILTRATION INRAT FOREBRAIN ISCHEMIA

The time course of ICAM-1 expression and leukocyte subset infiltration was studied in a model of CNS reperfusion injury in adult rats. Leuko cyte adhesion and infiltration, mediated in part by intercellular adhe sion molecule-1 (ICAM-1), appears to potentiate CNS reperfusion injury . The timing and relationship between ICAM-1 staining and leukocyte in filtration postglobal CNS ischemia is unknown. Reversible forebrain is chemia was produced in 32 adult Sprague-Dawley rats using the two-vess el occlusion model with histologic analysis performed at specific inte rvals postischemia: 1, 3, 6, 12, and 24 h, 4 and 7 d, or sham-operated controls (n = 4 each group). Monoclonal antibodies against ICAM-1 (1A 29 and TM8), a specific granulocyte (PMN) (HIS48), and a specific mono cyte/macrophage (Mempty set)(ED1) were used. No specific leukocyte and only rare ICAM-1 vessel immunoreactivity was observed in sham control s. ICAM-1: Significant expression in microvessels beginning at Ih with additional diffuse CA1 pyramidal layer staining beginning at 4 d. Leu kocytes: No PMN cells and rare Mempty set identified at 6 and 12 h. By 24 h: moderate infiltrate in areas of ICAM-1 expression of PMN and Me mpty set. At 4 and 7 d: only Mempty set accumulation, cellular morphol ogy now similar to microglia. The results of this study indicate that early and persistent ICAM-1 expression occurs following CNS ischemia w ith associated leukocyte infiltration.