Neutrophil Adhesion in Central Nervous System Ischemia in Rabbits

Activated neutrophils appear to be directly involved in potentiating central nervous system ischemic injury. After initial endothelial adherence, neutrophils can potentiate ischemia by causing capillary plugging and infiltrating ischemic tissue to release toxic metabolites. We used an endothelial component adherence assay to characterize neutrophil adhesion following reversible central nervous system ischemia. Rabbit spinal cord ischemia was produced by 40 min of reversible arterial occlusion. Neutrophils were isolated using density gradient centrifugation and adherence to laminin or fibronectin was determined using a myeloperoxidase assay. The baseline (N = 26) percentage of adherent neutrophils was 3.8 ± 0.3/5.6 ± 0.6 (laminin/fibronectin), sham-operated controls (2 h post) (N = 6) 3.3 ± 0.5/3.9 ± 0.4. 30 min post ischemia (N = 6) 2.5 ± 1.1/4.1 ± 1.9, 2 h (N = 6) 7.6 ± 1.4/9.9 ± 2.6 (p < .05 to baseline and sham), 18 h (N = 8)4.9 ± 1.5/7.1 ± 3.1. and 42 h (N = 6) 3.4 ± 0.4/6.6 ± 2.1. Concurrent serum fibrinogen values were baseline 142 ± 12, sham (18 h) 141 ±14, 2 h 166 ± 21, 18 h 512 ± 43 (p < .01), and 42 h 580 ± 86 (p < .01). These results suggest that neutrophil adherence is increased after acute central nervous system ischemia. There appears to be a limited period of increased adherence that occurs earlier than other acute phase reactants.