INTERCELLULAR-ADHESION MOLECULE-1 REGULATION IN THE CANINE LUNG AFTERCARDIOPULMONARY BYPASS

Objective(s): Neutrophil sequestration in the lung after cardiopulmona ry bypass has been shown to be dependent on the adhesion molecule CD18 . Thus we sought to determine whether endothelial expression of interc ellular adhesion molecule-1 (a ligand for CD18) in pulmonary capillari es mediates neutrophil adhesion in this setting, Methods: Seven adult mongrel dogs underwent 90 minutes of hypothermic cardiopulmonary bypas s with 60 minutes of cardioplegic arrest. After warming, dogs were rep erfused for up to 9 hours and lung biopsy specimens were obtained. Lun g tissue was examined by Northern and Western blot analysis and by imm unohistologic methods. Three sham-operated dogs served as time-matched controls. Results: Northern blots demonstrated increased expression o f intercellular adhesion molecule-1 messenger ribonucleic acid within 5 minutes of cessation of bypass (or approximately 30 minutes after ao rtic crossclamp release), which persisted at 9 hours of recovery and w as not present in controls. Western blots showed intercellular adhesio n molecule-1 protein expression before bypass but a measurable increas e in intercellular adhesion molecule-1 protein in four of seven dogs i n the bypass group by the ninth hour of recovery. Pulmonary neutrophil accumulation 9 hours after cardiopulmonary bypass was greater in thos e dogs with an increased intercellular adhesion molecule-1 protein exp ression, Immunoelectron microscopy demonstrated the pulmonary capillar y endothelium capable of increased intercellular adhesion molecule-1 p rotein expression at the 9-hour time point. Conclusions: Cardiopulmona ry bypass resulted in intercellular adhesion molecule-1 induction in t he canine lung during recovery. An increased expression of intercellul ar adhesion molecule-1 protein in the lung was associated with an incr eased accumulation of neutrophils in affected animals. Thus intercellu lar adhesion molecule-1 expression mag serve as a mechanism that predi sposes the lungs to inflammatory cell-mediated injury postoperatively.