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Intercellular adhesion molecule-1 regulation in the canine lung after cardiopulmonary bypass
W J Dreyer1, A R Burns, S C Phillips
1Lillie Frank Abercrombie Section of Cardiology, Department of Medicine, Baylor College of Medicine, Houston, Tex, USA.
Insights
Cardiopulmonary bypass increases intercellular adhesion molecule-1 (ICAM-1) in the lung. This ICAM-1 expression correlates with greater neutrophil accumulation, suggesting a role in post-operative lung injury.
Area of Science:
- Cardiovascular Surgery
- Pulmonary Medicine
- Immunology
Background:
- Neutrophil sequestration in the lungs post-cardiopulmonary bypass is CD18-dependent.
- Intercellular adhesion molecule-1 (ICAM-1) is a ligand for CD18.
- The role of ICAM-1 in mediating neutrophil adhesion during cardiopulmonary bypass requires investigation.
Purpose of the Study:
- To determine if endothelial ICAM-1 expression in pulmonary capillaries mediates neutrophil adhesion after cardiopulmonary bypass.
- To investigate the temporal expression of ICAM-1 in the lung following cardiopulmonary bypass.
Main Methods:
- Seven dogs underwent cardiopulmonary bypass and cardioplegic arrest.
- Lung biopsy specimens were collected for Northern blot, Western blot, and immunohistologic analysis.
- Three sham-operated dogs served as controls.
Main Results:
- Intercellular adhesion molecule-1 (ICAM-1) messenger RNA expression increased within 5 minutes of bypass cessation and persisted for 9 hours.
- Increased ICAM-1 protein expression was observed in four of seven dogs by 9 hours post-bypass.
- Higher ICAM-1 protein levels correlated with increased pulmonary neutrophil accumulation.
Conclusions:
- Cardiopulmonary bypass induces ICAM-1 expression in the canine lung during recovery.
- Increased ICAM-1 expression is associated with enhanced neutrophil accumulation.
- ICAM-1 may contribute to inflammatory cell-mediated lung injury following cardiopulmonary bypass.
Objective(S):
Neutrophil sequestration in the lung after cardiopulmonary bypass has been shown to be dependent on the adhesion molecule CD18. Thus we sought to determine whether endothelial expression of intercellular adhesion molecule-1 (a ligand for CD18) in pulmonary capillaries mediates neutrophil adhesion in this setting.
Methods:
Seven adult mongrel dogs underwent 90 minutes of hypothermic cardiopulmonary bypass with 60 minutes of cardioplegic arrest. After warming, dogs were reperfused for up to 9 hours and lung biopsy specimens were obtained. Lung tissue was examined by Northern and Western blot analysis and by immunohistologic methods. Three sham-operated dogs served as time-matched controls.
Results:
Northern blots demonstrated increased expression of intercellular adhesion molecule-1 messenger ribonucleic acid within 5 minutes of cessation of bypass (or approximately 30 minutes after aortic crossclamp release), which persisted at 9 hours of recovery and was not present in controls. Western blots showed intercellular adhesion molecule-1 protein expression before bypass but a measurable increase in intercellular adhesion molecule-1 protein in four of seven dogs in the bypass group by the ninth hour of recovery. Pulmonary neutrophil accumulation 9 hours after cardiopulmonary bypass was greater in those dogs with an increased intercellular adhesion molecule-1 protein expression. Immunoelectron microscopy demonstrated the pulmonary capillary endothelium capable of increased intercellular adhesion molecule-1 protein expression at the 9-hour time point.
Conclusions:
Cardiopulmonary bypass resulted in intercellular adhesion molecule-1 induction in the canine lung during recovery. An increased expression of intercellular adhesion molecule-1 protein in the lung was associated with an increased accumulation of neutrophils in affected animals. Thus intercellular adhesion molecule-1 expression may serve as a mechanism that predisposes the lungs to inflammatory cell-mediated injury postoperatively.