title: Intercellular adhesion molecule-1 regulation in the canine lung after cardiopulmonary bypass.
abstract: OBJECTIVE
  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.
authors.affiliation: Lillie Frank Abercrombie Section of Cardiology, Department of Medicine, Baylor College of Medicine, Houston, Tex, USA.
authors.forename: W J
authors.initials: WJ
authors.lastname: Dreyer
authors.forename: A R
authors.initials: AR
authors.lastname: Burns
authors.forename: S C
authors.initials: SC
authors.lastname: Phillips
authors.forename: M L
authors.initials: ML
authors.lastname: Lindsey
authors.forename: P
authors.initials: P
authors.lastname: Jackson
authors.forename: G L
authors.initials: GL
authors.lastname: Kukielka
mesh_terms: D000818:Animals; D015152:Blotting, Northern; D015153:Blotting, Western; D002315:Cardiopulmonary Bypass; D004285:Dogs; D004730:Endothelium, Vascular / Q000378:metabolism*; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D008168:Lung / Q000098:blood supply / Q000378:metabolism*; D008833:Microcirculation; D018375:Neutrophil Activation / Q000502:physiology*; D009504:Neutrophils / Q000378:metabolism*; D011184:Postoperative Period
chemical_list: D018799:Intercellular Adhesion Molecule-1