We have previously demonstrated a CD18-dependent sequestration of neutrophils in the dog lung within 3 hrs after CPB cessation that contributes to pulmonary dysfunction (Circulation 1995;92:2276-2283). To determine if expression of ICAM-1 (a ligand for CD18) on pulmonary capillary endothelium contributes to this response, 6 adult mongrel dogs underwent 90 mins of hypothermic CPB (26-28°C) with 60 mins of aortic cross-clamp time. After warming, dogs were reperfused open chest for 9 hrs. Lung biopsies were obtained prior to CPB, 10 to 30 mins after CPB, and at 1,2,3,6 and 9 hrs thereafter. Northern blots of lung biopsy homogenates demonstrated an early induction of the ICAM-1 gene which persisted at 9 hrs. In-situ hybridization showed mRNA expression within the alveolar wall, on alveolar macrophages, on bronchial epithelial cells, and on vascular endothelium of arterioles and venules. Western blots showed significant ICAM-1 expression prior to CPB, and against this background little or no increase in ICAM-1 protein expression was discernible after CPB. Immunohistochemistry performed at the light microscopic level confirmed ICAM-1 expression within the alveolar wall but failed to show an increase post-CPB, and failed to distinguish alveolar epithelial from capillary endothelial expression. Immunoelectron microscopy detected an increase in capillary ICAM-1 expression in only 1 dog at 9 hrs of reperfusion. Our data suggest that pulmonary neutrophil sequestration early after CPB, although CD18-dependent, is independent of pulmonary capillary ICAM-1 expression.