Differential cardiopulmonary recruitment of neutrophils during hemorrhagicshock: A role for ICAM-1?

Hemorrhagic shock and subsequent resuscitation can result in acute lung inj ury and cardiac dysfunction. Previous studies have demonstrated that tissue neutrophil accumulation contributes to cardiopulmonary injury associated w ith trauma. Thus, suppression of tissue neutrophil recruitment in an early therapeutic window after hemorrhagic shock may protect the cardiopulmonary system. It is unclear whether hemorrhagic shock induces cardiopulmonary rec ruitment of neutrophils before resuscitation. Intercellular adhesion molecu le-1 (ICAM-1) is one of the important factors that mediate tissue neutrophi l recruitment. The physiologic significance of ICAM-1 expression after hemo rrhage before resuscitation is not well delineated. The present study exami ned the role of ICAM-1 in neutrophil accumulation in the heart and lung aft er severe hemorrhage without resuscitation. Mice were subjected to hemorrha gic shock by removal of 30% of total blood volume. Lung neutrophil number a s determined by immunofluorescent staining increased by 1 h after hemorrhag e and was maximal at 4 h whereas myocardial neutrophil number was not chang ed. Lung neutrophil accumulation was not associated with an up-regulation o f ICAM-1 expression or an alteration in ICAM-1 subcellular distribution. Su rprisingly, deletion of the ICAM-1 gene enhanced hemorrhagic shock-induced lung neutrophil accumulation. These results suggest that hemorrhagic shock induces preferential neutrophil accumulation to the lung that appears to oc cur independent of ICAM-1-expression.