Faculty Collaboration Database

Differential cardiopulmonary recruitment of neutrophils during hemorrhagic shock: a role for ICAM-1? Shock 2001 Dec;16(6):444-8

Date

01/05/2002

Pubmed ID

11770042

DOI

10.1097/00024382-200116060-00007

Scopus ID

2-s2.0-0035655120 (requires institutional sign-in at Scopus site)   15 Citations

Abstract

Hemorrhagic shock and subsequent resuscitation can result in acute lung injury and cardiac dysfunction. Previous studies have demonstrated that tissue neutrophil accumulation contributes to cardiopulmonary injury associated with 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 recruitment of neutrophils before resuscitation. Intercellular adhesion molecule-1 (ICAM-1) is one of the important factors that mediate tissue neutrophil recruitment. The physiologic significance of ICAM-1 expression after hemorrhage before resuscitation is not well delineated. The present study examined the role of ICAM-1 in neutrophil accumulation in the heart and lung after severe hemorrhage without resuscitation. Mice were subjected to hemorrhagic shock by removal of 30% of total blood volume. Lung neutrophil number as determined by immunofluorescent staining increased by 1 h after hemorrhage and was maximal at 4 h whereas myocardial neutrophil number was not changed. Lung neutrophil accumulation was not associated with an up-regulation of ICAM-1 expression or an alteration in ICAM-1 subcellular distribution. Surprisingly, 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 occur independent of ICAM-1-expression.

Author List

Song Y, Ao L, Calkins CM, Raeburn CD, Harken AH, Meng X

Author

Casey Matthew Calkins MD Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Cell Movement
Gene Expression
Intercellular Adhesion Molecule-1
Lung
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardium
Neutrophils
Shock, Hemorrhagic