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Granulocytosis and increased adhesion molecules after resistive loading of the diaphragm

School of Rehabilitation Sciences, James Hogg iCapture Centre for Cardiovascular and Pulmonary Research, Vancouver Coastal Health Authority, Respiratory Division, University of British Columbia, Vancouver, BC, Canada.

CORRESPONDENCE: W. D. Reid, School of Rehabilitation Sciences, T325-2211 Wesbrook Mall, Vancouver, BC Canada V6T 2B5. Fax: 1 6048227624. E-mail: wdreid{at}interchange.ubc.ca

Keywords: Cell adhesion molecules, circulating leukocytes, lung diseases, respiratory muscles

Received: September 8, 2004
Accepted July 26, 2005

Upregulation of endothelial cell adhesion molecules, followed by an influx of granulocytes and macrophages, can contribute to exertion-induced skeletal muscle injury. The purpose of this study was to quantify circulating leukocyte subsets, diaphragm injury and infiltrating leukocyte subsets, and surface expression of vascular cell adhesion molecule (VCAM)-1 and intracellular adhesion molecule (ICAM)-1 in the diaphragm after inspiratory resistive loading (IRL).

Eight New Zealand white rabbits underwent 1.5 h of IRL and seven control rabbits underwent a sham procedure. Blood samples, taken at baseline and 2, 6, 12, 24, 48 and 72 h after the onset of IRL or sham, showed that band cell counts had increased at 6 h post-IRL. Point counting of haematoxylin and eosin-stained cross-sections, sampled at 72 h post-IRL, showed greater injury in diaphragms from IRL rabbits compared with controls. Immunohistochemical processing showed increased expression of ICAM-1 and VCAM-1, and higher granulocyte and macrophage counts in IRL diaphragms than control diaphragms. Macrophages were the predominant inflammatory cells.

Increased intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression, and infiltration of granulocytes and macrophages may contribute to inspiratory resistive loading-induced diaphragm injury.

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