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This Article Full Text Full Text (PDF) All Versions of this Article: 289/3/L407    most recent 00048.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Ichimura, H. Articles by Bhattacharya, J. Search for Related Content PubMed PubMed Citation Articles by Ichimura, H. Articles by Bhattacharya, J.

Pressure-induced leukocyte margination in lung postcapillary venules

¹Lung Biology Laboratory, Department of Physiology and Cellular Biophysics, and ²Department of Medicine, College of Physicians and Surgeons, Columbia University, Saint Luke's-Roosevelt Hospital Center, New York, New York; and ³Department of Pediatrics, Microbiology-Immunology and Pathology, Dalhousie University, Halifax, Nova Scotia, Canada

Submitted 25 January 2005 ; accepted in final form 3 May 2005

Although pressure elevation in lung postcapillary venules increases endothelial P-selectin expression, the extent to which P-selectin causes lung leukocyte margination remains controversial. To address this issue, we optically viewed postcapillary venules of the isolated blood-perfused rat lung by real-time fluorescence imaging. To determine leukocyte margination in single postcapillary venules, we quantified the fluorescence of leukocytes labeled in situ with rhodamine 6G (R6G). Although baseline fluorescence was sparse, a 10-min pressure elevation by 10 cmH₂O markedly increased R6G fluorescence. Both stopping blood flow during pressure elevation and eliminating leukocytes from the perfusion blocked the fluorescence increase, affirming that these fluorescence responses were attributable to pressure-induced leukocyte margination. A P-selectin-blocking MAb and the L- and P-selectin blocker fucoidin each inhibited the fluorescence increase, indicating that P-selectin was critical for inducing margination. Time-dependent imaging of blood-borne fluorescent beads revealed reduction of plasma velocity during pressure elevation. After pressure returned to baseline, a similar reduction of plasma velocity, established by manually decreasing the perfusion rate, prolonged margination. Our findings show that in lung postcapillary venules, the decrease in plasma velocity critically determines pressure-induced leukocyte margination.

P-selectin; plasma velocity; pulmonary circulation; pressure-induced; rhodamine 6G

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