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1 Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, St. Luke's-Roosevelt Hospital Center, New York, NY, USA;
2 Department of Pediatrics, Microbiology-Immunology & Pathology, Dalhousie University, Halifax, Nova Scotia, Canada
3 Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, St. Luke's-Roosevelt Hospital Center, New York, NY, USA; Department of Medicine, College of Physicians and Surgeons, Columbia University, St. Luke's-Roosevelt Hospital Center, New York, NY, USA
* To whom correspondence should be addressed. E-mail: jb39{at}columbia.edu.
Although pressure elevation in lung post-capillary 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 post-capillary venules of the isolated blood-perfused rat lung by real-time fluorescence imaging. To determine leukocyte margination, in single post-capillary 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 returning pressure to baseline, a similar reduction of plasma velocity, established by manually decreasing the perfusion rate, prolonged margination. Our findings show that in lung post-capillary venules, the decrease in plasma velocity critically determines pressure-induced leukocyte margination.
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