Role of L-selectin in leukocyte sequestration in lung capillaries in a rabbit model of endotoxemia

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Author list: Sckell A
Publisher: American Thoracic Society
Publication year: 2000
Volume number: 161
Issue number: 1
Start page: 36
End page: 43
Number of pages: 8
ISSN: 1073-449X
Languages: English-Great Britain (EN-GB)


After a variety of pathophysiologic stimuli, neutrophils accumulate in
lung capillaries and contribute to the pathogenesis of acute lung
injury. Lung neutrophil sequestration has previously been attributed to
mechanical retention of stiffened neutrophils, but L-selectin-mediated
leukocyte/endothelial interaction may be an essential step. We
investigated the effect of the anti-L-selectin antibody HuDreg 200 on
leukocyte sequestration and microhemodynamics in alveolar capillaries in
a model of acute endotoxemia. We used in vivo fluorescence microscopy
to analyze kinetics of fluorescently labeled red and white blood cells
in alveolar capillary networks of the rabbit lung. Investigations were
performed over 2 h after an intravenous infusion of 0.2 ml/kg body
weight (bw) NaCl, 2 mg/kg bw HuDreg 200, 20 μg/kg bw lipopolysaccharide
(LPS) of Escherichia coli 0111:B4, or the combination of HuDreg 200 and
LPS, respectively. Infusion of LPS induced leukocyte sequestration in
alveolar capillaries, which was accompanied by a reduction of alveolar
capillary perfusion and functional capillary density. These effects
could be completely blocked by pretreatment of animals with HuDreg 200.
We conclude that L-selectin-mediated leukocyte/endothelial interaction
is a necessary prerequisite for leukocyte sequestration in alveolar
capillaries in this model. Impaired alveolar capillary perfusion
appeared to result directly from capillary leukocyte sequestration.


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