Leukocyte sequestration in pulmonary microvessels and lung injury following systemic complement activation in rabbits

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Détails sur la publication

Liste des auteurs: Sckell A
Editeur: Karger Publishers
Année de publication: 1999
Numéro du volume: 36
Numéro de publication: 4
Page d'accueil: 289
Dernière page: 298
Nombre de pages: 10
ISSN: 1018-1172
Languages: Anglais-Royaume-Uni (EN-GB)


Résumé

Inflammatory reactions are associated with sequestration of leukocytes
in the lung. Complement activation leads to accumulation of leukocytes
in alveolar septa and alveoli, to lung edema and hemorrhage. Although in
organs other than the lung leukocytes interact with the vascular
endothelium only in postcapillary venules, alveolar capillaries are
considered to be the site of leukocyte sequestration in the lung.
However, pulmonary venules and arterioles have not been investigated
systematically after complement activation so far. A closed thoracic
window was implanted in anesthetized rabbits; leukocytes and red blood
cells were stained, and the movement of these cells was measured in
superficial pulmonary arterioles, venules and alveolar capillaries using
fluorescence video microscopy before and 30 and 60 min after infusion
of cobra venom factor (CVF). Erythrocyte velocity and macrohemodynamic
conditions did not change after CVF infusion and were not different from
the sham-treated controls. The number of sticking leukocytes increased
significantly compared to baseline and control: by 150% in arterioles
and in venules and by 740% in alveolar capillaries within 60 min after
CVF infusion. The width of alveolar septa in vivo was significantly
enlarged after CVF infusion, indicating interstitial pulmonary edema. At
the end of the experiments, myeloperoxidase activity was higher in the
CVF group, showing leukocyte sequestration in the whole organ. It is
concluded that complement activation by CVF induces leukocyte
sequestration in lung arterioles, venules and alveolar capillaries and
leads to mild lung injury.


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