Journal of Applied Physiology, Vol 77, Issue 1 252-261, Copyright © 1994 by American Physiological Society
Albumin exchange and inflammatory cell recruitment in lungs of antigen-challenged guinea pigs: role of histamine
M. F. Bureau, C. D. Arreto, J. Lefort and B. B. Vargaftig
Unite de Pharmacologie Cellulaire, Unite Associee Institut Pasteur-Institut National de la Sante et de la Recherche Medicale 285, Paris, France.
Microvascular albumin exchange and sequestration of inflammatory cells into
the lungs of anesthetized guinea pigs immunized to ovalbumin were evaluated
using radioactive tracers. Increased exchange of radiolabeled (*) albumin
from airways to blood was noted in immunized and boosted animals under
basal conditions. After the intratracheal injection of 300 micrograms of
ovalbumin, an additional increase in exchange through epithelium occurred,
since the rate of appearance of *albumin in blood was enhanced compared
with control (140 +/- 30 vs. 54 +/- 20% in 1 h). The augmentation of lung
content in extravascular *albumin compared with control (16.2 +/- 4.0 vs.
5.9 +/- 1.6%) indicates that transendothelial exchange was also
facilitated. Concomitment with the sequestration of *platelets into the
lungs of antigen-challenged sensitized animals (59.2 +/- 20% in 1 h),
leukocytes (> 60% polymorphonuclear neutrophils) did not marginate.
Histamine released during antigenic shock might promote leukocyte
demargination from the vascular bed through its vasomotor effect and/or by
inhibiting leukocyte activation and consequently may counteract the effects
of other inflammatory mediators acting to sequester neutrophils. In
confirmation, perfusion of histamine to the immunized animals induced
demargination of lung leukocytes. Histamine antagonists prevented the
increased exchange of *albumin through the epithelial and endothelial
barriers and uncovered *leukocyte sequestration (100.7 +/- 28.9% in 1 h) in
the lungs of antigen-challenged animals. Histamine antagonists may favor
antigen-induced leukocyte sequestration in the lungs by preventing the
effects of endogenous histamine on capillary recruitment and blood flow.
