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American Journal of Pathology, Vol 118, 128-133, Copyright © 1985 by American Society for Investigative Pathology
REGULAR ARTICLES |
TG Mundie, C Whitener and SK Ainsworth
New Zealand White rabbits were exposed intratracheally to aerosolized cotton dust extract (CDE) for 5 minutes of tidal breathing and lavaged 15 minutes 1, 4, and 6 hours after exposure. Bronchoalveolar lavage cells were counted, and the number of macrophages and polymorphonuclear leukocytes (PMNs) was determined. Cell recruitment, which began 1 hour after exposure to CDE and plateaued at 6 hours, consisted of both mononuclear cells and PMNs. Lavage fluid was analyzed for concentrations of prostaglandin F2 alpha (PGF2 alpha), prostaglandin E1 and E2 (PGE), thromboxane B2 (TxB2), and 5-hydroxytryptamine (5-HT). PGF2 alpha, PGE, TxB2, and 5-HT were maximally increased in the lavage 4 hours after exposure to CDE. This is the first study to demonstrate the in vivo release of arachidonic acid metabolites and 5-HT in the lung in response to CDE inhalation. This study also demonstrates that maximum mediator release occurs at 4 hours after exposure to aerosolized CDE. These findings strongly suggest that arachidonic acid metabolites are available to mediate either totally or partially the pathogenic mechanism(s) of bronchoconstriction seen in the acute byssinotic reaction of man.
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