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pubmed-article:1685118pubmed:abstractTextBecause tachykinins (TKs) cause severe bronchoconstriction in humans and animals, this study was carried out to examine whether depletion of TKs can prevent or ameliorate antigen-induced immediate bronchial constriction. Forty-five guinea pigs were randomly divided into six groups: control, antigen challenge, TK depletion + antigen challenge, ganglionic (Ggl) blockade, Ggl blockade + antigen challenge, and TK depletion + Ggl blockade + antigen challenge. Control animals received no treatment. Animals of all antigen challenge groups were sensitized with ovalbumin 10 days before the study. TK depletion was performed via 5-day pretreatment of capsaicin, which began 11 days before the study. On the day of the study, pulmonary resistance (RI), dynamic compliance (Cdyn), and breathing patterns were measured for 15 min just before (baseline) and for 30 min after intravenous injection of either saline (control) or ovalbumin (antigen challenge). In controls, saline injection did not produce any significant change within 30 min, whereas antigen challenge significantly increased RL at 4-15 min and significantly decreased Cdyn at 6-15 min, suggesting antigen-induced bronchoconstriction. Following TK depletion, antigen challenge produced pulmonary changes similar to those without depletion. Ggl blockade reduced RL and breathing frequency, and increased Cdyn and tidal volume; the blockade, however, did not significantly alter (in terms of % baseline) antigen challenge-induced changes in RL, Cdyn, or breathing patterns. These results suggest that TKs and reflexes via Ggl do not appear to be important contributing factors for antigen-induced immediate bronchial constriction in this animal model.lld:pubmed
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pubmed-article:1685118pubmed:pagination1047-60lld:pubmed
pubmed-article:1685118pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:1685118pubmed:articleTitleEndogenous tachykinins in antigen-induced acute bronchial responses of guinea pigs.lld:pubmed
pubmed-article:1685118pubmed:affiliationDivision of Pharmacology and Experimental Therapeutics, College of Pharmacy, University of Kentucky, Lexington.lld:pubmed
pubmed-article:1685118pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1685118pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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