Myogenic and neurogenic mechanisms and arachidonate metabolites in bronchial muscle response to allergen

The American Journal of Physiology
L J JanssenE E Daniel

Abstract

We investigated allergen-induced airway hyperresponsiveness (AH) in bronchial tissues obtained from dogs that inhaled Ascaris suum leading to AH (RESP) in vivo or that exhibited no change (NON-RESP) as well as from dogs that inhaled saline (SHAM). RESP tissues were not hyperresponsive to KCl or to carbachol, whereas contractions to electrical field stimulation (EFS) were reduced. This reduction was reversed partially by indomethacin and completely by replacement of the bathing fluid. Radioimmunoassay revealed marked elevation of prostaglandin (PG) E2 generation in RESP tissues compared with SHAM and NON-RESP tissues. EFS-evoked contractions were often followed by a slowly developing secondary contraction in RESP tissues but not in SHAM or NON-RESP tissues. However, indomethacin unmasked such secondary contractions in many SHAM and NON-RESP tissues and markedly enhanced those in RESP tissues, whereas L-655,240 (thromboxane A2/PGD2 receptor antagonist) abolished such contractions in all groups. We were unable to detect thromboxane using radioimmunoassay. We conclude that allergen-induced AH involves altered generation of cyclooxygenase metabolites of arachidonic acid (particularly PGE2) as well as of a nonprostanoid inhibitory fa...Continue Reading

References

May 1, 1988·The American Review of Respiratory Disease·W S BeckettH A Menkes
Nov 1, 1994·Canadian Journal of Physiology and Pharmacology·H JiangN L Stephens
Nov 1, 1994·American Journal of Respiratory Cell and Molecular Biology·M J WoolleyP M O'Byrne
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Citations

Feb 8, 2002·American Journal of Physiology. Cell Physiology·Dany SalvailEric Rousseau
Oct 16, 2016·American Journal of Physiology. Lung Cellular and Molecular Physiology·Y S Prakash
Apr 27, 2000·American Journal of Physiology. Lung Cellular and Molecular Physiology·L J JanssenS Keshavjee

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