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Updated: Aug 5, 2026
10:20
In vitro Measurements of Tracheal Constriction Using Mice
Published on: June 25, 2012
Eicosanoid and muscarinic receptor blockade abolishes hyperventilation-induced bronchoconstriction
A N Freed1, S McCulloch, Y Wang
1Department of Environmental Health Sciences, School of Hygiene and Public Health, The Johns Hopkins University, Baltimore, Maryland 21205, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|October 29, 2000
Summary
Hyperventilation-induced bronchoconstriction (HIB) involves prostanoid and leukotriene pathways. Blocking these pathways and muscarinic receptors significantly reduces HIB in dogs.
Area of Science:
- Pulmonary Medicine
- Respiratory Physiology
Background:
- Hyperventilation-induced bronchoconstriction (HIB) is a significant respiratory response.
- The roles of prostanoid and leukotriene metabolism in HIB are not fully understood.
Purpose of the Study:
- To investigate the contribution of prostanoid and leukotriene metabolism to HIB.
- To determine the efficacy of combined cyclooxygenase and 5-lipoxygenase inhibition on HIB.
Main Methods:
- Anesthetized dogs were used to measure peripheral airway resistance and HIB.
- Airways were treated with indomethacin (cyclooxygenase inhibitor) and MK-0591 (5-lipoxygenase inhibitor).
- Bronchoalveolar lavage fluid (BALF) was analyzed for cells and mediators.
Main Results:
- Combined indomethacin and MK-0591 significantly attenuated HIB.
- Atropine nearly abolished the residual HIB response.
- Eicosanoid blockade reduced eicosanoid concentrations in BALF after hyperventilation.
Conclusions:
- Both prostanoid and leukotriene pathways contribute to HIB.
- Eicosanoid and muscarinic-receptor blockade effectively prevents HIB.
- Mucosal injury may contribute to mediator release during hyperventilation.
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