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Calcium chelators induce bronchoconstriction in the canine lung periphery
K S Lindeman1, C A Hirshman, A N Freed
1Department of Environmental Health Science, Johns Hopkins University, Baltimore, Maryland 21205.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|March 1, 1990
Summary
Disodium EDTA (Na2EDTA) causes airway narrowing in dogs by chelating calcium, not just due to solution concentration. This mechanism is independent of muscarinic pathways, offering insights into airway hyperresponsiveness.
Area of Science:
- Pulmonary Physiology
- Pharmacology
Background:
- Nonspecific airway hyperresponsiveness is a key feature of asthma.
- Divalent cation chelators, like disodium EDTA (Na2EDTA), are known to affect airway smooth muscle function.
Purpose of the Study:
- To investigate the mechanism by which Na2EDTA induces bronchoconstriction in the peripheral airways.
- To model nonspecific small airway hyperresponsiveness using mongrel dogs.
Main Methods:
- Utilized a wedged bronchoscope technique to measure collateral system resistance (Rcs) in mongrel dogs.
- Administered aerosolized Na2EDTA at varying concentrations and durations.
- Assessed the role of muscarinic pathways using atropine and compared Na2EDTA with calcium-containing CaNa2EDTA.
Main Results:
- Isotonic Na2EDTA significantly increased Rcs by 91% +/- 21%.
- Na2EDTA induced a dose-dependent increase in Rcs with increasing concentration and duration.
- Atropine did not significantly alter the Na2EDTA-induced bronchoconstriction, but it did attenuate the response to distilled water.
- Na2EDTA caused a significantly greater increase in Rcs compared to CaNa2EDTA, indicating hyperosmolality alone does not explain the effect.
Conclusions:
- Na2EDTA induces dose-dependent bronchoconstriction in the canine lung periphery.
- The mechanism of Na2EDTA-induced bronchoconstriction is not solely due to hyperosmolality.
- The observed effect is independent of muscarinic activity and appears to involve calcium chelation.