Calcium chelators induce bronchoconstriction in the canine lung periphery

K. S. Lindeman, C. A. Hirshman, A. N. Freed

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We studied the mechanism by which Na2EDTA, a divalent cation chelator, induces bronchoconstriction in the lung periphery of mongrel dogs as a model of nonspecific small airway hyperresponsiveness. Using a wedged bronchoscope technique, we measured collateral system resistance (Rcs) before and after challenges with aerosolized Na2EDTA. An isotonic solution (4% Na2EDTA, 0.28 osmol/kg) increased Rcs 91 ± 21%. Na2EDTA increased Rcs in a dose-dependent fashion after challenges of increasing concentration (0, 1, 3, and 6%) or duration (15, 30, 60, and 90 s) with 6% Na2EDTA. Atropine (1 mg/kg iv) significantly (P = 0.01) attenuated the response to an aerosol challenge with distilled H2O. Atropine did not significantly (P = 0.35) alter the response to a challenge with 4% Na2EDTA. Challenge with 6% Na2EDTA (0.42 osmol/kg) increased Rcs to a significantly greater (P < 0.01) extent than did challenge with 6% CaNa2EDTA (0.37 osmol/kg, 250 ± 55 vs. 29 ± 11%, respectively). We conclude that Na2EDTA induces bronchoconstriction in the canine lung periphery in a dose-dependent fashion. As suggested by the Na2EDTA-CaNa2EDTA comparison, hyperosmolality of the solution alone cannot explain this phenomenon. The mechanism does not depend on muscarinic activity and appears to involve chelation of calcium.

Original languageEnglish (US)
Pages (from-to)1114-1120
Number of pages7
JournalJournal of applied physiology
Issue number3
StatePublished - 1990


  • collateral resistance
  • ethylenediaminetetraacetic acid

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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