Effects of a β2-agonist on airway hyperreactivity in subjects with cervical spinal cord injury

Richard V. DeLuca, David R. Grimm, Marvin Lesser, William A. Bauman, Peter L. Almenoff

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Study Objective: Aerosolized ipratropium bromide or orally administered baclofen or oxybutynin chloride (Ditropan) block methacholine-associated airway hyperreactivity in subjects with chronic cervical spinal cord injury (SCI), whereas these agents do not inhibit airway hyperreactivity associated with the inhalation of histamine. The present study was performed to determine whether pretreatment with a β2-agonist attenuates airway hyperresponsiveness in these subjects. Participants: Subjects with chronic cervical SCI previously demonstrating airway hyperreactivity were challenged with methacholine (n = 9) or histamine (n = 16) alone and, on a separate day, 25 min following inhalation of nebulized metaproterenol sulfate. Results: Inhalation of the β2-agonist was associated with an increase in provocative concentration causing a 20% decrease in FEV1 (PC20) values (geometric mean) from 1.01 ± 2.76 to 20.54 ± 6.24 mg/mL for methacholine and from 2.29 ± 2.26 to 19.82 ± 5.93 mg/mL for histamine. No correlation was found between specific PC20 values for individual subjects and percentage improvement in FEV1 (liter) following inhalation of metaproterenol sulfate and between PC20 values and baseline FEV1 percent. Conclusion: These data, combined with findings that patients with chronic high cervical SCI experience increased breathlessness following exposure to exogenous agents, suggest that long-term prophylactic β2-agonist therapy may reduce respiratory symptoms associated with airway hyperreactivity in these patients.

Original languageEnglish
Pages (from-to)1533-1538
Number of pages6
JournalChest
Volume115
Issue number6
DOIs
StatePublished - 1999

Keywords

  • Bronchial hyperresponsiveness
  • Histamine
  • Methacholine
  • Quadriplegia
  • Spinal cord injury
  • β-Agonist

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