Albuterol improves alveolar-capillary membrane conductance in healthy humans

Natalie E. Taylor, Sarah E. Baker, Thomas P. Olson, Sophie Lalande, Bruce D. Johnson, Eric M. Snyder

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Background: Beta-2 adrenergic receptors (β2ARs) are located throughout the body including airway and alveolar cells. The β2ARs regulate lung fluid clearance through a variety of mechanisms including ion transport on alveolar cells and relaxation of the pulmonary lymphatics. We examined the effect of an inhaled β2-agonist (albuterol) on alveolar-capillary membrane conductance (DM) and pulmonary capillary blood volume (VC) in healthy humans. Methods: We assessed the diffusing capacity of the lungs for carbon monoxide (DLCO) and nitric oxide (DLNO) at baseline, 30 minutes, and 60 minutes following nebulized albuterol (2.5 mg, diluted in 3 mL normal saline) in 45 healthy subjects. Seventeen subjects repeated these measures following nebulized normal saline (age = 27 ± 9 years, height = 165 ± 21 cm, weight = 68 ± 12 kg, BMI = 26 ± 9 kg/m2). Cardiac output (Q), heart rate, systemic vascular resistance (SVR), blood pressure, oxygen saturation, forced expiratory volume at one-second (FEV1), and forced expiratory flow at 50% of forced vital capacity (FEF50) were assessed at baseline, 30 minutes, and 60 minutes following the administration of albuterol or saline. Results: Albuterol resulted in a decrease in SVR, and an increase in Q, FEV1, and FEF50 compared to saline controls. Albuterol also resulted in a decrease in VC at 60 minutes post albuterol. Both albuterol and normal saline resulted in no change in DLCO or DM when assessed alone, but a significant increase was observed in DM when accounting for changes in VC. Conclusion: These data suggest that nebulized albuterol improves pulmonary function in healthy humans, while nebulization of both albuterol and saline results in an increase in DM/VC.

Original languageEnglish (US)
Pages (from-to)19-25
Number of pages7
JournalClinical Medicine Insights: Circulatory, Respiratory and Pulmonary Medicine
Volume10
DOIs
StatePublished - Oct 12 2016

Bibliographical note

Funding Information:
This work was supported by NIH Grants HL71478 and AHA Grant 56051Z. The authors confirm that the funder had no influence over the study design, content of the article, or selection of this journal.

Publisher Copyright:
© the authors, publisher and licensee Libertas Academica Limited.

Keywords

  • CFTR
  • Lung diffusion
  • Lung fluid
  • Sodium channels

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