title: Hypertonic saline nasal provocation and acoustic rhinometry.
abstract: BACKGROUND
  Hypertonic saline (HTS) acts as an airway irritant in human nasal mucosa by stimulating nociceptive nerves and glandular secretion. HTS does not change vascular permeability. In asthma, HTS causes airflow obstruction.
  
  
  OBJECTIVE
  To determine the effect of HTS on mucosal swelling using acoustic rhinometry (AcRh). Potential vasodilator effects were controlled by maximally constricting mucosal vessels with oxymetazoline (Oxy).
  
  
  METHODS
  Normal subjects had AcRh before and 30 min after either 0.05% Oxy or saline (0.9% NaCl) nasal treatments. Nasal provocations followed immediately with five step-wise incremental escalating doses of HTS administered at 6-min intervals. AcRh was performed 1, 3 and 5 min after each HTS administration, and then after blowing the nose at 5 min. The minimum cross-sectional area (Amin), volume of the anterior 6 cm of nasal cavity (V6) and incremental changes from pre-drug treatment baseline levels (delta, mean +/- SEM) were calculated.
  
  
  RESULTS
  Oxy increased Amin by 46% (delta = 0.48 +/- 0.07 cm2, P = 0.0001) and V6 by 53% (Delta = 9.9 +/- 1.5 mL, P < 1 x 10-7) during the first 30 min. Saline (vehicle) treatment had no effect. The maximum HTS dose had no effect after 1 or 3 min. However, in the 4th and 5th minutes there were reductions in Amin (delta = 0.07 +/- 0.03 cm2, P = 0.035) and V6 (delta = 1.57 +/- 0.42 mL, P = 0.004) with an increase in the weight of secretions (delta = 700 +/- 100 mg, P < 0.05). Blowing the nose returned Amin and V6 towards baseline. Oxy had no effect on HTS-induced changes in Amin, V6, pain, rhinorrhea or weight of secretions.
  
  
  CONCLUSIONS
  HTS induced nociceptive nerve stimulation and mucus secretion, and reduced V6 and Amin. Oxy caused vasoconstriction but did not alter HTS-induced effects. HTS may stimulate neurogenic axon response-mediated glandular secretion that contributes to perceptions of nasal obstruction in normal subjects.
authors.affiliation: Division of Rheumatology, Immunology and Allergy, Georgetown University, Washington, DC 20007, USA. baraniuj@georgetown.edu
authors.forename: J N
authors.initials: JN
authors.lastname: Baraniuk
authors.forename: M
authors.initials: M
authors.lastname: Ali
authors.forename: K
authors.initials: K
authors.lastname: Naranch
mesh_terms: D000281:Administration, Intranasal; D004305:Dose-Response Relationship, Drug; D006801:Humans; D006982:Hypertonic Solutions / Q000008:administration & dosage / Q000494:pharmacology*; D007700:Kinetics; D009296:Nasal Cavity / Q000033:anatomy & histology; D014663:Nasal Decongestants / Q000494:pharmacology; D017817:Nasal Lavage Fluid / Q000737:chemistry; D009297:Nasal Mucosa / Q000033:anatomy & histology / Q000187:drug effects* / Q000378:metabolism; D015508:Nasal Obstruction / Q000139:chemically induced; D009299:Nasal Provocation Tests; D010109:Oxymetazoline / Q000494:pharmacology; D010146:Pain / Q000139:chemically induced; D023842:Rhinometry, Acoustic; D012965:Sodium Chloride / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D006982:Hypertonic Solutions; D014663:Nasal Decongestants; D012965:Sodium Chloride; D010109:Oxymetazoline