title: Simulated reflux decreases vocal fold epithelial barrier resistance.
abstract: OBJECTIVE
  The vocal fold epithelium provides a barrier to the entry of inhaled and systemic challenges. However, the location of the epithelium makes it vulnerable to damage. Past research suggests, but does not directly demonstrate, that exposure to gastric reflux adversely affects the function of the epithelial barrier. Understanding the nature of reflux-induced epithelial barrier dysfunction is necessary to better recognize the mechanisms for vocal fold susceptibility to this disease. Therefore, we examined the effects of physiologically relevant reflux challenges on vocal fold transepithelial resistance and gross epithelial and subepithelial appearance.
  
  
  METHODS
  Ex vivo, mixed design with between-group and repeated-measures analyses.
  
  
  METHODS
  Healthy, native porcine vocal folds (N = 52) were exposed to physiologically relevant acidic pepsin, acid-only, or pepsin-only challenges and examined with electrophysiology and light microscopy. For all challenges, vocal folds exposed to a neutral pH served as control.
  
  
  RESULTS
  Acidic pepsin and acid-only challenges, but not pepsin-only or control challenges significantly reduced transepithelial resistance within 30 minutes. Reductions in transepithelial resistance were irreversible. Challenge exposure produced minimal gross changes in vocal fold epithelial or subepithelial appearance as evidenced by light microscopy.
  
  
  CONCLUSIONS
  These findings demonstrate that acidic environments characteristic of gastric reflux compromise epithelial barrier function without gross structural changes. In healthy, native vocal folds, reductions in transepithelial resistance could reflect reflux-related epithelial disruption. These results might guide the development of pharmacologic and therapeutic recommendations for patients with reflux, such as continued acid-suppression therapy and patient antireflux behavioral education.
authors.affiliation: Department of Speech, Language, and Hearing Sciences, Purdue University, West Lafayette, Indiana, USA.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Erickson
authors.forename: Mahalakshmi
authors.initials: M
authors.lastname: Sivasankar
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D017097:Electric Impedance; D005764:Gastroesophageal Reflux / Q000503:physiopathology*; D005765:Gastrointestinal Agents / Q000494:pharmacology*; D006851:Hydrochloric Acid / Q000494:pharmacology*; D007820:Laryngeal Mucosa / Q000187:drug effects / Q000503:physiopathology*; D057045:Laryngopharyngeal Reflux / Q000503:physiopathology; D010434:Pepsin A / Q000494:pharmacology*; D013552:Swine; D014827:Vocal Cords / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D005765:Gastrointestinal Agents; D010434:Pepsin A; D006851:Hydrochloric Acid