title: Modulatory impact of acid and pepsin on esophageal hydrophobicity in humans.
abstract: OBJECTIVE
  The role of hydrophobicity in the pathophysiology of the gastrointestinal tract is well established as a protective mechanism against the impact of lumenal acid and pepsin. Hydrophobic properties of esophageal secretion in humans remain largely unknown.
  
  
  METHODS
  We have studied, therefore, hydrophobicity by using fluorescence probe in human esophageal secretion, elaborated under the impact of saline followed by HCl, HCl/pepsin, and final saline.
  
  
  RESULTS
  Basal hydrophobicity of human esophageal secretion, elaborated during mucosal exposure to saline, was 237 +/- 32. This value, however, declined 72% during mucosal exposure to HCl (66 +/- 14 vs 237 +/- 32; p < 0.001) and 87% during mucosal exposure to acid supplemented with pepsin (30 +/- 4 vs 237 +/- 32; p < 0.001). Moreover, hydrophobicity upon perfusion with HCl/pepsin was 55% lower than after perfusion with HCl alone (30 +/- 4 vs 66 +/- 14), although the result was insignificant. Substitution of saline for HCl/pepsin solution during the last perfusion period resulted in a partial recovery of hydrophobicity in esophageal secretion (131 +/- 30 vs 30 +/- 4; p < 0.001), although this value was lower than the basal hydrophobicity value (131 +/- 30 vs 237 +/- 32; p = 0.028). In addition, we continuously observed a significant shift in the fluorescence emission maximum from 508 +/- 6.4 to 486 +/- 0.9 (p < 0.001) during perfusion with starting saline, to 492 +/- 1.6 (p < 0.001) during exposure to HCl, to 493 +/- 1.1 (p < 0.001) during perfusion with HCl/pepsin, and to 488 +/- 0.9 (p < 0.001) during infusion of final saline. The maximum emission wavelength after esophageal exposure to initial saline also was significantly lower than the maximum emission upon perfusion with HCl (492 +/- 1.6 vs 486 +/- 0.9; p < 0.05) and HCl/pepsin (493 +/- 1.1 vs 486 +/- 0.9; p < 0.05). Although basal hydrophobicity in males was similar to corresponding values recorded in females, mucosal exposure to HCl (pH 2.1) resulted in an 84% decline in females but only 60% in males. Therefore, the hydrophobicity value in females during the perfusion period with HCl was 52% lower than in males (p = 0.129).
  
  
  CONCLUSIONS
  Esophageal secretion exhibits its hydrophobic nature presumably through the presence of mucus components such as mucin and mucin-associated phospholipids. The inhibitory impact of HCl and HCl/pepsin solutions on esophageal hydrophobicity may play a role in the pathogenesis of mucosal damage by gastroesophagel refluxate.
mesh_terms: D000328:Adult; D004942:Esophagitis, Peptic / Q000209:etiology; D004947:Esophagus / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D005764:Gastroesophageal Reflux / Q000209:etiology; D006801:Humans; D006851:Hydrochloric Acid / Q000494:pharmacology*; D008297:Male; D009077:Mucins / Q000032:analysis / Q000378:metabolism*; D009092:Mucous Membrane / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D010434:Pepsin A / Q000494:pharmacology*; D010743:Phospholipids / Q000032:analysis / Q000378:metabolism; D012737:Sex Factors; D012965:Sodium Chloride / Q000494:pharmacology; D013050:Spectrometry, Fluorescence; D014867:Water
chemical_list: D009077:Mucins; D010743:Phospholipids; D014867:Water; D012965:Sodium Chloride; D010434:Pepsin A; D006851:Hydrochloric Acid