MODULATORY IMPACT OF ACID AND PEPSIN ON ESOPHAGEAL HYDROPHOBICITY IN HUMANS

Objectives: The role of hydrophobicity in the pathophysiology of the g astrointestinal tract is well established as a protective mechanism ag ainst the impact of lumenal acid and pepsin. Hydrophobic properties of esophageal secretion in humans remain largely unknown. Methods: We ha ve studied, therefore, hydrophobicity by using fluorescence probe in h uman esophageal secretion, elaborated under the impact of saline follo wed by HCl, HCl/pepsin, and final saline. Results: Basal hydrophobicit y of human esophageal secretion, elaborated during mucosal exposure to saline, was 237 +/- 32. This value, however, declined 72% during muco sal exposure to HCl (66 +/- 14 vs 237 +/- 32; p < 0.001) and 87% durin g mucosal exposure to acid supplemented with pepsin (30 +/- 4 vs 237 /- 32; p < 0.001). Moreover, hydrophobicity upon perfusion with HCl/pe psin was 55% lower than after perfusion with HCl alone (30 +/- 4 vs 66 +/- 14), although the result was insignificant. Substitution of salin e 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 ba sal hydrophobicity value (131 +/- 30 vs 237 +/- 32; p = 0.028). In add ition, we continuously observed a significant shift in the fluorescenc e 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 expo sure to HCl, to 493 +/- 1.1 (p < 0.001) during perfusion with HCl/peps in, and to 488 +/- 0.9 (p < 0.001) during infusion of final saline. Th e maximum emission wavelength after esophageal exposure to initial sal ine also was significantly lower than the maximum emission upon perfus ion with HCl (492 +/- 1.6 vs 486 +/- 0.9; p < 0.05) and HCl/pepsin (49 3 +/- 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 on ly 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 pr esumably through the presence of mucus components such as mucin and mu cin-associated phospholipids. The inhibitory impact of HCl and HCV-pep sin solutions on esophageal hydrophobicity may play a role in the path ogenesis of mucosal damage by gastroesophageal refluxate.