DeRosa J, Marcinkiewicz M, Sarosiek J, Edmunds M, McCallum R W
University of Virginia Health Sciences Center, Charlottesville, USA.
Am J Gastroenterol. 1995 Nov;90(11):2020-4.
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.
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.
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).
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.
疏水性在胃肠道病理生理学中的作用已被充分确认为一种抵御管腔酸和胃蛋白酶影响的保护机制。人类食管分泌物的疏水性特性在很大程度上仍不为人所知。
因此，我们使用荧光探针研究了人类食管分泌物的疏水性，该分泌物在生理盐水、随后的盐酸、盐酸/胃蛋白酶以及最后的生理盐水作用下产生。
在黏膜暴露于生理盐水期间产生的人类食管分泌物的基础疏水性为237±32。然而，在黏膜暴露于盐酸期间，该值下降了72%（66±14对比237±32；p<0.001），在黏膜暴露于添加胃蛋白酶的酸期间下降了87%（30±4对比237±32；p<0.001）。此外，用盐酸/胃蛋白酶灌注后的疏水性比单独用盐酸灌注后低55%（30±4对比66±14），尽管结果不显著。在最后灌注期用生理盐水替代盐酸/胃蛋白酶溶液导致食管分泌物疏水性部分恢复（131±30对比30±4；p<0.001），尽管该值低于基础疏水性值（131±30对比237±32；p = 0.028）。此外，在灌注起始生理盐水期间，我们持续观察到荧光发射最大值从508±6.4显著移至486±0.9（p<0.001），在暴露于盐酸期间移至492±1.6（p<0.001），在灌注盐酸/胃蛋白酶期间移至493±1.1（p<0.001），在灌注最后生理盐水期间移至488±0.9（p<0.001）。食管暴露于初始生理盐水后的最大发射波长也显著低于用盐酸灌注时的最大发射波长（492±1.6对比486±0.9；p<0.05）以及用盐酸/胃蛋白酶灌注时的最大发射波长（493±1.1对比486±0.9；p<0.05）。尽管男性的基础疏水性与女性记录的相应值相似，但黏膜暴露于盐酸（pH 2.1）导致女性下降84%，而男性仅下降60%。因此，在盐酸灌注期女性的疏水性值比男性低52%（p = 0.129）。
食管分泌物可能通过黏蛋白和黏蛋白相关磷脂等黏液成分表现出其疏水性。盐酸和盐酸/胃蛋白酶溶液对食管疏水性的抑制作用可能在胃食管反流物引起的黏膜损伤发病机制中起作用。
