Marcinkiewicz M, Sarosiek J, Edmunds M, Scheurich J, Weiss P, McCallum R W
University of Virginia Health Sciences Center, Charlottesville 22908, USA.
J Clin Gastroenterol. 1995 Dec;21(4):268-74. doi: 10.1097/00004836-199512000-00003.
Normal human esophageal mucosa exhibits biphasic secretory responses to intraluminal stimuli in terms of PGE2 release with a decline under the impact of HCl and an increase in PGE2 release during mucosal exposure to HCl/Pepsin. PGE2 secretory patterns in patients with reflux esophagitis (RE) remain unknown. We have studied, therefore, luminal release of PGE2 in 28 patients with nonhealed and healed RE, and compared the obtained results with corresponding values recorded in controls. The rate of luminal release of PGE2 in nonhealed RE exhibited a monophasic patterns, i.e., significantly decreased both during mucosal exposure to HCl (2,273 +/- 444, vs. 3,655 +/- 600 pg/min, p = 0.025) and HCl/pepsin (1,271 +/- 244, vs. 3,655 +/- 600 pg/min. p = 0.003) as compared to its basal value. However, the rate of luminal PGE2 release in patients with nonhealed RE in basal conditions and during mucosal exposure to HCl was significantly higher than corresponding values in controls. Luminal release of PGE2 in patients with healed endoscopic esophagitis was significantly lower as compared to corresponding values recorded in patients with nonhealed endoscopic changes and in controls. In conclusion, (a) monophasic inhibitory responses of the esophageal mucosa to intraluminal HCl and HCl/pepsin solutions in patients with RE indicate a different pattern of mucosal secretory response to intraluminal stimuli; (b) inhibition of the rate of luminal release of PGE2 under the impact of HCl/pepsin may play a role in the development and/or progression of mucosal damage; and (c) the decline in the rate of luminal PGE2 release in healed RE indicates that its elevated value in active esophageal disease should be considered as an implication of mucosal damage induced by HCl/pepsin.
正常人类食管黏膜在PGE2释放方面对腔内刺激表现出双相分泌反应，即在盐酸作用下下降，而在黏膜暴露于盐酸/胃蛋白酶期间PGE2释放增加。反流性食管炎（RE）患者的PGE2分泌模式尚不清楚。因此，我们研究了28例未愈合和已愈合RE患者的腔内PGE2释放情况，并将所得结果与对照组记录的相应值进行比较。未愈合RE患者的腔内PGE2释放率呈现单相模式, 即与基础值相比，在黏膜暴露于盐酸（2273±444，vs. 3655±600 pg/min，p = 0.025）和盐酸/胃蛋白酶（1271±244，vs. 3655±600 pg/min，p = 0.003）时均显著降低。然而，未愈合RE患者在基础条件下和黏膜暴露于盐酸期间的腔内PGE2释放率显著高于对照组的相应值。与未愈合内镜改变的患者和对照组记录的相应值相比，内镜食管炎已愈合患者的腔内PGE2释放显著降低。总之，（a）RE患者食管黏膜对腔内盐酸和盐酸/胃蛋白酶溶液的单相抑制反应表明黏膜对腔内刺激的分泌反应模式不同；（b）在盐酸/胃蛋白酶作用下腔内PGE2释放率的抑制可能在黏膜损伤的发生和/或进展中起作用；（c）已愈合RE患者腔内PGE2释放率的下降表明，在活动性食管疾病中其升高的值应被视为盐酸/胃蛋白酶诱导的黏膜损伤的一种表现。
