Esophageal exposure to ethanol increases risk of acid damage in rabbit esophagus

Esophageal exposure to ethanol increases risk of acid damage in rabbit esophagus
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DOI:
10.1023/a:1026646215879
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发表时间:
1999-02-01
影响因子:
3.1
通讯作者:
Orlando, RC
Orlando, RC
中科院分区:
医学3区
文献类型:
--
作者:
Bor, S;Bor-Caymaz, C;Orlando, RC

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大量饮酒与反流性食管炎的发生有关。其原因包括抗反流屏障受损、酸分泌刺激和组织抵抗力改变。为了探讨组织抵抗力改变对食管炎发展的影响,将兔食管上皮切片置于Ussing室中,并在光照下暴露于10%乙醇、酸(HCl、pH 2)或两者的组合中。通过测量电位差(PD)、短路电流(I-sc)和电阻(R)以及组织学来评估组织损伤。与林格对照组相比,组织在光照下暴露于HCl 1小时,在电或形态学上几乎没有变化,而在光照下暴露于10%乙醇1小时,PD(53 +/- 4%)、I-sc(30 +/- 1%)和R(31 +/- 5%)降低,上层细胞水肿。同时暴露于乙醇和酸导致PD(81 +/- 1%)和I-sc(70 +/- 2%)显著下降,但R(40 +/- 4%)没有显著下降,形态学损伤更大。此外,在一般无害的酸度水平(pH值2-4)下,暴露于乙醇的组织对酸的脆弱性是显而易见的,只需要很短的乙醇暴露时间(10分钟),并且在从沐浴液中去除乙醇后,酸暴露的延迟时间长达1小时。综上所述,乙醇对食管上皮有直接的毒性作用,使食管上皮易发生酸损伤。即使短时间暴露于临床相关浓度的乙醇也会产生组织易损性,在乙醇清除后至少持续1小时,并将相对无害的酸浓度转化为破坏性物质。这些结果支持乙醇改变组织抵抗的能力在人类反流性食管炎的发展中起重要作用的可能性。
Heavy alcohol consumption is associated with the development of reflux esophagitis. Among the reasons for this are impairment of the antireflux barrier, stimulation of acid secretion, and altered tissue resistance. To explore the contribution of altered tissue resistance to the development of esophagitis, sections of rabbit esophageal epithelium were mounted in Ussing chambers and exposed luminally to 10% ethanol, acid (HCl, pH 2), or combinations of both. Tissue injury was assessed by measurements of potential difference (PD), short circuit current (I-sc) and electrical resistance (R) and by histology. Tissues exposed luminally to HCl for 1 hr exhibited little or no change electrically or morphologically compared to Ringer controls, while luminal exposure to 10% ethanol for 1 hr lowered PD (53 +/- 4%), I-sc (30 +/- 1%), and R (31 +/- 5%) and produced cellular edema in the upper layers. Simultaneous exposure to ethanol and acid resulted in significantly greater declines in PD (81 +/- 1%) and I-sc (70 +/- 2%), but not R (40 +/- 4%), and greater morphologic damage. Moreover, this vulnerability of ethanol-exposed tissues to acid was demonstrable at generally innocuous levels of acidity (pH 2-4), after only short periods of ethanol exposure (10 min) and with delays for acid exposures of up to 1 hr following ethanol removal from the bathing solution. In conclusion, ethanol has a direct noxious effect on esophageal epithelium, which predisposes the tissue to acid injury. Tissue vulnerability develops with even short exposures to clinically relevant concentrations of ethanol, lasts for at least 1 hr after ethanol clearance, and transforms relatively innocuous concentrations of acid into damaging agents. These results support the likelihood that ethanol's ability to alter tissue resistance plays an important role in the development of reflux esophagitis in humans.