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首页> 外文学位 >A model for the development and recovery from acid-induced esophagitis in the opossum: Changes in motor function and in the mucosal defensive repertoire.
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A model for the development and recovery from acid-induced esophagitis in the opossum: Changes in motor function and in the mucosal defensive repertoire.

机译：负鼠酸诱发食管炎发展和恢复的模型：运动功能和黏膜防御性功能改变。

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摘要

The pathogenesis of gastroesophageal reflux disease (GERD) is poorly understood. Two prevailing hypotheses propose that GERD is either an epithelial disease or is a result of altered motility. The development of esophagitis is, in fact, likely a consequence of failures of both motor function, allowing access of refluxate to the esophageal lumen, and of mucosal defenses that may be inadequate to resist the resulting acid exposure. This thesis describes an integrated series of studies that used a "subacute" model of esophagitis in anesthetized opossums to examine alterations in esophageal motor function and in epithelial and mucosal components of the defensive repertoire.; Changes in esophageal length and swallow-induced motor responses were recorded before and after three consecutive days of 45-minute luminal perfusion with saline or with physiologically relevant concentrations of acid. Electrical and mechanical longitudinal muscle (LM) responses were also assessed. Repeated acid challenge produced erosive esophagitis that was partially resolved over a subsequent one-week period. Acid-induced esophageal shortening was associated with enhanced LM responses to carbachol, depolarization of resting cell membrane potentials, and abnormal spike patterns. Lower esophageal sphincter resting pressure and swallow-induced peristalsis were unaffected, but acid did impair the deglutition reflex. The role of vagal afferent pathways in this deficit was established by its attenuation by bilateral cervical vagotomy.; Regional heterogeneity was described in epithelial thickness and in quantity and content of esophageal glands. Exposure to acid produced site-specific increases in the extent of gland secretion and changes in gland mucin composition. There were also decreases in mast cells, and changes in structure and integrity of the luminal epithelium. Damage was associated with increased glutathione peroxidase (GPx) and heat shock protein (HSP) 90, and with decreased reduced glutathione (GSH) and HSP72. Resolution of injury eight days after acid exposure was associated with distally decreased GPx and GSH.; These studies provide new insights into the pathogenesis of GERD and highlight the existence of certain site-specific structural and functional defenses against gastric refluxate. Esophageal shortening associated with LM hyperresponsiveness is identified as the earliest motor disorder induced by acid injury, while changes in antioxidant levels further support the involvement of free radicals in acid-induced esophagitis.
机译：胃食管反流病（GERD）的发病机理知之甚少。两种流行的假设表明GERD要么是上皮疾病，要么是运动性改变的结果。事实上，食管炎的发展可能是由于两种运动功能衰竭（允许回流物进入食管腔）和粘膜防御层（可能不足以抵抗由此产生的酸暴露）导致的。本论文描述了一系列综合研究，这些研究在麻醉的负鼠中使用了“亚急性”食管炎模型，以检查食管运动功能以及防御库中上皮和粘膜成分的变化。连续三天腔内灌注盐水或生理相关浓度的酸之前和之后的三天，记录食管长度的变化和吞咽引起的运动反应。还评估了纵向和纵向肌电（LM）反应。反复的酸刺激产生了侵蚀性食管炎，其在随后的一周内部分缓解。酸诱导的食管缩短与LM对卡巴胆碱的反应增强，静息细胞膜电位去极化以及异常峰形有关。食管下括约肌的静息压力和吞咽引起的蠕动不受影响，但酸确实会影响脱胶反射。迷走神经传入途径在此缺陷中的作用是通过双侧子宫颈迷走神经切断术减轻其建立的。区域异质性在上皮厚度以及食管腺的数量和含量上都有描述。暴露于酸会使腺体分泌的程度和腺黏蛋白组成的变化产生位点特异性。肥大细胞也减少，并且腔上皮的结构和完整性改变。损伤与谷胱甘肽过氧化物酶（GPx）和热休克蛋白（HSP）90的增加有关，与减少的谷胱甘肽（GSH）和HSP72减少有关。酸暴露八天后，伤口的消退与远端GPx和GSH降低有关。这些研究为GERD的发病机理提供了新的见解，并突出了某些针对胃反流的特定部位结构和功能防御的存在。与LM高反应性相关的食管缩短被认为是酸损伤引起的最早的运动障碍，而抗氧化剂水平的变化进一步支持了自由基参与酸诱导的食管炎。

著录项

  • 作者

    White, Robert Joseph.;

  • 作者单位

    Queen's University at Kingston (Canada).;

  • 授予单位 Queen's University at Kingston (Canada).;
  • 学科 Biology Animal Physiology.; Health Sciences Pathology.
  • 学位 Ph.D.
  • 年度 2002
  • 页码 213 p.
  • 总页数 213
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生理学;病理学;
  • 关键词

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