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脂肪酶在兔实验性食管炎发病机制中的作用。

Role of lipase in the pathogenesis of experimental esophagitis in the rabbit.

作者信息

Salo J A, Lehto V P, Karonen S L, Kivilaakso E

机构信息

Department of Thoracic and Cardiovascular Surgery, Helsinki University Central Hospital, Finland.

出版信息

Arch Surg. 1987 Oct;122(10):1160-4. doi: 10.1001/archsurg.1987.01400220070014.

DOI:10.1001/archsurg.1987.01400220070014
PMID:3662797
Abstract

The role of lipase in the pathogenesis of reflux esophagitis was investigated in an experimental model in which an in situ isolated segment of rabbit esophagus was perfused (at pH 7) with a solution containing lipase in concentrations of 2 and 10 mg/ml. The severity of mucosal damage was assessed using the following indicators of mucosal integrity: transmucosal potential difference, net flux of sodium, and mucosal permeability to erythritol labeled with carbon 14, a neutral molecule with a greatest molecular diameter of 8.2 nm. Furthermore, the morphologic characteristics of esophageal damage were studied by light and scanning electron microscopy. The results suggest that lipase significantly decreased transmucosal potential difference and increased mucosal permeability to sodium and erythritol labeled with carbon 14. Morphologically, lipase induced cytoplasmatic vesiculation and widening of intercellular spaces within the basal cell layer. The epithelial cell layers were also often seen to be sloughed off with consequent exposure of the subepithelial connective tissue at the mucosal surface. The findings suggest that lipase has an adverse effect on the esophageal mucosa that may have pathogenetic significance in clinical reflux esophagitis.

摘要

在一个实验模型中研究了脂肪酶在反流性食管炎发病机制中的作用。该模型是用浓度为2毫克/毫升和10毫克/毫升的含脂肪酶溶液(pH值为7)灌注原位分离的兔食管段。使用以下黏膜完整性指标评估黏膜损伤的严重程度:跨黏膜电位差、钠的净通量以及黏膜对用碳14标记的赤藓糖醇的通透性,赤藓糖醇是一种最大分子直径为8.2纳米的中性分子。此外,通过光学显微镜和扫描电子显微镜研究了食管损伤的形态学特征。结果表明,脂肪酶显著降低了跨黏膜电位差,并增加了黏膜对钠和用碳14标记的赤藓糖醇的通透性。在形态学上,脂肪酶诱导了细胞质空泡化以及基底细胞层内细胞间隙增宽。还经常可见上皮细胞层脱落,随后黏膜表面的上皮下结缔组织暴露。这些发现表明,脂肪酶对食管黏膜有不良影响,这可能在临床反流性食管炎的发病机制中具有重要意义。

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