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Jarmo A. Salo, MD; Veli-Pekka Lehto, MD; Sirkka-Liisa Karonen, MD; Eero Kivilaakso, MD

Arch Surg. 1987;122(10):1160-1164.

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.

(Arch Surg 1987;122:1160-1164)

Author Affiliations
From the Departments of Thoracic and Cardiovascular Surgery (Dr Salo) and Pathology (Dr Lehto), University of Helsinki; and the Department of Clinical Chemistry (Dr Karonen) and Second Department of Surgery (Dr Kivilaakso), Helsinki University Central Hospital.

Footnotes
Accepted for publication Oct 31, 1986.

Reprint requests to Department of Thoracic and Cardiovascular Surgery, Helsinki University Central Hospital, Haartmanikatu 4, SF-00290 Helsinki, Finland (Dr Salo).

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