283122 The Role of Mucous Viscosity and Esophageal Strictures On Bolus Flow in Diseased Esophagi

Monday, October 29, 2012
Hall B (Convention Center )
Hedieh Saffari, Chemical Engineering, University of Utah, Salt Lake City, UT, Mike Hansen, Chemical Engineering , university of Utah, salt lake city, UT, Kathryn Peterson, Department of Internal Medicine, Division of Gastroenterology, University of Utah, Salt Lake City, UT, Gerald Gleich, Department of Dermatology, University of Utah, Salt Lake City, UT and Leonard F. Pease III, Chemical Engineering, Internal Medicine (Gastroenterology), and Pharmaceutics & Pharmaceutical Chemistry, University of Utah, Salt Lake City, UT

Hydrodynamic flow through the gastrointestinal tract is significantly perturbed in diseased states. For example, in eosinophil esophagitis (EoE), an allergic condition of the esophagus putatively caused by invasion of white blood cells called eosinophils, the diameter of the esophagus narrows dramatically in a feature called a stricture and mucin genes are upregulated affecting the viscosity of the thin mucous layer lining the esophageal wall. No existing model of esophageal peristalsis accounts for these changes and their impact on wall stresses, which may affect patient sensation or pain.

Here we model the flow of a swallowed bolus in normal and diseased esophagi by solving the non-dimensionalized axisymmetric Navier-Stokes equations for both the bolus and mucous layers. We calculated wall stresses and mean flow rates, as well as their dependencies upon esophageal stricture length ratios and mucous-to-bolus viscosity ratios. We find that sharp strictures generate large increases in both normal and shear stresses in the esophagus wall, and that a more viscous mucous layer reduces these stresses. These results have significant implications for understanding EoE symptoms (e.g. patient pain) and the role of mucous in peristaltic transport throughout the entire GI tract.


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See more of this Session: Fluid Mechanics Poster Session
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