Strain induced esophageal growth in a novel rodent model

Longitudinal esophageal strain has been shown to increase esophageal length but the contribution of tissue hyperplasia to this growth is unknown. We used a novel model of esophageal stretch to determine the cellular response to the strain stimulus.

Male Sprague-Dawley rats underwent transection of the distal esophagus. The distal stump was ligated and stretched over a silicone tube. The proximal esophageal stump was anastomosed to the stomach to restore continuity. After two, four, or seven days, the silicone tube was removed and the esophageal segment was measured and compared to its initial length. Sham animals had only a thin piece of silicone tubing placed. Standardized histologic sections were evaluated for wall thickness. Immunofluorescence with DAPI, Ki-67, and Myogenin antibodies was used to assess nuclear density, proliferation indices, and myoblast differentiation indices.

Experimental animals demonstrated a significant increase in esophageal length compared to sham controls at four and seven days with no difference at two days. There was significant lengthening between four and seven days among the experimental animals. There was no change in wall thickness between experimental and sham animals at any time point. Nuclear density was increased at all time points, although this only reached significance at day four. Proliferation indices were significantly increased relative to sham controls at all time points. Esophageal strain induced significantly increased myoblast differentiation.

In this novel rat model of esophageal strain, lengthening is associated with stable esophageal wall thickness, increased nuclear density, increased cellular proliferation, and increased myogenin expression. These data suggest that true tissue hyperplasia may contribute to the increased length seen after esophageal strain.