REDUCTION OF CELL PROLIFERATIVE ACTIVITIES OF GASTRIC STUMP ADENOMATOUS HYPERPLASIAS AFTER BILE REFLUX DIVERSION IN RATS

Previously we reported the majority of lesions induced hy bile reflux, in the absence of chemical carcinogens, in the rat remnant stomach to consist primarily of gastric type and secondarily of intestinal type cells, and that they are reversible after diversion of bile reflux. Th e present study was designed to evaluate changes in proliferative acti vities in cells of each type under these conditions. The frequency of adenomatous hyperplasia (AH) induced in the gastric stump mucosa by du odenal content reflux after Billroth II partial gastrectomy (BII) incr eased until the 54th week of the experiment. Roux-en-Y (RY) surgical p rocedure which prevents duodenal reflux performed at the 24th or 36th week after BII led to a decrease in AH. Cell content of the lesions wa s analyzed using routine H&E staining, immunohistochemical staining fo r pepsinogen isoenzyme 1 and histochemical procedures for mucins (para doxical concanavalin A, galactose oxidase Schiff and sialidase galacto se oxidase Schiff reactions) and proliferation in each compartment eva luated by an immunohistochemical method using bromodeoxyuridine (BrdU) and a monoclonal antibody against BrdU. At the 54th week the number o f BrdU-labeled cells per normal pyloric column was significantly (P < 0.05) increased to 10.63/pit after the BII operation, while it diminis hed to 5.23/pit after RY diversion, this being the same level as with the RY procedure alone. AH maintained a high rate of BrdU incorporatio n at 12.7% after BII operation, which was also significantly reduced ( P < 0.01) to 7.0% by the RY surgery. The intestinal type cell showed h ighest (22.2%), the surface mucous type cell showed the next (16.5%) a nd the pyloric gland type cell showed lowest (5.2%) BrdU labeling indi ces after BII operation. All the cell types in AH showed similar propo rtional decreases in BrdU incorporation after RY diversion. Thus surgi cal intervention reverses the cell proliferation caused by bile reflux in the gastric stump.