G-cell hyperplasia in rats with pyloric stenosis

Abstract

Since little is known about the pathophysiology of pyloric stenosis, we created a partial gastric outlet obstruction in 13 Wistar rats by placing a nonabsorbable ligature of defined size around the pylorus. Sham operations were performed in 10 rats. The animals from both groups were killed after four months. G-cell count and gastrin content were determined in 10 parallel strips, which were cut by razor blades mounted on a handle. Gastric size and weight as well as thickness of mucosal and muscular layers and serum gastrin concentration were also determined. Body weight of the animals with pyloric stenosis was lower and gastric weight higher than that of the controls. Furthermore, we found an enlarged G-cell area and G-cell hyperplasia, an increased surface area and thickness of the mucosal and muscular layers of the stomach, and in the majority of rats, elevated serum gastrin levels. Total G-cell count was 583,720 +/- 90,561 in the rats with pyloric stenosis and 385,775 +/- 15,820 (mean +/- SEM) in the control rats (P less than 0.04). We conclude that partial gastric outlet obstruction in rats leads to G-cell hyperplasia and that this experiment may serve as a model for pyloric stenosis in man.

Increased Sensitivity of Gastrin Cells to Gastric Distension following Antral Denervation in the Rat

“…In both cases there is gastric retention secondary to decreased emptying. Chronic pyloric obstruction, like antral denervation, leads to hypergastrinaemia (Feurle, Tischbirek & Baca, 1988;Chen, Zhao, Nylander, Sundler & Hakanson, 1995). However, pyloric obstruction is associated with increased acid secretion, whereas antral denervation leads to decreased acid output.…”