Received November 13, 2002.
Topical application of benzalkonium chloride to the stomach serosa increases gastric emptying time, acid secretion, serum gastrin and size of the mucosa
Article first published online: 14 FEB 2003
Volume 110, Issue 11, pages 795–801, November 2002
How to Cite
ZUCOLOTO, S., ROMANELLO, L. M. F., GARCIA, S. B., SOBREIRA, L. F. R., BARBOSA, A. J. A. and TRONCON, L. E. A. (2002), Topical application of benzalkonium chloride to the stomach serosa increases gastric emptying time, acid secretion, serum gastrin and size of the mucosa. APMIS, 110: 795–801. doi: 10.1034/j.1600-0463.2002.1101105.x
Accepted September 19, 2002.
- Issue published online: 14 FEB 2003
- Article first published online: 14 FEB 2003
- Stomach denervation;
- gastric emptying;
- gastric acid secretion;
- parietal cell;
- G cell
Aim: In the present study we evaluated the effects of gastric myenteric denervation using benzalkonium chloride (BAC) on the time for gastric emptying, as well as gastric secretion, and mucosal epithelial cell size and population in rats. Methods and Results: Wistar rats were treated with topical serosal application of BAC to the stomach. Control animals received saline. Ninety days after surgery, gastric emptying time, gastric acid secretion and serum gastrin levels were studied. Next, the animals were sacrificed and the stomachs were removed, fixed in formalin and histologically processed for histomorphometry of the height, area and volume of the glandular portion, and volume and population of mucous, chief, parietal, G- and labelled cells. BAC animals showed a significant delay in gastric emptying and an increase in gastric acid secretion and serum gastrin levels. These animals also presented a significant reduction of myenteric neuron number, hypertrophy of parietal and chief cells, hyperplasia of G cells and an increase in the gastric mucosa area. Conclusion: The absence of the myenteric plexus seems to protect the stomach from the hyperplastic effects of hypergastrinemia. Gastric food stasis may act as a factor triggering morphological and functional alterations of the gastric epithelium. Although gastric food stasis is a common finding in medical practice, its physiopathological consequences are poorly understood and have not been frequently discussed in the literature.