Gastric nitrite processing in the surgically altered maximal and minimal bile reflux ferret model.
Ingested nitrate and nitrite have been shown to contribute to endogenous, N-nitroso compound formation in man and experimental animals. N-nitroso compounds have long been suspected of contributing to higher levels of gastric cancer in various populations. Reconstructive gastric surgery to treat ulcers is accompanied by a change in bile reflux, gastritis and an increased incidence of gastric cancer in humans. To evaluate possible connections between gastric nitrite processing, reconstructive surgery and gastric cancer, the surgically altered domestic ferret, Mustela putorius furo, was used as an experimental model. The aim of the study was to determine if surgery would alter the stomach in a way which would increase gastric nitrite concentration, and thereby enhance the likelihood of gastric N-nitroso compound formation. Three groups of ferrets, one control group (n = 6) and two groups of surgically altered ferrets, one to simulate maximal bile reflux (MABR, n = 6), and the other to model minimal bile reflux (MIBR, n = 7), were studied. Each group's response to an exogenously administered dose of sodium nitrite did not differ significantly with respect to rate of gastric nitrite absorption, with half-lives in the 13-min range. Permeability of gastric mucosa to nitrite did not differ between controls and MIBR ferrets. Mean doubling time of gastric nitrate appeared slowed in surgically altered ferrets. Mean rate of gastric emptying was the same in the three groups, but appeared delayed initially in MIBR ferrets. Thiocyanate concentrations, pH and HCl secretion, all parameters which have been shown to affect gastric nitrite processing, did not differ significantly between groups. Gastric mucosal endoscopic biopsies obtained at 6-month intervals showed no clear difference in degree of mucosal inflammation and/or dysplasia in the three groups. These findings indicate that gastric mucosal neoplasia has not occurred in this model and that changes in parameters favoring gastric N-nitrosation, even if relevant to the disease process, are not apparent at this time.
Ryden
E B
EB
Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge 02139.
Licht
W R
WR
Cabot
E B
EB
Fox
J G
JG
D000818:Animals; D001655:Bile Reflux / Q000378:metabolism*; D001660:Biliary Tract Diseases / Q000378:metabolism*; D005260:Female; D005289:Ferrets; D005744:Gastric Acid / Q000378:metabolism; D005745:Gastric Acidity Determination; D005746:Gastric Emptying; D005753:Gastric Mucosa / Q000378:metabolism*; D009573:Nitrites / Q000378:metabolism*; D010539:Permeability; D013274:Stomach Neoplasms / Q000209:etiology; D013861:Thiocyanates / Q000378:metabolism
D009573:Nitrites; D013861:Thiocyanates; C031760:thiocyanate