title: Trophic effects in the acid-producing part of the rat stomach after pyloric stenosis.
abstract: BACKGROUND
  Pyloric stenosis produces gastric hypersecretion and is thought to stimulate the growth of the gastric mucosa in the rat, the dog, and man. However, the mechanisms behind the hypersecretion and the trophic effect of pyloric stenosis are little known. The purpose of the present study was to examine whether the postulated trophic effects described include growth of the histamine-producing enterochromaffin-like (ECL) cells and whether circulating gastrin can be held responsible.
  
  
  METHODS
  Pyloric stenosis was produced in rats by tying a ligature around the pylorus, thereby narrowing the passage through the sphincter. The animals were left for 4 to 12 weeks.
  
  
  RESULTS
  The operation dilated the stomach, increased the serum gastrin concentration approximately twofold, and increased the oxyntic mucosal weight, volume, and surface area but not the mucosal thickness and total DNA content. The interglandular space was increased, and the DNA concentration was reduced. The density of the ECL cells (that is, the number of ECL cells per visual field) was reduced at 4 weeks and back to control values at 8 and 12 weeks. The calculated total volume of the ECL cell population was unchanged at first but showed a less than twofold increase 12 weeks after the operation. The volume density of the ECL cells (that is, the proportion of the mucosa made up of ECL cells) was reduced at 4 and 8 weeks and was back to normal at 12 weeks. The ECL cells are rich in histidine decarboxylase (HDC); whenever the cells are stimulated, the enzyme activity increases. The HDC activity in the oxyntic mucosa was reduced at first and returned to control values 12 weeks later.
  
  
  CONCLUSIONS
  Pyloric stenosis per se does not affect the total number of oxyntic mucosal cells, but causes the ECL cell population to grow somewhat, probably because of the moderate hypergastrinemia. Interestingly, however, there was no increase in the HDC activity, suggesting that the ECL cells are not much activated by the operation.
authors.affiliation: Dept. of Pharmacology, University of Lund, Sweden.
authors.forename: D
authors.initials: D
authors.lastname: Chen
authors.forename: C M
authors.initials: CM
authors.lastname: Zhao
authors.forename: A G
authors.initials: AG
authors.lastname: Nylander
authors.forename: F
authors.initials: F
authors.lastname: Sundler
authors.forename: R
authors.initials: R
authors.lastname: Håkanson
mesh_terms: D000818:Animals; D002452:Cell Count; D004195:Disease Models, Animal; D004759:Enterochromaffin Cells / Q000473:pathology*; D005755:Gastrins / Q000502:physiology; D005758:Gastritis, Hypertrophic / Q000209:etiology* / Q000473:pathology*; D008297:Male; D010295:Parietal Cells, Gastric / Q000473:pathology; D011707:Pyloric Stenosis / Q000150:complications*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D005755:Gastrins