Effect of testosterone, its 5?-reduced metabolites, estradiol, and progesterone on experimental duodenal ulcer formation in male rats

1986 ◽  
Vol 102 (4) ◽  
pp. 1343-1345
Author(s):  
L. A. Loseva ◽  
V. G. Degtyar' ◽  
V. A. Vinogradov ◽  
V. G. Smagin
2005 ◽  
Vol 289 (4) ◽  
pp. G753-G759 ◽  
Author(s):  
Yasutada Akiba ◽  
Michael Jung ◽  
Samedy Ouk ◽  
Jonathan D. Kaunitz

The cystic fibrosis (CF) transmembrane conductance regulator (CFTR) plays a crucial role in mediating duodenal bicarbonate (HCO3−) secretion (DBS). Although impaired DBS is observed in CF mutant mice and in CF patients, which would predict increased ulcer susceptibility, duodenal injury is rarely observed in CF patients and is reduced in CF mutant mice. To explain this apparent paradox, we hypothesized that CFTR dysfunction increases cellular [HCO3−] and buffering power. To further test this hypothesis, we examined the effect of a novel, potent, and highly selective CFTR inhibitor, CFTRinh-172, on DBS and duodenal ulceration in rats. DBS was measured in situ using a standard loop perfusion model with a pH stat under isoflurane anesthesia. Duodenal ulcers were induced in rats by cysteamine with or without CFTRinh-172 pretreatment 1 h before cysteamine. Superfusion of CFTRinh-172 (0.1–10 μM) over the duodenal mucosa had no effect on basal DBS but at 10 μM inhibited acid-induced DBS, suggesting that its effect was limited to CFTR activation. Acid-induced DBS was abolished at 1 and 3 h and was reduced 24 h after treatment with CFTRinh-172, although basal DBS was increased at 24 h. CFTRinh-172 treatment had no effect on gastric acid or HCO3− secretion. Duodenal ulcers were observed 24 h after cysteamine treatment but were reduced in CFTRinh-172-pretreated rats. CFTRinh-172 acutely produces CFTR dysfunction in rodents for up to 24 h. CFTR inhibition reduces acid-induced DBS but also prevents duodenal ulcer formation, supporting our hypothesis that intracellular HCO3− may be an important protective mechanism for duodenal epithelial cells.


Author(s):  
H.X. Bui ◽  
A. delRosario ◽  
M. Abdulla ◽  
F. Ballouk ◽  
V. Bajakian ◽  
...  

Various animal models have often been utilized as the basis of studies of the pathophysiology of peptic ulcer disease, however the ultrastructural changes in the evolution of duodenal ulcers produced in experimental animals have not been well elucidated. Utilizing a surgical method developed for the study of gastric ulcers we have established an experimental duodenal ulcer production technique in the rat which is highly reproducible and readily standardized. In the following time sequence study of experimental duodenal ulcers we present the ultrastructural features of ulcer induction and evolution.Duodenal ulcers were produced in 150-200 gram male Sprague Dawley rats by application of 50% acetic acid for 30 seconds through a 3 mm polyethylene tube to the serosa 1.0-1.5 cm distal to the pyloric sphincter. Routine transmission and scanning electron microscopy were performed on duodenal specimens at specific time points subsequent to surgical ulcer generation. Thin sections were stained with uranyl acetate and lead citrate and examined with a Phillip's EM 300 transmission electron microscope. For SEM, specimens were post-fixed in 2% osmium for two days, coated with gold/palladium and examined with JEOL JSM-6100 scanning electron microscope (JEOL, Inc., Peabody, MA).


1982 ◽  
Vol 32 (6) ◽  
pp. 1167-1170
Author(s):  
Haruyo KUNIMI ◽  
Susumu OKABE

1986 ◽  
Vol 10 (1) ◽  
pp. 74-77 ◽  
Author(s):  
Tariq Mahmood ◽  
Steven Tenenbaum ◽  
X.T. Niu ◽  
Stanley M. Levenson ◽  
Eli Seifter ◽  
...  

1956 ◽  
Vol 30 (4) ◽  
pp. 583-592 ◽  
Author(s):  
Asher Winkelstein ◽  
Ben F. Bryer ◽  
Leonard J. Druckerman ◽  
Franklin Hollander

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