epidermal-growth-factor has been researched along with Gastric-Fistula* in 2 studies
2 other study(ies) available for epidermal-growth-factor and Gastric-Fistula
Article | Year |
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Effects of orally administered human epidermal growth factor on natural and delayed healing of acetic acid-induced gastric ulcers in rats.
We examined the effects of orally administered human epidermal growth factor (hEGF) on healing of acetic acid-induced gastric ulcers in rats. hEGF, given twice daily at 30 and 100 micrograms/kg for 2 weeks or at 100 micrograms/kg for 4 weeks to rats with ulcers, had no effect on natural healing or the gastric secretion, delayed one caused by indomethacin. Oral hEGF had no effect on basal histamine-stimulated gastric secretion, and stomach weight. These results indicate that oral hEGF has no biological activity on the pathophysiology of the stomach. Topics: Acetates; Animals; Anti-Ulcer Agents; Epidermal Growth Factor; Gastric Acid; Gastric Fistula; Histamine; Indomethacin; Male; Pylorus; Rats; Stomach Ulcer | 1990 |
Effects of epidermal growth factor on gastrointestinal secretions.
Epidermal growth factor (EGF) has been reported to stimulate epithelial cell proliferation and to inhibit gastric H+ secretion, but no details of the latter effect have been studied. This paper reports the effects of EGF on gastric and pancreatic secretions induced by various stimulants in vivo on conscious dogs and in vitro on isolated rabbit gastric glands. EGF was found to be an effective inhibitor of H+ secretion induced from the fully innervated and vagally denervated portions of the stomach stimulated by secretagogues activating receptors of the parietal cells (pentagastrin, histamine, and urecholine) and by natural stimulants such as sham or ordinary feeding. It appears to act directly on the parietal cells, as the inhibitory effect in vivo was not accompanied by any change in postprandial serum gastrin level. In addition, EGF was found to suppress H+ formation in the isolated gastric glands, both under resting conditions and after stimulation with histamine, carbachol, or dibutyryl cAMP. EGF failed to affect pancreatic response to exogenous hormones (secretin and cholecystokinin) but reduced postprandial secretion probably because of inhibition of H+ secretion from the subsequent reduction in duodenal acid loads. We conclude that EGF is a potent, specific, and direct inhibitor of H+ secretion from the parietal cells and that it does not affect alkaline gastroduodenal or pancreatic secretion. Topics: Animals; Dogs; Epidermal Growth Factor; Gastric Acid; Gastric Fistula; Gastric Juice; Kinetics; Mice; Pancreatic Juice; Pentagastrin; Secretin; Sincalide; Time Factors | 1984 |