BACKGROUND: Transforming growth factor beta3 (TGF-beta3) has been shown to accelerate gastric ulcer healing in rats. However, little is known about the mechanism. In this study we investigated the influence of TGF-beta3 on gastric acid secretion, since gastric hyperacidity is a major cause of gastroduodenal ulcer disease. MATERIAL/METHODS: Male Sprague Dawley rats were equipped with gastric Thomas cannulas and jugular vein catheters. The acute effect of either intravenous TGF-beta3 (400 and 1200 pg/kg/h) or saline (0.15 M) on pentagastrin-stimulated (10 pg/kg/h) gastric acid secretion was evaluated by gastric acid back-titration after 5 days of recovery. Additionally, pentagastrin-stimulated gastric acid secretion was assessed after 48 hours following TGF-beta3 (1200 microg/kg/h) or saline treatment. RESULTS: Pentagastrin significantly increased gastric acid production. TGF-beta3 significantly reduced pentagastrin-stimulated gastric acid secretion in a dose-dependent manner as early as 15 minutes after application (saline: 124.9+/-14.9 microEq H+/15 min, TGF-beta3: 97.7+/-13.1 9 microEq H+/15 min, p

Keywords: Gastric Fistula - surgery, Pentagastrin - administration & dosage, Pentagastrin - antagonists & inhibitors, Transforming Growth Factor beta3, Animals, Dose-Response Relationship, Drug, Gastric Acid - secretion, Gastric Fistula - surgery, Humans, Injections, Intravenous, Intubation, Gastrointestinal, Male, Pentagastrin - pharmacology, Rats, Rats, Sprague-Dawley, Recombinant Proteins - pharmacology, Stomach Ulcer - physiopathology, Time Factors, Transforming Growth Factor beta - pharmacology, Transforming Growth Factor beta3, Wound Healing - drug effects