59Ferrous sulfate was administered i.v. to 12 male beagles. Beginning 11 days later, gastrointestinal microbleeding was determined by comparison of the 59Fe specific activities of 24-h stool collections and of whole blood. During the following 48-day period the dogs received p.o. twice daily a placebo, two tablets containing 650 mg of acetylsalicylic acid (ASA), 22 mg/kg of phenylbutazone, or 24 mg/kg of N-2-[5'-(3"-bromophenyl-2'H-tetrazole]propionyl piperidine (broperamole) in four 7-day tratment periods (each of which was preceded by a 5-day period of no treatment) in complete crossover fashion. Average daily fecal blood volumes of 2.55 ml, 1.94 ml, 0.54 ml, and 0.48 ml were observed after treatment with ASA, phenylbutazone, broperamole, and placebo, respectively. The influence of ASA and phenylbutazone on gastrointestinal microbleeding was statistically greater than that of broperamole, which was equivalent to placebo.
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Stress is known to cause severe adverse effects in the human gastrointestinal tract including mucosal microbleedings and erosions or even gastric ulceration but the mechanism of these complications has not been fully elucidated. The pathogenesis of stress-induced gastric damage involves the fall in Gastric Blood Flow (GBF), an increase in gastric acid secretion and gastric motility, enhanced adrenergic and cholinergic nerve activity and the rise in gastric mucosal generation of reactive oxygen species. The gastric mucosal defense mechanisms against the deleterious effect of stress include the activation of the hypothalamic-pituitary-adrenal axis which has been linked with glucocorticoids release capable of counteracting of stress-induced gastric lesions.
View Article and Find Full Text PDFBackground: Capsaicin is a specific compound acting on capsaicin-sensitive afferent nerves.
Aim: Capsaicin was used to study the different events of human gastrointestinal physiology, pathology, and clinical pharmacology, and possible therapeutic approaches to enhance gastrointestinal mucosal defense in healthy human subjects and in patients with various different gastrointestinal disorders as well as its use with nonsteroidal anti-inflammatory drugs (NSAIDs) in healthy subjects and in patients.
Materials And Methods: The observations were carried out in 198 healthy human subjects and in 178 patients with different gastrointestinal (GI) diseases (gastritis, erosions, ulcer, polyps, cancer, inflammatory bowel diseases, colorectal polyps, cancers), and in 69 patients with chronic (Helicobacter pylori positive and negative) gastritis (before and after eradication treatment).
J Pineal Res
May 2010
Department of Medicine, Thuringia Clinic Georgius Agricola Saalfeld, Teaching Hospital, Gemany.
Melatonin and its precursor, l-tryptophan, have been shown to exert gastroprotective effects in animals, but their influence on the gastric damage by aspirin (ASA) in humans has been sparingly investigated. In this study, we designed to determine the effects of melatonin and l-tryptophan on ASA-induced gastric mucosal damage, gastric microbleeding, mucosal generation of prostaglandin E(2), and plasma melatonin, and gastrin levels. Three groups of healthy male volunteers (n = 30) with intact gastric mucosa received daily for 11 days either ASA alone or that combined with melatonin or tryptophan.
View Article and Find Full Text PDFAim: to study the clinical and morphological manifestations of portal gastropathy in patients with liver cirrhosis (LC).
Subjects And Methods: One hundred and sixty-nine patients with Child-Pugh Classes B and C CL and 150 patients with gastritis and peptic ulcer disease without LC were examined. All the patients underwent fibrogastroscopy and morphological study of the gastric mucosa (GM).
Med Hypotheses
January 2010
Medical Service, Comando Brigata Alpina Julia, Udine, Italy.
A consensus view has emerged favoring an anticancer effect of long-term aspirin use. Aspirin-induced loss of stored iron from chronic gastrointestinal bleeding is proposed as a mechanism underlying this beneficial effect. In iron depletion, less iron may be available for carcinogenesis through free-radical mediated mechanisms and for promotion of tumor growth.
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