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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinically, it is true that gastric ulcer is more common along the lesser curvature and less common along the greater curvature. To elucidate this difference in ulcerognesis, two experimental ulcers were prepared in dogs at the sites, one at the angular incisure and the other at the corresponding greater curvature after the method by Hatafuku & Thal. The fates of these ulcers studied endoscopically, macroscopically, histologically and with the use of microangiography. The results obtained are summarized as follows. 1) When two ulcers only were prepared, better healing was consistent for the greater curve ulcer. 2) Experimental ulcers with simultaneous ligation of gastric vessels resulted in poor healing of both ulcers, though the greater curve ulcer showed better healing than the lesser curve ulcer. 3) Endoscopically, dogs with vessel ligation showed antral congestion and edema. These findings, however, disappeared in 3 to 4 weeks. 4) Histamine injection accelerated the rate of early perforation and both experimental ulcers showed no tendency of healing. In conclusion, delayed healing was almost consistent for the lesser curve ulcer under various conditions. The cause for this may be explained by the increased motility with repeated ischemic condition at the lesser curvature.
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PMID:[Studies on predilection area of gastric ulcer viewed from healing process of experimental gastric ulcers (author's transl)]. 75 Jun 85

Effects of carbenoxolone Na on acute or chronic types of gastric lesions or ulcer models produced in rats, guinea pigs, or dogs were studied. Carbenoxolone Na, given either orally or intraperitoneally, produced a significant inhibition of stress-induced gastric lesions in intact or in pylorus-ligated rats. Acetylsalicylic acid (ASA)-induced or serotonin-induced gastric lesions in rats were also inhibited significantly by pretreatment with the drug. However, carbenoxolone Na did not affect the development of Shay ulceration in rats even though the peptic activity in gastric juices was markedly reduced by the drug. Histamine-induced gastric lesions in guinea pigs were not prevented by pretreatment with carbenoxolone Na. Although carbenoxolone Na, given for 10-20 days, did not promote the healing of stress-induced gastric lesions and acetic acid gastric jlcers in rats, it significantly accelerated the healing of chronic gastric ulcer produced in dogs by 3 weeks' treatment. Carbenoxolone Na prevented the acid back-diffusion caused by ASA without any influence on Na+ efflux in pylorus-ligated rats.
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PMID:Effects of carbenoxolone Na on acute and chronic gastric ulcer models in experimental animals. 98 16

Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) can cause varying degrees of gastroduodenal mucosal damage. These agents are most frequently used for the treatment of rheumatic diseases because they are highly effective in reducing joint pain and swelling. Histamine H2-receptor antagonists, omeprazole, sucralfate, and misoprostol are drugs available for the treatment of gastric mucosal damage caused by NSAIDs. In controlled clinical studies, all these drugs effectively heal gastric and duodenal injury if NSAIDs are discontinued. However, current data suggest that if NSAIDs are continued while gastrointestinal damage is present, only misoprostol and omeprazole have demonstrated efficacy in healing gastric mucosal injury. Misoprostol also effectively heals NSAID-induced duodenal injury. At this time, no data exist on the efficacy of other antiulcer drugs in healing duodenal erosions or ulceration if NSAID administration is continued. Regarding prevention of NSAID-induced gastric ulcer, controlled clinical studies with H2 antagonists and sucralfate have failed to show any therapeutic benefit. Ranitidine, however, has shown efficacy in preventing NSAID-induced duodenal ulcers. The coadministration of misoprostol with NSAIDs to patients who have either osteoarthritis or rheumatoid arthritis prevents the development of gastric and duodenal ulcers. Based on current published information, this property distinguishes misoprostol from other antiulcer drugs.
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PMID:Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs. 139 9

The effects of antrectomy and proximal gastric vagotomy on the metabolism of histamine in the human gastric mucosa were studied in the basal state and during pentagastrin stimulation in patients with duodenal or gastric ulcer disease. Mucosal biopsy specimens were taken from the antral and oxyntic gland areas, whereafter histamine content, histidine decarboxylase activity, and histamine methyltransferase activity were simultaneously assayed. Vagotomy was followed by a decrease in the acid secretory capacity and an increase in basal serum gastrin levels. Histamine content of the oxyntic mucosa increased after vagotomy, but the ability of pentagastrin to form new amounts of the amine was impaired. Antrectomy caused a decrease in acid secretion and a fall in gastrin concentrations. Basal histamine content and rate of amine formation in the remaining oxyntic mucosa were unaffected by antrectomy. Antrectomy impaired the ability of pentagastrin to release histamine. Histamine methyltransferase was not affected by pentagastrin, vagotomy, or antrectomy. In conclusion, both antral gastrin and the vagus nerve seem to exert a regulatory influence on the metabolism of histamine in the human oxyntic mucosa. The withdrawal of these factors either causes impaired ability of pentagastrin to release histamine from its storage site or counteracts the ability of pentagastrin to accelerate histamine synthesis.
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PMID:The role of the antrum and the vagus nerve in the metabolism of histamine in the human gastric mucosa. 177 87

Histamine is formed by decarboxylation of the amino acid histidine and is found both in plants and in animals, including man. In man it has important biologic functions. To assess the physiologic role of histamine, however, it is necessary to have a reliable and convenient method to determine its concentration in biologic fluids and tissue. Histamine has been determined by bioassay, chemically by different modification of a fluorometric method, by radioenzymatic methods, and, recently, by immunoassays. Immunoassay of histamine has, however, been difficult to establish, mainly as a result of problems with the production of an antibody with histamine specificity. This is due to the general occurrence of histamine in all animal species. By binding histamine to different ligands, several researchers have succeeded in producing antibodies against antigens in which histamine is integrated. Treating samples and histamine standard with the same coupling agent, reliable and specific radioimmunoassays of histamine have been established. We have for some years utilized a commercial radioimmunoassay of histamine and confirmed its convenience, specificity, and sensitivity. In some patients taking a histamine-2 blocker (cimetidine or ranitidine) we have detected an increase in plasma histamine which also tended to be increased after proximal gastric vagotomy and in patients with gastric ulcer compared with patients with duodenal ulcer. In rats treated with high doses of omeprazole for 90 days we found an increase in the enterochromaffin-like cell mass and in histamine concentration in the oxyntic mucosa which was reflected by an increase in plasma histamine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Radioimmunoassay of histamine. 204 35

Changes in the contents of various amines and histidine decarboxylase (HDC) activity in the gastric mucosa during the healing process of acetic acid induced gastric ulcer in rats were sequentially examined in the ulcer region and intact region at 2, 10, 40, 80, 180 and 365 days after the operation. The following results were obtained: 1) Histamine (HA) content in the ulcer region was decreased as compared with the intact region at 2 and 10 days and returned to the control level in 40 days. After 180 days, the contents in the ulcer region and intact region were also increased as compared with that of the normal control region. 2) Changes in serotonin (5-HT) content as well as HA content were observed. 3) Norepinephrine content in the ulcer region was decreased as compared with the intact region at 2, 10, 80 and 180 days. 4) HDC activity in the ulcer region was decreased as compared with the intact region at 2, 10 and 40 days, and a lower level was maintained still at 180 days. 5) In the relapse and recurrence of gastric ulcer at 365 days, HA and 5-HT contents in the intact region and ulcer region were not different from those in healing rats, but the contents of these amines were higher at 180 days. The results suggest that the change of HA, 5-HT contents and HDC activity in the gastric mucosa may be one of the factors involved in the relapse and recurrence of chronic ulcers.
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PMID:[Changes in amine contents and regulating enzyme activity of gastric mucosa during the healing process of acetic acid induced ulcer in rats]. 273 3

Isolated human gastric glands provide an in vitro model that can yield significant information about the mechanisms regulating gastric acid secretion at the parietal cell level. Aminopyrine, a weak base that accumulates in acid compartments, has been used as an indirect probe of H+ secretion. By means of a microscale technique it was possible to isolate oxyntic glands from gastroscopic biopsy specimens and thereby enable studies of healthy subjects and non-operated ulcer patients. Histamine (5.4 X 10(-5) M) and db-cAMP (10(-3) M) both induced a pronounced response, whereas the response to carbachol (4.5 X 10(-6) M), although still statistically significant, was less potent. The response to stimuli was twice as high in duodenal ulcer patients as in normal individuals. In contrast, the response in patients with a gastric ulcer located either in the prepyloric region or at the minor curvature on the antrum-corpus border was of the same magnitude as in healthy subjects. Pentagastrin did not induce any response in isolated gastric glands from normal individuals. Gastric acid secretion in vitro, measured as aminopyrine accumulation, did not decrease with increasing age of the individuals.
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PMID:Acid secretion in isolated gastric glands from healthy subjects and ulcer patients. 299 68

Adenylate cyclase (AC) in response to prostaglandin E2 (PGE2) and histamine was studied in morphologically different biopsy specimens from human gastric mucosa. The activities of the enzyme were log-normally distributed and did not differ between males and females. PGE2 activated AC in a concentration-dependent manner in normal gastric mucosa (n = 57), chronic superficial gastritis (GI, 18), chronic gastritis with beginning atrophy (GII, 10), chronic atrophic gastritis (GIII, 24), gastric ulcer (GU, 39), duodenal ulcer (DU, 32), and biopsies of patients operated according to Billroth II (BII, 20) and was most efficacious in GIII and BII. Histamine, which was studied in normal gastric mucosa (n = 27), DU (n = 20), GU (n = 13), and BII (n = 18), stimulated AC most efficaciously and potently in DU, was less effective in normal gastric mucosa and GU, and had no effect at all in BII. Cimetidine treatment of DU patients did not change the PGE2 action, while the degree of stimulation by histamine was reduced. The data indicate characteristic differences of the PGE2- and histamine-sensitive AC in the mucosal samples of these patients.
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PMID:Morphologically different biopsy specimens of the human gastric mucosa. II. Adenylate cyclase activity in response to prostaglandin E2 and histamine. 346 52

Mild stress of restraint for 10 min at an ambient temperature of 18 degrees C increased serum corticosterone levels in rats considerably. Histamine given intravenously prior to restraint alone significantly further intensified the stress-induced elevation of serum corticosterone. Dimaprit and cimetidine failed to modify corticosterone responses to the mild stress. Severe stress of restraint and cold of 3 h duration increased serum corticosterone and free fatty acid levels considerably. Histamine given prior to stress exposure left the corticosterone and hyperlipaemic responses to severe stress unchanged. Dimaprit inhibited and cimetidine intensified the stress-induced hyperlipaemia. The most striking finding in the present experiment was a powerful inhibition of gastric stress ulcer generation by intraventricularly administered histamine. Dimaprit was similarly effective. This strong anti-ulcer effect of histamine was abolished by intraventricular pretreatment of rats with either H1- or H2-receptor antagonists, chloropyramine or cimetidine. The results may suggest that in the rat a mild stress does not fully activate central histaminergic pathways involved in corticosterone responses. During severe stress histamine considerably prevents gastric ulcer generation and both H1- and H2-receptors mediate this action of histamine.
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PMID:The involvement of central histamine receptors in stress-induced responses of serum corticosterone and free fatty acids and in gastric ulcer development. 611 42

Nonsteroidal anti-inflammatory drugs (NSAIDs) are most frequently used for the treatment of rheumatic disease due to their anti-inflammatory and analgesic properties. All NSAIDs have the potential to cause damage to the gastrointestinal (GI) tract and have been associated with the induction of peptic ulcers and massive life-threatening bleeding. The therapeutic approaches for the treatment and prevention of NSAID-induced ulcers is critically reviewed using data derived from carefully controlled, world-wide clinical studies with anti-ulcer drugs. Histamine (H2) antagonists, omeprazole, sucralfate and E-prostaglandin (PGE) analogs are effective for the treatment of NSAID-induced gastric and duodenal ulcers, if NSAIDs are discontinued. However, if NSAIDs are continued while GI damage is present, the PGE analogs misoprostol, arbaprostil and enprostil have shown efficacy in healing NSAID-induced ulcers. Furthermore, one limited clinical study demonstrated that omeprazole has efficacy in healing NSAID-associated ulcers. Neither H2 antagonists, sucralfate and sulglycotide (a cytoprotective drug) have shown efficacy in preventing NSAID-induced gastric ulcers. However H2 antagonists have shown efficacy in preventing NSAID-induced duodenal ulcers. In contrast, only misoprostol prevents the development of NSAID-induced gastric and duodenal ulcers. Such pharmacological observations suggest that the pathophysiologic mechanisms for the induction of NSAID-induced gastric ulcer are distinctly different from those of NSAID-induced duodenal ulcers. Mild diarrhea and GI intolerance were the predominant adverse reactions experienced by patients receiving synthetic PGEs, particularly enprostil and arbaprostil. From the published data, we conclude that misoprostol is the only anti-ulcer drug proven to be well tolerated and effective for the treatment and prevention of NSAID-induced gastric and duodenal ulcers in patients receiving chronic NSAIDs therapy.
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PMID:Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update. 759 35


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