dinoprost and Gastritis

Aspirin causes peptic ulcers predominately by reducing gastric mucosal cyclooxygenase (COX) activity and prostaglandin synthesis. Because aspirin circulates for only a few hours, we hypothesized that aspirin's inhibitory effect on gastric COX activity must be prolonged. We performed a placebo-controlled experiment in healthy humans to determine the duration of inhibition of aspirin on gastric mucosal COX activity (PGE(2) and PGF(2alpha) synthesis rates). Recovery of gastric COX activity after stopping aspirin was slow and linear. Seventy-two hours after 325-mg aspirin, gastric COX activity was still reduced by 57% (P < 0.001). Duration of inhibition of gastric COX activity was estimated to be 7-8 days after 325-mg aspirin and 5 days after 81-mg aspirin. Recovery of gastric prostaglandin synthesis after 325-mg but not after 81-mg aspirin occurred at slower rates in subjects with Helicobacter pylori-associated gastritis than in those with normal histology. In conclusion, aspirin inhibits gastric COX activity for much longer than predicted from its pharmacokinetic profile, explaining why aspirin at widely spaced intervals is ulcerogenic.

Topics: Adolescent; Adult; Aspirin; Blood Platelets; Cyclooxygenase Inhibitors; Dinoprost; Dinoprostone; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Prostaglandin-Endoperoxide Synthases; Regression Analysis; Stomach Ulcer; Thromboxane A2; Time Factors

To study role of E2 and F2alpha prostaglandins in development of erosive-ulcerative lesions of gastrointestinal tract.. were examined patients with mucosal erosive-ulcerative and inflammatory lesions of gastrointestinal tract, as well as patients with osteoarthritis who received selective and non selective NSAIDs. Determination of E2 and F2alpha endogenous PG group was investigated with help of immunefuoration method with help of R&D Systems, Inc. Control group was 15 healthy patients.. in presented work you can find that there is relationship between degree of reduction of PG level and severity of gastrointestinal mucosal lesion area. The lowest values of PGE2 and PG F2alpha observed in patients with gastric ulcer disease, especially during exacerbation. Patients with low PG synthesis in body increases likelihood of gastropathy as to reception of non-selective COX inhibitors, and at receiving selective COX-2 inhibitors.

Topics: Case-Control Studies; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase Inhibitors; Dinoprost; Dinoprostone; Duodenitis; Gastric Mucosa; Gastritis; Humans; Intestinal Mucosa; Osteoarthritis; Peptic Ulcer

The results of experimental studies support the hypothesis that decreased prostaglandin production might play a part in the gastric mucosal injury induced by alcohol. In this study, it was investigated whether alcohol misuse impairs the synthesis of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) in gastric mucosa.. Fifty six alcoholic patients and 66 subjects without alcohol misuse were included in the study.. Mucosal biopsy specimens were obtained from the antrum and body of the stomach. Maximal synthesis rates of PGE2 and PGF2 alpha were determined in the microsomal fraction of the biopsy specimens.. The rates of synthesis of both prostaglandins in biopsy specimens from the antrum were not significantly different from those obtained in the body. Synthesis of both prostaglandins was significantly reduced in alcoholic patients who abstained less than five days compared with the non-alcoholic group with normal mucosa (PGE2-40%, PGF2 alpha-42% respectively). In non-alcoholic patients with severe gastritis PGE2 synthesis was increased (+30%, p < 0.05) and PGF2 alpha synthesis was decreased (-42.5%, p < 0.025). In alcoholic patients with severe gastritis PGE2 synthesis was depressed by almost 60% (p < 0.001) compared with the non-alcoholic group with severe gastritis. Neither colonisation of Helicobacter pylori nor smoking had a significant influence on the prostaglandin synthesis.. Chronic alcohol misuse is associated with significantly reduced capacity for prostaglandin synthesis in gastric mucosa and this alcohol induced decrease in prostaglandin synthesis is modulated by the presence and degree of gastritis.

Topics: Alcoholism; Dinoprost; Dinoprostone; Female; Gastric Mucosa; Gastritis; Helicobacter pylori; Humans; Male; Middle Aged; Pyloric Antrum; Smoking; Temperance

CI-986 is a potent inhibitor of 5-lipoxygenase and cyclooxygenase pathway product biosynthesis from rat basophilic leukemia (RBL) cells. Because metabolites from these pathways have proinflammatory properties, CI-986 was evaluated in several acute and chronic models of inflammation and hyperalgesia. The compound inhibited swelling in the carrageenan footpad edema, Mycobacterium foot-pad edema and adjuvant arthritis models of inflammation with ID40 values of 1.0, 7.7., and 7.2 mg/kg, respectively. It was roughly equivalent in potency to the standard selective cyclooxygenase inhibitor, naproxen (ID40 = 0.7, 6.3, and 3.8 mg/kg, respectively). CI-986 was also evaluated in the acetic acid induced writhing hyperalgesia assay (ID50 = 0.23 mg/kg) and was approximately equipotent with indomethacin (ID50 = 0.87 mg/kg). Although the effects of CI-986 were similar to those of standard nonsteroidal antiinflammatory drugs (NSAIDs) in the inflammation models, its gastrointestinal profile was unique. CI-986 caused no gastrointestinal irritation at doses up to 200 mg/kg in acute and chronic studies. In contrast, standard NSAIDs caused ulcers at doses of 3.7-37 mg/kg after a single dose. Moreover, CI-986 inhibited the release of LTC4 and PGE2 by gastric mucosa and reduced mucosal and vascular damage induced by oral administration of absolute ethanol to rats. These results indicate that CI-986 is a potent nonulcerogenic antiinflammatory agent with novel pharmacologic properties.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Arachidonic Acid; Arthritis, Experimental; Cyclooxygenase Inhibitors; Dinoprost; Disease Models, Animal; Ethanol; Female; Gastritis; Inflammation; Leukotriene B4; Lipoxygenase Inhibitors; Male; Mice; Pain; Rats; Rats, Wistar; Thiadiazoles; Tumor Cells, Cultured

The blood and urine prostaglandin E2 (PGE2), Prostaglandin F2 alpha (PGF2 alpha) in 106 cases of chronic gastritis and peptic ulcer were investigated by RIA. Meanwhile, the relationship among PGE2, PGF2 alpha and the Syndromes of TCM were approached. The result showed: In comparing with the normal control, the blood and urine PGE2 of 106 cases were obviously higher (P < 0.01), but PGF2 alpha was not (P > 0.05). The urine PGE2 and PGF2 alpha of moderate gastritis were markedly higher than those of mild gastritis (P < 0.05), but there were no significant difference between blood PGE2, PGF2 alpha of moderate gastritis and those of mild gastritis (P > 0.05). The blood PGE2, PGE2/PGF2 alpha ratio of Dampness-Heat in Spleen-Stomach Syndrome and the blood PGE2/PGF2 alpha ratio of incoordination between Liver and Stomach Syndrome were higher than those of Spleen Stomach Deficiency Syndrome in all the cases (P < 0.05). Compared with the normal control, both the decreased amplitude of blood PGE2/urine PGE2 and increased amplitude of blood PGF2 alpha/urine PGF2 alpha ratio showed as following: Spleen-Stomach Deficiency Syndrome > incoordination between Liver and stomach Syndrome > Dampness-Heat in Spleen-Stomach Syndrome. This study suggested: (1) There was a close relation between PGE2 and chronic gastritis and peptic ulcer; (2) There was no correlation between blood PGE2, PGF2 alpha and urine PGE2, PGF2 alpha; (3) PG was possibly a useful objective parameter to the Syndrome Differentiation in TCM.

Topics: Adult; Aged; Dinoprost; Dinoprostone; Female; Gastritis; Humans; Male; Medicine, Chinese Traditional; Middle Aged; Peptic Ulcer; Radioimmunoassay

We measured gastric and duodenal mucosal prostaglandin concentrations in 69 patients with active or inactive duodenal or gastric ulcer disease and 26 non-ulcer controls. Each underwent endoscopy enabling us to obtain multiple biopsies from the gastric body and antrum and from the duodenal bulb and postbulbar duodenum for measurement of mucosal prostaglandin concentrations, as well as a single biopsy from each region for mucosal histology. Using a multivariate linear regression model, we found that neither gastric nor duodenal ulcer disease significantly affected gastric or duodenal mucosal prostaglandin concentrations. Mucosal prostaglandin concentrations were similar at the edge of the ulcer and in the adjacent non-ulcerated mucosa. Neither gender symptoms, smoking, use of H2-receptor antagonists, disease activity, nor Helicobacter pylori infection had an independent effect on mucosal prostaglandins in any region. Gastritis in the body of the stomach was associated with significantly higher prostaglandins, while older age was associated with significantly lower gastric and duodenal prostaglandins. Gastroduodenal mucosal prostaglandins are thus not altered in patients with active or inactive peptic ulcer disease, even when multiple demographic and histologic variables are taken into consideration.

Topics: Age Factors; Dinoprost; Dinoprostone; Duodenal Ulcer; Female; Gastric Mucosa; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metaplasia; Middle Aged; Prevalence; Prospective Studies; Stomach Ulcer

In patients with functional disorders of the stomach and chronic gastroduodenitis, the content of cellular bioregulaters (prostaglandins) in the blood and gastric mucosa was abnormal. The revealed alterations may give rise to a reduction of mucosal resistance because of cytoprotection weakening and derangement of the control over gastric secretion. The data obtained make great contributions to our concepts of the pathogenesis of gastroduodenal pathology and children and provide evidence for new approaches to its prevention and treatment.

Topics: Adolescent; Child; Child, Preschool; Chronic Disease; Dinoprost; Dinoprostone; Duodenitis; Gastric Acid; Gastric Mucosa; Gastritis; Gastroenteritis; Humans

The content of prostaglandins E(PGE) and prostaglandins F2 alpha (PGF2 alpha) was studied in 32 patients with different morphological forms of chronic gastritis at the stage of exacerbation before and after treatment. The PGE content was increased and the PGF2 alpha level was reduced. At the beginning of remission the PGE level was reduced. At the beginning of remission the PGE level decreased as compared with findings before the beginning of treatment while the content of PGF2 alpha did not show essential changes.

Topics: Adolescent; Adult; Chronic Disease; Dinoprost; Female; Gastritis; Humans; Male; Middle Aged; Prostaglandins E; Remission Induction

A study of prostaglandins (PGE2 and PGF2) and cyclic nucleotides (cAMP, cGMP) in the blood and gastric mucosa biopsies was carried out. In peptic ulcer the level of cyclic nucleotides in the blood and gastric mucosa was on an increase. The level of prostaglandins increased in the blood and decreased in the gastric mucosa. A decrease in the level of prostaglandins and cAMP in the blood and gastric mucosa was noted in patients with chronic atrophic histamine refractory gastritis with a simultaneous rise of the cAMP level. It was shown that stable stimulation of cyclic nucleotides resulting in an increase of gastric acid production, might cause ulcer development and exacerbation of disease. In patients with chronic atrophic gastritis changes of prostaglandins and cyclic nucleotides as compared to those in patients with peptic ulcer, were contrary.

Topics: Achlorhydria; Adolescent; Adult; Chronic Disease; Dinoprost; Dinoprostone; Gastric Mucosa; Gastritis; Humans; Middle Aged; Nucleotides, Cyclic; Peptic Ulcer; Prostaglandins E; Prostaglandins F