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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of hypertonic solutions on gastric acidity and on experimental gastric and duodenal ulcers as well as on gastric prostaglandins (PGs) were studied in the rat. The oral administration of a 10% NaCl solution resulted in complete absence of free acidity and very significant reductions in total acidity 24 h after pyloric ligation. The antiulcer effect of hypertonic saline was studied in three experimental models. In pyloric-ligated rats, both the incidence and the severity of gastric ulcers were remarkably reduced by hypertonic saline treatment. Indomethacin-induced gastric erosions were significantly reduced by hypertonic NaCl or sorbitol and completely prevented by hypertonic xylitol. Cysteamine-induced duodenal ulcers were also significantly reduced by hypertonic solutions of NaCl, xylitol or sorbitol. In the latter model, indomethacin potentiated the ulcerogenic effect of cysteamine and also reduced the efficacy of the hypertonic NaCl gavage. The possible contribution of PGs to these effects was further investigated by analysing PGE in the gastric mucosa and juice. Rats treated orally with hypertonic NaCl solutions had several-fold higher PGE contents in their gastric mucosa as well as higher PGE levels in the gastric juice. It is concluded that hypertonic solutions stimulate endogenous PGE biosynthesis and also exert profound antiulcer effects in the rat. A causal relationship between the two phenomena is suggested.
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PMID:Antiulcer activity of hypertonic solutions in the rat: possible role of prostaglandins. 4 25

To assess the effect of indomethacin on gastric acidity and to identify a potential pharmacodynamic interaction between indomethacin and ranitidine, we measured nocturnal acidity on half-hourly aliquots of gastric contents from 10 volunteers on the seventh day of four dosing regimens given in a randomized double-blind manner. These were indomethacin (50 mg t.d.s.) and ranitidine (300 mg in the evening) together or alone with matching placebos. Median nocturnal acidity on placebo was 41.7 mmol/L (range 67.6-25.1 mmol/L) and was 39.8 mmol/L (63.1-24.0 mmol/L) on indomethacin (N.S.). During ranitidine dosing it was 0.4 mmol/L (21.3-0.0 mmol/L) without and 0.8 mmol/L (43.7-0.0 mmol/L) with concurrent indomethacin, representing 99 and 98% decreases in gastric acidity (P less than 0.01) compared with placebo. Indomethacin did not increase overnight gastric acidity and did not influence the suppression of acidity produced by ranitidine. It is unlikely that the ulcerogenic potential of indomethacin is explicable by an effect on gastric acidity.
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PMID:Effect of ranitidine and indomethacin on nocturnal gastric acidity in normal subjects. 210 83

In the present study the effect of indomethacin-induced prostaglandin deficiency was examined on the release of bombesin-like immunoreactivity (BLI), a putative peptidergic neurotransmitter, from the isolated perfused rat stomach. In addition, gastrin and somatostatin (SLI) secretion was determined. Pretreatment of rats with indomethacin (2 mg/kg X h) resulted in a 3-fold increase of basal BLI secretion. In response to acetylcholine (2 X 10(-6) M) BLI rose from 2,000 to 4,000 pg/min, whereas in controls BLI increased from 400 to 1,400 pg/min. While absolute values for BLI secretion were higher in indomethacin-treated stomachs the relative increase above baseline was lower (100 vs. 250%). In control rats the increase in BLI secretion in response to acetylcholine was abolished when the acidity in the gastric lumen was increased from pH 7 to pH 2. After indomethacin, however, the stimulatory effect of acetylcholine during luminal pH 7 and pH 2 was identical. The decrease of SLI by acetylcholine at luminal pH 7 was abolished in indomethacin-treated stomachs in response to 10(-6) M acetylcholine, and 2 X 10(-6) M had even a stimulatory effect on SLI secretion. Indomethacin pretreatment reduced gastrin secretion at luminal pH 7. These data demonstrate that endogenous prostaglandins exert an inhibitory tone on basal and stimulated BLI and stimulated SLI secretion in the rat stomach. It is suggested that endogenous prostaglandins also inhibit the release of a peptidergic neurotransmitter, similar to their effect on the classical neurotransmitters acetylcholine and norepinephrine.
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PMID:Effect of indomethacin on bombesin-like immunoreactivity, somatostatin and gastrin secretion from rat stomach. 288 61

The purpose of these studies was to determine the role played by endogenous prostaglandins in the development of gastric ulcers produced by indomethacin, and of duodenal ulcers produced by mepirizole in rats. Indomethacin (10 mg/kg subcutaneously) produced gastric ulcers, whereas mepirizole (100 mg/kg subcutaneously) produced exclusively duodenal ulcers. Both drugs, given at ulcerogenic doses, reduced the gastric and duodenal generation of PGE2, PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane B2. In this regard, the extent of reduction was more pronounced after indomethacin than after mepirizole. Despite this greater inhibition of prostaglandin synthesis by indomethacin, this drug did not produce duodenal ulcers, whereas mepirizole was duodenoulcerogenic. In addition, mepirizole increased gastric acid secretion by 74%, whereas indomethacin had no effect on acid secretion. Oral administration of 16,16-dimethyl PGE2, given at nonantisecretory doses (0.5-5 micrograms/kg), prevented formation of indomethacin-induced gastric ulcers, whereas antisecretory doses were required to prevent formation of mepirizole-induced duodenal ulcers. We conclude that a reduction of prostaglandin formation in the duodenal mucosa is not by itself sufficient to induce duodenal ulcers. We hypothesize that three changes, produced by mepirizole, must be present for duodenal ulcers to develop: increased gastric acid secretion, decreased duodenal bicarbonate secretion (as demonstrated earlier), and decreased duodenal content of prostaglandins. The decreased prostaglandin formation, although not causing duodenal ulcers, may lower the resistance of duodenal mucosa to the hyperacidity induced by mepirizole. On the other hand, in the case of gastric ulcers following administration of indomethacin, a decrease in gastric mucosal levels of prostaglandins may play a more important role than changes in gastric acidity.
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PMID:Prostaglandin deficiency by itself is not the cause of mepirizole-induced duodenal ulcers in rats. 362 95

Vagal stimulation by modified shamfeeding in healthy subjects induced about fourfold increases of gastric outputs of acid, chloride, sodium and potassium. Prior oral 15(R)15 methyl prostaglandin E2 inhibited dose-dependently the peak and total gastric acid response to modified shamfeeding by lowering both the secreted volumes and the acidity. The inhibition by 15 micrograms of the analogue exceeded 50% and the suppression was submaximal by 140 micrograms. Gastric output of chlorides decreased in a dose-related way. The hydrogen ion output was proportionally more reduced than the chlorides. The analogue did not affect the gastric output of sodium. Potassium decreased in a dose-related way. Indomethacin was without effect on the gastric acid response to shamfeeding but reduced the sodium output compared to in controls and in series with the analogue. Plasma gastrin was slightly but significantly elevated by the shamfeeding procedure. This elevation was absent or even reversed by 15(R)15 Me PGE2. No effect was recorded by indomethacin pretreatment. Vagal stimulation augments both the parietal and non-parietal components of the gastric secretion. Low doses of oral 15(R)15 Me PGE2 were effective in suppressing the vagally stimulated acid secretion. Neutralization by the gastric non-parietal secretion can contribute to reduce the acid response. Blocking of the prostaglandin biosynthesis decreased gastric sodium output, suggesting indirectly that endogenous prostaglandins may be involved in modulating the gastric non-parietal secretion.
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PMID:Effect of graded 15(R)15 methyl prostaglandin E2 and of indomethacin on the gastric secretory and plasma gastrin response to modified shamfeeding. 651 89

The effect of indometacin (3 X 50 mg daily), carprofen (Imadyl) (2 X 150 mg daily) and placebo (3 X daily) on gastric juice secretion, acidity, prostanoid concentration (PGE2, PGF2 alpha and TXB2) and excretion of the major urinary metabolite of PGF (PGF-MUM) were investigated in a single-blind cross-over study in nine healthy volunteers after 3-day treatment periods separated by one-week washout periods between treatments. Indometacin proved to be a classical cyclooxygenase inhibitor (strong inhibition of PGE2 and TXB2 before and after pentagastrin stimulation and of PGF-MUM) while carprofen was an atypical inhibitor (weak inhibition of PGE2 before pentagastrin stimulation and no inhibition after, strong inhibition of TXB2 but without influence on PGF-MUM). The weak inhibition of PGE2-biosynthesis by carprofen might be related to its low incidence of gastric side effects.
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PMID:[The effect of indomethacin and carprofen on gastric prostaglandin biosynthesis]. 659 21

We aimed to evaluate the protective effects of pentoxifylline on alcohol-induced gastric injury, its relation with nitric oxide and prostaglandin synthesis, as well as gastric acidity in rats. Acute gastric mucosal injury was induced by intragastric infusion of 2 ml 98% alcohol. Pentoxifylline was given at 100 mg/kg intraperitoneally. Indomethacin and N(G)-nitro-L arginine were used to inhibit prostaglandin and nitric oxide synthesis, respectively. Macroscopic and microscopic gastric injuries were evaluated. Gastric pH, tissue malondialdehyde levels, oxidized and reduced glutathion (GSSG/GSH) levels, and effects of pentoxifylline on gastric acid output were measured. Pentoxifylline pretreatment significantly reduced macroscopic and microscopic gastric injury. Malondialdehyde level was lower in pentoxifylline treated rats (351.1 +/- 94.1 nmol/g vs 624.3 +/- 234.2 nmol/g). Pentoxifylline has a protective role on alcohol-induced gastric mucosal injury in rats. This effect is not related to synthesis of prostaglandins and changes in gastric acidity but does seem to be related to nitric oxide-mediated pathways. In contrast, pentoxifylline increases gastric acid output significantly.
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PMID:Effects of pentoxifylline on alcohol-induced gastric injury and acid secretion in rats. 1287 Aug 2

This study investigated the involvement of neutrophil infiltration, disturbances in nitric oxide (NO) generation and oxidative stress in indomethacin-induced gastric ulcer, and the possible gastroprotective potentials of leptin, known for its angiogenic effect. Male Wistar albino rats (180-220 g) were allocated into a normal control group, ulcer control group (received a single dose of indomethacin 40 mg/kg p.o.) and an ulcer group pretreated with leptin (10 microg/kg i.p. 30 min before ulcer induction). The animals were killed 6 h after indomethacin administration and their gastric juice, serum and mucosal tissue were used for gastric injury evaluation. Indomethacin produced multiple lesions in glandular mucosa, evidenced by marked increase in gastric ulcer index (GUI) accompanied by significant increases in gastric juice acidity, tissue myeloperoxidase (MPO) activity, serum NO and tissue conjugated diene (CD), and marked decreases in tissue NO and glutathione (GSH) as well as glutathione reductase (GR) and superoxide dismutase (SOD) activities, while gastric juice mucin and tissue glutathione peroxidase (GPx) were not affected. Leptin exerted significant gastroprotection as evidenced by significantly decreased GUI and attenuated neutrophil infiltration. Leptin significantly increased mucin and tissue NO, restored GR and SOD activities and up-regulated GPx activity. It failed to affect acidity, serum NO, GSH and CD. These results suggest that leptin confers significant gastroprotection against indomethacin-induced injury through interfering with neutrophil infiltration, NO production and oxidative stress.
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PMID:Gastroprotective effect of leptin in indomethacin-induced gastric injury. 1818 Oct 30

The gastroprotective mechanism of the natural diterpene ferruginol was assessed in mice and rats. The involvement of gastric prostaglandins (PGE(2)), reduced glutathione, nitric oxide or capsaicin receptors was evaluated in mice either treated or untreated with indometacin, N-ethylmaleimide (NEM), N-nitro-L-arginine methyl ester (L-NAME) or ruthenium red, respectively, and then orally treated with ferruginol or vehicle. Gastric lesions were induced by oral administration of ethanol. The effects of ferruginol on the parameters of gastric secretion were assessed in pylorus-ligated rats. Gastric PGE(2) content was determined in rats treated with ferruginol and/or indometacin. The reduction of gastric glutathione (GSH) content was determined in rats treated with ethanol after oral administration of ferruginol, lansoprazole or vehicle. Finally, the acute oral toxicity was assessed in mice. Indometacin reversed the gastroprotective effect of ferruginol (25 mg kg(-1)) but not NEM, ruthenium red or L-NAME. The diterpene (25 mg kg(-1)) increased the gastric juice volume and its pH value, and reduced the titrable acidity but was devoid of effect on the gastric mucus content. Ferruginol (25, 50 mg kg(-1)) increased gastric PGE(2) content in a dose-dependent manner and prevented the reduction in GSH observed due to ethanol-induced gastric lesions in rats. Single oral doses up to 3 g kg(-1) ferruginol did not elicit mortality or acute toxic effects in mice. Our results showed that ferruginol acted as a gastroprotective agent stimulating the gastric PGE(2) synthesis, reducing the gastric acid output and improving the antioxidant capacity of the gastric mucosa by maintaining the GSH levels.
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PMID:Gastroprotective activity of ferruginol in mice and rats: effects on gastric secretion, endogenous prostaglandins and non-protein sulfhydryls. 1823 73

Several reports have indicated that indomethacin-induced gastropathy is mediated through generation of free radicals, neutrophil infiltration and disturbance in nitric oxide production. Rutin is a potent antioxidant flavonoid. Recently, rutin was reported to inhibit neutrophil infiltration and to modulate nitric oxide production in gastric mucosa. Therefore, the aim of this study was to investigate the protective effect of rutin against indomethacin-induced gastric injury. Accordingly, four groups of rats were used. The first three groups were injected orally with vehicle, rutin (200 mg/kg) and indomethacin (48 mg/kg) respectively. The fourth group was injected with rutin 1 hr before indomethacin. Animals were killed after 6 hr of indomethacin administration. Gastric juice acidity and gastric injury were evaluated directly. Moreover, the activities of myeloperoxidase, superoxide dismutase and the contents of reduced glutathione, thiobarbituric acid reactive substance and total nitrite/nitrate (as a marker of nitric oxide production) were determined in mucosal tissues. Indomethacin increased gastric ulcer index, gastric myeloperoxidase activity, gastric acidity and thiobarbituric acid reactive substance contents compared with control. On the other hand, indomethacin decreased glutathione, nitrite/nitrate contents and superoxide dismutase activity. Histopathological examination of the stomachs of indomethacin-treated rats revealed degenerative changes in gastric tissues. Pre-treatment with rutin protected gastric tissues against indomethacin-induced gastropathy as demonstrated from reduction in the ulcer index, attenuation of histopathological changes and amelioration of the altered oxidative stress and biochemical parameters. These results indicate that rutin has a protective effect against indomethacin-induced gastropathy probably through inhibiting neutrophil infiltration, suppression of oxidative stress generation and replenishing nitrite/nitrate levels regardless of gastric acidity.
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PMID:Gastroprotective effect of rutin against indomethacin-induced ulcers in rats. 2037 37


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