Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of Rhinax on gastric damage in different animal models including gastric ulceration induced by a necrotic agent such as 0.6 N HCl, indomethacin, and intragastric distension was studied. Treatment with Rhinax at a dose of 160 mg/kg protected gastric mucosa against the damage induced by oral administration of indomethacin and intragastric distension. The volume and acidity of gastric juice in pyloric ligated rats was reduced by Rhinax. It also significantly promoted gastric mucus secretion in normal animals. On the basis of these observations, we conclude that Rhinax possesses anti-ulcer activity and that the observed activity may be due to the modulation of defensive factors by improvement in gastric cytoprotection.
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PMID:Protection by Rhinax in various models of ulceration in rats. 1003 Jul 26

Heavy alcohol consumption is associated with the development of reflux esophagitis. Among the reasons for this are impairment of the antireflux barrier, stimulation of acid secretion, and altered tissue resistance. To explore the contribution of altered tissue resistance to the development of esophagitis, sections of rabbit esophageal epithelium were mounted in Ussing chambers and exposed luminally to 10% ethanol, acid (HCl, pH 2), or combinations of both. Tissue injury was assessed by measurements of potential difference (PD), short circuit current (Isc) and electrical resistance (R) and by histology. Tissues exposed luminally to HCl for 1 hr exhibited little or no change electrically or morphologically compared to Ringer controls, while luminal exposure to 10% ethanol for 1 hr lowered PD (53 +/- 4%), Isc (30 +/- 1%), and R (31 +/- 5%) and produced cellular edema in the upper layers. Simultaneous exposure to ethanol and acid resulted in significantly greater declines in PD (81 +/- 1%) and Isc (70 +/- 2%), but not R (40 +/- 4%), and greater morphologic damage. Moreover, this vulnerability of ethanol-exposed tissues to acid was demonstrable at generally innocuous levels of acidity (pH 2-4), after only short periods of ethanol exposure (10 min) and with delays for acid exposures of up to 1 hr following ethanol removal from the bathing solution. In conclusion, ethanol has a direct noxious effect on esophageal epithelium, which predisposes the tissue to acid injury. Tissue vulnerability develops with even short exposures to clinically relevant concentrations of ethanol, lasts for at least 1 hr after ethanol clearance, and transforms relatively innocuous concentrations of acid into damaging agents. These results support the likelihood that ethanol's ability to alter tissue resistance plays an important role in the development of reflux esophagitis in humans.
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PMID:Esophageal exposure to ethanol increases risk of acid damage in rabbit esophagus. 1006 14

Croton cajucara Benth. (Euphorbiaceae) is widely used in Amazonian folk medicine for the treatment of a wide range of gastrointestinal symptoms. The essential oil from its bark was investigated for acute toxicity in mice and for its ability to prevent the formation of ulceration of the gastric mucosa in different models of experimentally induced gastric ulcer in mice and rats. When previously administered orally at a dose of 100 mg kg(-1), the essential oil significantly reduced (P < 0.01) the gastric injury induced by hypothermic restraint stress (48%), indomethacin (47%), ethanol (86%) and pylorus ligature models (87%) in rats. In the HCl/ethanol-induced gastric ulcer model in mice, at oral doses of 100 and 200 mg kg(-1), the essential oil from C. cajucara significantly reduced (P < 0.01) the formation of gastric lesions by 52% and 67%, respectively, when compared with the control group. In rats submitted to pylorus ligature, the essential oil given orally increased the volume of gastric juice when compared with the control group (P < 0.01). When the essential oil (100 mg kg(-1)) was administered intraduodenally to mice, significant modifications were found in gastric parameters such as pH and total acid content after oil treatment. We observed significant changes (P < 0.01) in gastric juice parameters such as an increase in volume and a decrease in gastric acidity (pH and total acid content). The acute toxicologic effects of the essential oil from C. cajucara were assessed in mice. The LD50 values were 9.3 g kg(-1) by the oral route and 680 mg kg(-1) by the intraperitoneal route. The good yield of essential oil obtained from dried C. cajucara bark (1%) as well as its anti-ulcerogenic activity and low toxicity suggest that pharmacological studies of this substance as a potential new anti-ulcerogenic drug are warranted.
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PMID:Effects of an essential oil from the bark of Croton cajucara Benth. on experimental gastric ulcer models in rats and mice. 1034 36

Two varieties of finger millet (Eleusine coracana)-a tannin-containing red variety, CO13, and nontannin white variety, CO9-processed by treatment with enzymes (cellulase and hemicellulase) and fermentation with starters (from previously fermented finger millet batter), achieved the desirable goals of reduced fermentation time (12 h), increased acidity (2.2 to 2.4%), enhanced in vitro protein digestibility (IVPD) (14 to 26%), and mineral availability compared to 48 h uncontrolled natural fermentation (Usha Antony and Chandra, 1998). Fermentation with starters alone increased titratable acidity (1.02 to 1.88%), IVPD (5. 5 to 22%) and mineral availability, and decreased phytate (23 to 26%) and tannin (10.8 to 40.5%) in the millets. Enzymatic treatment (3 h, 50 degrees C) did not significantly alter the pH, phytate, tannins, IVPD, or HCl-mineral extractability but enhanced fermentative changes. Overall, the changes were marked when the 48 h starter was used and the improvements in nutrient availability was greater in the CO13 variety.
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PMID:Enzymatic treatment and use of starters for the nutrient enhancement in fermented flour of red and white varieties of finger millet (Eleusine coracana). 1055 88

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.
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PMID:Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection. 1058 48

It was established in the experiments determining the influence of the mushroom powder on acidity of the HCl solution by means of ionometrical method that in 15 minutes after introduction 3 gram of the powder pH of the solution increases from 1.62 up to 2.64. The stable meaning of the solution pH (without fall) can be (held) the same in the presence of the powder more than 23 hours. The mushroom powder reduces the high content of the ions Pb2+ and Cu2+ in the solution from 8.8 x 10(-6) up to 3.3 x 10(-6) and from 11.8 x 10(-6) up to 8.6 x 10(-6) mole/ml correspondingly. The trustworthy reduction (fall) of the concentration of the ions Zn2+ and Cd2+ in the filtrate was not discovered (found out). To determine the content of metal in the solution the method of flaming atomic adsorption.
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PMID:[Antacid and sorption properties of mushroom powder made of dried solids (Pleurotus ostreatus)]. 1064 Dec 77

In the rat stomach, evidence has been provided that capsaicin-sensitive sensory nerves (CSSN) are involved in a local defense mechanism against gastric ulcer. In the present study capsaicin or resiniferatoxin (RTX), a more potent capsaicin analogue, was used to elucidate the role of these sensory nerves in gastric mucosal protection, mucosal permeability, gastric acid secretion and gastrointestinal blood flow in the rat. In the rat stomach and jejunum, intravenous RTX or topical capsaicin or RTX effected a pronounced and long-lasting enhancement of the microcirculation at these sites, measured by laser Doppler flowmetry technique. Introduction of capsaicin into the rat stomach in very low concentrations of ng-microg x mL(-1) range protected the gastric mucosa against damage produced by topical acidified aspirin, indomethacin, ethanol or 0.6 N HCl. Resiniferatoxin exhibited acute gastroprotective effect similar to that of capsaicin and exerted marked protective action on the exogenous HCl, or the secretagogue-induced enhancement of the indomethacin injury. The ulcer preventive effect of both agents was not prevented by atropine or cimetidine treatment. Capsaicin given into the stomach in higher desensitizing concentrations of 6.5 mM markedly enhanced the susceptibility of the gastric mucosa and invariably aggravated gastric mucosal damage evoked by later noxious challenge. Such high desensitizing concentrations of capsaicin, however, did not reduce the cytoprotective effect of prostacyclin (PGI2) or beta-carotene. Capsaicin or RTX had an additive protective effect to that of atropine or cimetidine. In rats pretreated with cysteamine to deplete tissue somatostatin, capsaicin protected against the indomethacin-induced mucosal injury. Gastric acid secretion of the pylorus-ligated rats was inhibited with capsaicin or RTX given in low non-desensitizing concentrations, with the inhibition being most marked in the first hour following pylorus-ligation. Low intragastric concentrations of RTX reduced gastric hydrogen ion back-diffusion evoked by topical acidified salicylates. It is concluded that the gastropotective effect of capsaicin-type agents involves primarily an enhancement of the microcirculation effected through local release of mediator peptides from the sensory nerve terminals. A reduction in gastric acidity may contribute to some degree in the gastric protective action of capsaicin-type agents. The vasodilator and gastroprotective effects of capsaicin-type agents do not depend on vagal efferents or sympathetic neurons, involve prostanoids, histaminergic or cholinergic pathways.
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PMID:Capsaicin-sensitive afferent sensory nerves in modulating gastric mucosal defense against noxious agents. 1067 23

(R)-alpha-methylhistamine, a selective agonist of histamine H(3) receptors, is capable of protecting the gastric mucosa against differently acting damaging agents. The objective of the present study was to determine whether H(3) receptors mediate its protective action in the rat. Gastric mucosal lesions were induced intragastrically (i.g.) by 0.6 N HCl, 1 ml rat(-1). (R)-alpha-methylhistamine, 100 mg kg(-1) i.g., substantially reduced the severity of macroscopically and histologically assessed damage caused by concentrated acid. Prior treatment with highly selective H(3)-receptor antagonists, ciproxifan (0.3, 1 and 3 mg kg(-1) i.g.) and clobenpropit (3, 10 and 30 mg kg(-1) i.g.), dose-dependently inhibited the protection exerted by (R)-alpha-methylhistamine up to a complete reversal. When given alone at high doses, both antagonists tended to worsen the HCl-induced histologic damage. During basal conditions, (R)-alpha-methylhistamine, 100 mg kg(-1) i. g., caused a significant increase in titratable acidity of the gastric juice. Prior treatment with ciproxifan (3 mg kg(-1) i.g.) and clobenpropit (30 mg kg(-1) i.g.) did not alter the secretory response to (R)-alpha-methylhistamine. Clobenpropit alone, but not ciproxifan, increased the volume of gastric juice, and both compounds alone had no effect on titratable acid. Present findings support evidence that H(3) receptors are actively involved in the maintenance of gastric mucosal integrity, with no apparent role in the regulation of basal gastric acid secretion.
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PMID:Histamine H(3)-receptor antagonists inhibit gastroprotection by (R)-alpha-methylhistamine in the rat. 1078 Sep 63

A method has been developed for the speciation of trace dissolved Fe(II) and Fe(II) in water by on-line coupling of flow injection separation and preconcentration with inductively coupled plasma mass spectrometry (ICPMS). Selective determination of Fe(III) in the presence of Fe(II) was made possible by on-line formation and sorption of the Fe(III)-pyrrolidinecarbodithioate (PDC) complex in a PTFE knotted reactor over a sample acidity range of 0.07-0.4 mol L(-1) HCl, elution with 1 mol L(-1) HNO3, and detection by ICPMS. Over a sample acidity range of 0.001-0.004 mol L(-1) HCl, the sum of Fe(III) and Fe(II), i.e., Fe(III + II), could be determined without the need for preoxidation of Fe(II) to Fe(III). The concentration of Fe(II) was obtained as the difference between those of Fe(III + II) and Fe(III). With a sample flow rate of 5 mL min(-1) and a 30-s preconcentration time, an enhancement factor of 12, a retention efficiency of 80%, and a detection limit (3s) of 0.08 microg L(-1) were obtained at a sampling frequency of 21 samples h(-1). The relative standard deviation (n = 11) was 2.9% at the 10 microg L(-1) Fe(III) level. Recoveries of spiked Fe(III) and Fe(II) in local tap water, river water, and groundwater samples ranged from 95% to 103%. The concentrations of Fe(III) and Fe(II) in synthetic aqueous mixtures obtained by the proposed method were in good agreement with the spiked values. The result for total iron concentration in the river water reference material SLRS-3 was in good agreement with the certified value. The method was successfully applied to the determination of trace dissolved Fe(III) and Fe(II) in local tap water, river water, and groundwater samples.
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PMID:Speciation of dissolved iron(III) and iron(II) in water by on-line coupling of flow injection separation and preconcentration with inductively coupled plasma mass spectrometry. 1078 57

The ability to promote chloride-attachment ions of the form [M + Cl]- in negative ion electrospray ionization mass spectrometry (ESI-MS) has been developed using chlorinated solvents such as chloroform and carbon tetrachloride. This approach expands the current capabilities of negative ion ESI-MS by enabling detection of analytes that lack acidic sites and thus exhibit weak [M - H]- signals. In contrast to the remote-site collision-induced dissociation (CID) often observed in positive ion ESI-MS/MS for alkali metal cation adducts, the decomposition of chloride adducts usually proceeds via competitive dissociations to form Cl-, which is not structurally informative, or [M - H]-. The latter can provide structural information via consecutive decompositions. For compounds having higher gas-phase acidities than HCl, a low CID collision energy can promote the formation of [M - H]-, whereas for the majority of compounds with lower gas phase acidities than HCl, higher collision energies generally improve the relative yield of [M- H] . Because chloride attachment occurs primarily at electrophilic hydrogens, the daughter ion ratio, Cl-/[M - H]-, depends primarily upon the difference in gas phase acidity between the analyte molecule and HCl. At higher collision energies, entropic factors take on increased importance in determining the product ratio. The difference between the deltaS(0) terms for formation of Cl and formation of [M - H]- has been estimated for a series of substituted phenols and a series of acetic acid analogs. Finally, a novel neutral loss of CH3Cl from glycerophosphocholine and from ganglioside GM3 methyl ester is reported.
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PMID:Formation and decompositions of chloride adduct ions, 1107 56


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