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  • 1
    Electronic Resource
    Electronic Resource
    Oxidation of alcohols by Fenton's reagent. Effect of copper ion (1971)
    s.l. : American Chemical Society
    Journal of the American Chemical Society 93 (1971), S. 4275-4281 
    Details
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ja00746a031
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  • 2
    Electronic Resource
    Electronic Resource
    Homogeneous Precipitation of Hydrous Tin Oxide Powders at Room Temperature Using Enzymatically Induced Gluconic Acid as a Precipitant (2000)
    Westerville, Ohio : American Ceramics Society
    Journal of the American Ceramic Society 83 (2000), S. 0 
    Details
    ISSN: 1551-2916
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Notes: Hydrous tin oxide powders were precipitated at room temperature via the neutralization of sodium stannate with gluconic acid. The gluconic acid was generated by the oxidation of glucose, with the assistance of a glucose oxidase/catalase system. The hydrous tin oxide, which had a large surface area, was obtained when a high concentration of enzymes was used as a solution. However, the apparent sizes of the precipitates were ∼0.3 μm, independent of the enzyme concentration. The precipitates were converted to tin oxide via calcination at temperatures 〉400°C.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1151-2916.2000.tb01313.x
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  • 3
    Electronic Resource
    Electronic Resource
    Pathways mediating pentagastrin-induced mucosal blood flow response in rat stomachs (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 485-491 
    Details
    ISSN: 1573-2568
    Keywords: pentagastrin ; gastric mucosal blood flow ; acid secretion ; prostaglandin ; adenosine ; luminal H+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanisms of pentagastrin-induced gastric mucosal blood flow (GMBF) response were investigated in anesthetized rats. A rat stomach was mounted on anex vivo chamber, perfused with saline, and GMBF was measured by a laser Doppler flowmetry simultaneously with acid secretion. Pentagastrin infused intravenously produced a dose-dependent increase of GMBF as well as acid secretion, and its effect reached a maximum at 120 µg/kg/hr (maximal dose). Pretreatment with omeprazole (60 mg/kg, intraperitoneally) completely inhibited the acid secretory response and the enhancement of GMBF induced by both submaximal (60 µg/kg/hr) and maximal doses of pentagastrin. In contrast, the luminal perfusion with glycine (200 mM) to remove luminal H+ almost totally attenuated the increase of GMBF caused by the submaximal dose of pentagastrin, without any effect on acid secretion, but partially suppressed such GMBF responses caused by the maximal dose. Subcutaneous pretreatment with indomethacin, a cyclooxygenase inhibitor, significantly mitigated GMBF response caused by both submaximal and maximal doses of pentagastrin, whereas 8-phenyltheophylline (8-PT), an adenosine antagonist, showed a significant inhibition of GMBF response caused by only the maximal dose. However, the combined administration of 8-PT with glycine perfusion further attenuated GMBF response caused by the maximal dose of pentagastrin, and the additional treatment with indomethacin completely blocked this GMBF response. We conclude that pentagastrin-induced GMBF responses are mediated by at least two different pathways; one is related to luminal H+ and the other to the parietal cell activity, depending on the dose of pentagastrin. In addition, the latter pathway may be mediated by adenosine, while endogenous prostaglandins may be involved in both pathways.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02282323
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  • 4
    Electronic Resource
    Electronic Resource
    Mucosal Ulcerogenic Action of Monochloramine in Rat Stomachs (Effects of Polaprezinc and Sucralfate) (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 2156-2163 
    Details
    ISSN: 1573-2568
    Keywords: AMMONIA ; MONOCHLORAMINE ; GASTRIC MUCOSAL LESIONS ; POLAPREZINC ; ZINC L-CARNOSINE ; SUCRALFATE ; H. PYLORI
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of a novel zinc compound polaprezinc[N-(3-aminopropionyl)-L-histidinatozinc] and sucralfateon the mucosal ulcerogenic responses induced bymonochloramine (NH2Cl) were examined in ratstomachs. Oral administration of NH2Cl (≥60mM) produced severe lesions in unanesthetized ratstomachs, with concomitant increase of lipidperoxidation. These lesions were aggravated by sensorydeafferentation but not affected by pretreatment with indomethacinor L-NAME. The mucosal ulcerogenic response toNH2Cl was significantly inhibited by oralpretreatment with either dmPGE2 (10μg/kg), capsaicin (30 mg/kg), or NOR-3 (3 mg/kg), the NO donor. Gastriclesions induced by NH2Cl were also inhibitedby prior oral administration of polaprezinc (3-30 mg/kg)as well as sucralfate (30 and 100 mg/kg). The protectiveeffect of polaprezinc was not affected by anypretreatments such as indomethacin, L-NAME, or sensorydeafferentation, while that of sucralfate wassignificantly mitigated in the presence of eitherindomethacin or L-NAME. On the other hand, mucosal exposureto NH2OH (60 mM) caused a marked PD reductionin ex vivo stomachs made ischemic by bleeding from thecarotid artery, followed by severe gastric lesions.These ulcerogenic and PD responses caused by NH OHplus ischemia were also attenuated by prior applicationof polaprezinc, while dmPGE2 and sucralfateprevented such lesions without affecting the reduced PDresponse. These results suggest that: (1)NH2Cl generated either exogenously orendogenously damages the gastric mucosa, (2) bothpolaprezinc and sucralfate protect the stomach againstinjury caused by NH2Cl, and (3) the mechanisms underlying the protectiveaction of sucralfate may be partly mediated by bothendogenous PGs and NO but may be different from those ofpolaprezinc.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018847324172
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  • 5
    Electronic Resource
    Electronic Resource
    Mechanism by which histamine increases gastric mucosal blood flow in the rat (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 1224-1232 
    Details
    ISSN: 1573-2568
    Keywords: histamine ; gastric mucosal blood flow ; acid secretion ; luminal H+ ; cimetidine ; tripelennamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanism by which histamine increases gastric mucosal blood flow (GMBF) was investigated in the anesthetized rat. The experiment was performed in the presence of tripelennamine, an H1 antagonist, to focus on the relationship between acid secretion (H2-receptor-mediated response) and GMBF. The stomach was mounted on a Lucite chamber, perfused with saline, and GMBF was measured by laser Doppler flowmetry simultaneously with acid secretion. Under these conditions, histamine at the submaximal dose significantly increased GMBF as well as acid secretion, and this increase of GMBF was completely blocked when acid secretion was inhibited by cimetidine or omeprazole. The elevation of GMBF caused by histamine was also significantly attenuated when luminal H+ was removed by intraluminal perfusion with NaHCO3 or glycine. Glycine by itself did not affect the increase of acid secretion induced by histamine and the increase of GMBF caused by isoproterenol, yet significantly inhibited the GMBF response induced by pentagastrin. Intraluminal perfusion with HCl also produced an increase of GMBF in a concentration-related manner, even in the presence of omeprazole during histamine infusion. Pretreatment of the animals with indomethacin significantly blocked the GMBF responses induced by either histamine or luminal HCl. These results suggest that the increase of GMBF during acid secretion induced by histamine may be caused by luminal H+ and involve endogenous prostaglandins in its mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01296071
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  • 6
    Electronic Resource
    Electronic Resource
    Gastric Motility and Mucosal Ulcerogenic Responses Induced by Rats Under Prostaglandin-Deficient Conditions Prokinetic Drugs in (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 251-258 
    Details
    ISSN: 1573-2568
    Keywords: PROKINETIC DRUG ; GASTRIC MOTILITY ; GASTRIC LESION ; PROSTAGLANDIN DEFICIENCY
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was performed to examinewhether gastric prokinetic drugs may induce damage inthe rat stomach under normal and prostaglandin(PG)-deficient conditions. Male SD rats fasted for 18 hrwere administered subcutaneously with threedifferent prokinetic drugs such as metoclopramide (3-60mg/kg), ondansetron (0.3-3 mg/kg), and cisapride (3-30mg/kg). Half the number of these animals were pretreated with indomethacin (5 mg/kg) subcutaneously forinduction of PG deficiency in the stomach.Administration of these drugs increased gastric motoractivity in a dose-dependent manner and expeditedgastric emptying at lower doses than those affectinggastric motility; the potency of the hypermotilityeffect was in the following order: metoclopramide =ondansetron 〉 cisapride. None of these drugs alonecaused gross damage in the stomach, although whitishrough areas were observed in the gastric mucosa alongthe folds. In the rats pretreated with indomethacin,however, both metoclopramide and ondansetron provoked multiple hemorrhagic lesions in the gastricmucosa. Indomethacin at this dose showed over 90%inhibition of cyclooxygenase activity without causingany damage in the stomach, and this PG-deficient effect was not affected by coadministration with theprokinetic drugs. The mucosal ulcerogenic responsesinduced by metoclopramide in the presence ofindomethacin were significantly inhibited by prioradministration of atropine (1 mg/kg) or PGE2 (300μg/kg) at doses that inhibited gastric hypermotilityinduced by metoclopramide. These results suggest that:(1) gastric prokinetic drugs induce damage in ratstomachs under PG-deficient conditions at the doses that enhance gastric motility and emptying but notat the doses that expedite gastric emptying only, and(2) gastric hypermotility has the potential to causegross damage in the stomach, supporting the importance of gastric motility as a pathogenic element ofgastric lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018889129410
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  • 7
    Electronic Resource
    Electronic Resource
    Luminal Calcium in Regulation of Nitric Oxide Release and Acid Secretion in Rat Stomachs After Damage (1999)
    Springer
    Digestive diseases and sciences 44 (1999), S. 515-522 
    Details
    ISSN: 1573-2568
    Keywords: TAUROCHOLATE ; BARRIER DISRUPTION ; LUMINAL Ca2+ ; NITRIC OXIDE ACID SECRETION ; RAT
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated The role of luminalCa2+ in The regulation of nitric oxide (NO)release and acid secretion in The rat stomach followingdamage by sodium taurocholate (TC). Under urethaneanesthesia, a rat stomach was mounted in an exvivo chamber,perfused with saline, and transmucosal potentialdifference (PD), luminal pH, acid secretion, and luminalcontents of Ca2+ and NO were measured beforeand after exposure to 20 mM TC for 30 min, with orwithout coapplication of EGTA (5 mM) and/orCaCl2 (10 mM). Mucosal exposure to TC causeda reduction in PD and a decrease of acid secretion, witha concomitant increase of NO as well as Ca2+ content in thegastric lumen. The increase of NO release as well as The reduced acid response were attenuated by pretreatmentwith L-NAME or coapplication of EGTA, and the latterinhibited the luminal increase of Ca2+. Thechanges caused by L-NAME were antagonized bycoadministration of L-arginine, while those induced byEGTA were partially antagonized by coinstillation ofCaCl2. NeiThe r treatment tested had any effect on gastric PDresponses to TC. These results suggest that: (1) damagein the stomach increases The release of Ca2+as well as NO in the lumen; (2) acid secretion decreases in response to damage by both an NO- andCa2+-dependent mechanism; and (3) theincrease of luminal Ca2+ is an adaptiveresponse of the stomach to damage and may play animportant role in increasing NO production and hence in regulating acidsecretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1026645004918
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  • 8
    Electronic Resource
    Electronic Resource
    Mechanism of Acid Secretory Changes in Rat Stomach After Damage by Taurocholate Role of Nitric Oxide, Histamine, and Sensory Neurons (1997)
    Springer
    Digestive diseases and sciences 42 (1997), S. 645-653 
    Details
    ISSN: 1573-2568
    Keywords: STOMACH ; TAUROCHOLATE ; BARRIER DISRUPTION ; ACID SECRETION ; NITRIC OXIDE ; HISTAMINE ; SENSORY NEURON
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was performed to investigatethe mechanism underlying the acid stimulatory responsein the stomach after damage under the inhibition ofnitric oxide (NO) production byNG-nitro-L-arginine methyl ester (L-NAME). A rat stomach wasmounted in an ex vivo chamber, perfused with saline, andthe potential difference (PD) and acid secretion weremeasured before and after the application of 20 mM taurocholate (TC) for 30 min. Exposure of thestomach to TC caused a PD reduction and a decrease ofacid secretion. Pretreatment with L-NAME did not affectbasal acid secretion but significantly enhanced the acid secretion in the stomach after damagewith TC, without any effect on the PD response. Thiseffect of L-NAME was antagonized by simultaneousadministration of L-arginine but not D-arginine. The luminal appearance of NO was significantlyincreased in the stomach after exposure to TC, and thischange was completely blocked in the presence of L-NAMEor when EGTA was applied together with TC. The enhanced acid secretory response to TC in thepresence of L-NAME was inhibited by pretreatment withcimetidine, FPL-52694 (a mast cell stabilizer), orspantide (a substance P antagonist) or by chemical ablation of capsaicinsensitive sensory neurons.Mucosal exposure to TC increased histamine output in thelumen and decreased the number of metachromaticallystaining cells in the stomach, and these changes were also significantly prevented by FPL-52694,spantide, or sensory deafferentation. These resultssuggest that 1) damage in the stomach may activate theacid stimulatory pathway in addition to the NO-dependent inhibitory mechanism, but the latter effectovercomes the former, resulting in a decrease in acidsecretion, 2) the acid stimulation in the damagedstomach may be mediated by histamine released from the mucosal mast cell which may interact withcapsaicin-sensitive sensory nerves, and 3) L-NAMEunmasks the acid stimulatory response by suppressing theinhibitory mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018875932503
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  • 9
    Electronic Resource
    Electronic Resource
    Effects of Cyclooxygenase-2 Selective and Nitric Oxide-Releasing Nonsteroidal Antiinflammatory Drugs on Mucosal Ulcerogenic and Healing Responses of the Stomach (1998)
    Springer
    Digestive diseases and sciences 43 (1998), S. 2003-2011 
    Details
    ISSN: 1573-2568
    Keywords: CYCLOOXYGENASE-2 INHIBITORS ; NONSTEROIDAL ANTIINFLAMMATORY DRUGS ; ASPIRIN ; GASTRIC ULCER ; ULCER HEALING ; ANTIINFLAMMATORY ACTION
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of selective cyclooxygenase-2 (COX-2)inhibitors (NS-398) and nitric oxide (NO)-releasingaspirin (NO-ASA) on gastric ulcerogenic and healingresponses were examined in comparison with nonselective COX inhibitors such as indomethacin and aspirin(ASA). Hypothermic stress (28-30°C, 4 hr) inducedgastric lesions in anesthetized rats with an increase ofacid secretion. The lesions induced by hypothermic stress were markedly worsened by subcutaneousadministration of both indomethacin and ASA but were notaffected by either NS-398 or NO-ASA, although theincreased acid secretion during hypothermia was not affected by any of the drugs. On the otherhand, the healing of gastric ulcers induced in mice bythermal cauterization (70°C, 15 sec) wassignificantly delayed by daily subcutaneousadministration of indomethacin and ASA as well as NS-398, but not by NO-ASA.COX-2 mRNA was not detected in the intact mucosa but waspositively expressed in the ulcerated mucosa, mostpotently on day 3 after ulceration. Prostaglandin contents in the intact mouse stomach werereduced by indomethacin, ASA, and NO-ASA, while theincreased prostaglandin generation in the ulceratedmucosa was inhibited by all drugs including NS-398.After subcutaneous administration of NO-ASA topylorus-ligated rats and mice, high amounts ofNOx were detected in both the gastriccontents and serum. In addition, both NS-398 and NO-ASAshowed an equipotent antiinflammatory effect againstcarrageenan-induced paw edema in rats as compared withindomethacin and ASA. These results suggest that bothindomethacin and ASA not only increased the mucosalulcerogenic response to stress but impaired the healingresponse of gastric ulcers as well. The former actionwas due to inhibition of COX-1, while the latter effectwas accounted for by inhibition of COX-2 and was mimicked by the COX-2-selective inhibitorNS-398. NO-ASA, although it inhibited both COX-1 andCOX-2 activity, had no deleterious effects on gastriculcerogenic and healing responses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1018846912032
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  • 10
    Electronic Resource
    Electronic Resource
    Increased susceptibility of rat gastric mucosa to ulcerogenic stimulation with aging (1996)
    Springer
    Digestive diseases and sciences 41 (1996), S. 339-345 
    Details
    ISSN: 1573-2568
    Keywords: aging ; mucosal blood flow ; acid back-diffusion ; capsaicin-sensitive sensory neurons ; taurocholate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the influences of aging on gastric damage and gastric mucosal blood flow (GMBF) responses induced by acid back-diffusion, following the barrier disruption, and investigated the relation of capsaicin-sensitive sensory nerves to these changes. Male Fischer rats 3, 13, and 24 months old were used. Under urethane anesthesia, a rat stomach was mounted on a chamber, and gastric potential difference (PD), luminal H+ loss, and GMBF were measured before, during, and after exposure to 20 mM sodium taurocholate (TC) for 30 min, in the presence of 50 mM HCl. Mucosal exposure to TC caused surface cell damage, PD reduction, and acid back-diffusion (luminal H+ loss) in all groups of rats; ΔPD reduction and the amount of H+ loss were not significantly different between young and aged rats. In young rats, a marked increase of GMBF was observed with luminal acid loss following TC treatment, yet it resulted in less damage in the gastric mucosa. In aged rats, however, such GMBF responses were apparently mitigated, leading to a significant worsening of gastric mucosal lesions induced by TC. Mucosal application of capsaicin (0.1 mg/ml) caused an increase of GMBF in young rats, but this response was significantly attenuated in aged rats. In addition, the amount of calcitonin gene-related peptide (CGRP) released in the isolated stomach in response to capsaicin (1 × 10−5 M) was significantly lower in aged animals when compared to young rats. These findings suggest that the gastric mucosa of aged rats is more vulnerable to acid back-diffusion following the barrier disruption, partly because of dysfunction of GMBF responses mediated by capsaicin-sensitive sensory neurons in the acidic conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02093826
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