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  • 1
    Electronic Resource
    Electronic Resource
    A study of the antiulcer mechanisms of propanolol in rats (1996)
    Springer
    Inflammation research 45 (1996), S. 370-375 
    Details
    ISSN: 1420-908X
    Keywords: Propranolol ; Gastric damage ; Ethanol ; Indomethacin ; Stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Although propranolol has been shown to protect against enthanol and stress ulceration, the antiulcer mechanisms are still unclear. The present study examined the antiulcer mechanisms of propranolol in three different types of ulceration induced respectively by ethanol (60%), indomethacin (30 mg/kg) and stress (cold-restraint). Propranolol pretreatment in the highest dose (10 mg/kg) given either intraperitoneally (i.p.) or orally (p.o.) prevented gastric mucosal damage in these three ulcer models. The three doses of the drug (2.5, 5 or 10 mg/kg) dose-dependently decreased systemic blood pressure which was accompanied by a reduction of gastric mucosal blood flow. These findings suggest that the protection was unrelated to an improvement of local circulation in the stomach. However, propranolol preserved the mucus levels in the three types of ulcer models. The β-adrenoceptor blocker also increased the basal gastric mucosal potential difference. These findings indicate that propranolol strengthens the mucosal barrier by the preservation of mucosal mucus and enhancement of the mucosal integrity in the stomach.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02252930
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  • 2
    Electronic Resource
    Electronic Resource
    The role of non-protein sulfhydryl compounds in gastric adaptive cytoprotection against ethanol-induced mucosal damage in rats (1995)
    Springer
    Inflammation research 44 (1995), S. 242-244 
    Details
    ISSN: 1420-908X
    Keywords: Adaptive cytoprotection ; Lesions ; Nonprotein sulfhydryl compounds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The contribution of the endogenous nonprotein sulfhydryl compounds (SH) in gastric adaptive cytoprotection was investigated in rats. N-ethylmaleimide (NEM) treatment significantly reduced mucosal SH level, and aggravated the mucosal injury induced by absolute ethanol. Oral administration of the mild irritants, 20% ethanol, 5% NaCl or 0.3 M HCl, significantly increased the basal mucosal SH level. These agents also showed a cytoprotective action against the necrotizing effect of absolute ethanol. Administration of NEM did not alleviate this cytoprotective potential, although it abolished the increased SH level evoked by these mild irritants. Thus, it is concluded that modulation of endogenous SH by mild irritants perhaps only plays a minor role in the gastric adaptive cytoprotection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01782975
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  • 3
    Electronic Resource
    Electronic Resource
    Co-regulation of mucosal nitric oxide and prostaglandin in gastric adaptive cytoprotection (1999)
    Springer
    Inflammation research 48 (1999), S. 471-478 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Nitric oxide — Prostaglandins — Adaptive cytoprotection — Ethanol — Gastric defense — Mucosa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: The correlation between mucosal generation of nitric oxide (NO) and prostaglandin E2 (PGE2) in gastric adaptive cytoprotection was investigated.¶Materials and Treatment: Male Sprague-Dawley rats were pretreated with either Nw-nitro-L-arginine methyl ester (L-NAME, 12.5mg/kg i.v.) or indomethacin (5mg/kg s.c.). Following that, mild irritant 20% ethanol was administered, 15min prior to 100% ethanol challenge.¶Methods: Macroscopic gastric mucosal damage, NO synthase activity, mucosal PGE2 and leukotriene C4 (LTC4) levels were measured.¶Results: Administration of L-NAME and indomethacin significantly reduced the protective action of 20% ethanol against 100% ethanol-induced gastric mucosal damage. Besides, mucosal activity of constitutive NO (cNO) synthase, but not of the inducible isozyme (iNO synthase), was elevated following 20% ethanol treatment. This was accompanied by a reduction in mucosal leukotriene C4 level. Indomethacin significantly inhibited mucosal PGE2 biosynthesis but increased cNO synthase activity. Nevertheless, L-NAME reduced both cNO and iNO formation and prevented the increase in cNO formation caused by 20% ethanol, while enhancing mucosal PGE2 production. Combined L-NAME and indomethacin treatment markedly potentiated ethanol-induced mucosal damage, and completely prevented the increase in cNO or PGE2 biosynthesis when either compound was given alone.¶Conclusions: These findings suggest a co-regulatory relationship between mucosal NO and PG in the gastric defense system, which will be released after activation by the mild irritants to induce cytoprotection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050489
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  • 4
    Electronic Resource
    Electronic Resource
    The importance of gastric emptying and mucosal folds in the adaptive cytoprotection of mild irritants in rats (1995)
    Springer
    Inflammation research 44 (1995), S. 518-522 
    Details
    ISSN: 1420-908X
    Keywords: Mild irritants ; Ethanol ; Gastric lesions ; Gastric emptying rate ; Mucosal folds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This study examines the involvement of gastric emptying and mucosal folds in the adaptive cytoprotection of different mild irritants against 100% ethanolinduced gastric mucosal damage. Pre-exposure to either 20% ethanol, 5% NaCl or 0.3M HCl significantly reduced the gastric mucosal damage caused by 100% ethanol in rats. Administration of either one of the three mild irritants increased the basal gastric residual volume and decreased the area occupied by gastric mucosal folds, but only 20% ethanol reduced the gastric emptying rate. Indomethacin (5 mg/kg, s.c.) pretreatment did not affect ethanol ulceration and gastric emptying rate when given by itself, but reversed the flattening of mucosal folds produced by the three mild irritants, and abolished the protective effect of 20% ethanol. These results suggest that the gastric adaptive cytoprotection induced by the three mild irritants acts through luminal dilution of the noxious agent, possibly caused by gastric retention. The reduction of mucosal folds could also contribute to the anti-lesion action of 20% ethanol. It is therefore suggested that the protective actions of the three mild irritants act through different mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01757355
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  • 5
    Electronic Resource
    Electronic Resource
    The gastric cytoprotective action of adenosine and prostaglandin E2 in rabbits (1994)
    Springer
    Inflammation research 42 (1994), S. 146-148 
    Details
    ISSN: 1420-908X
    Keywords: Adenosine ; Prostaglandin E2 ; Gastric gland ; Damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The direct protective action of adenosine and prostaglandin E2 (PGE2) was examined in an isolated gastric gland preparation in rabbits. Ethanol, (8%, v/v) incubation markedly increased the release of lactate dehydrogenase (LDH) and number of non-viable glands in the preparation. Both effects were prevented by PGE2 preincubation in a concentration (10−6, 1.4×10−5 or 2.8×10−5 M)-dependent manner. The protective action was smaller in adenosine-treated groups, and yet the highest concentration (10−4 M) of the compound also significantly inhibited the cytotoxic effects of ethanol. These findings indicate that both adenosine and PGE2 possess cytoprotective action on gastric glands in rabbits, but the former compound exerts its action beyond physiological concentrations. It is concluded that endogenous PGE2, but not adenosine may act as an ulcer modulator in the stomach.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01983481
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  • 6
    Electronic Resource
    Electronic Resource
    The effect of nicotine on ethanol-induced gastric ulcers in rats (1985)
    Springer
    Cellular and molecular life sciences 41 (1985), S. 1140-1141 
    Details
    ISSN: 1420-9071
    Keywords: Nicotine ; ethanol ; gastric ulcers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Nicotine, in concentrations of 5 and 25 μg/ml drinking water, given ad libitum for 10 days, dose-dependently increased lesion formation and worsened ethanol-induced ulceration in rat stomachs. Daily fluid intake and b.wt gain were not adversely affected by nicotine pretreatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01951697
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  • 7
    Electronic Resource
    Electronic Resource
    The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats (1992)
    Springer
    Cellular and molecular life sciences 48 (1992), S. 389-391 
    Details
    ISSN: 1420-9071
    Keywords: Nicotine ; cold-restraint stress ; gastric ulcers and motility
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Ten-day treatment with nicotine, (5, 25 or 50 μg/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923437
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  • 8
    Electronic Resource
    Electronic Resource
    Sulphasalazine and experimental stress ulcers (1985)
    Springer
    Inflammation research 17 (1985), S. 153-157 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of sulphasalazine on gastric ulceration induced by restraint at 4°C (stress) for 2 h were studied in rats. Doses of 63 or 125 mg/kg s.c., which had no effect on stomach wall prostaglandin E2 (PGE2) levels, prevented stress ulceration but not the lesions produced by indomethacin. Stress significantly increased gastric glandular mucosal PGE2 levels. Indomethacin pretreatment (20 mg/kg, p.o.) markedly reduced PGE2 levels in the same region of the stomachs, and worsened stress-induced lesion formation. Pretreatment with sulphasalazine of animals given indomethacin and then subjected to stress did not appear to affect the indomethacin component of indomethacin-stress ulceration. Oral administration of PGE2 200 μg/kg significantly elevated gastric PGE2 levels, but had no effect on stress ulceration. It appears that neither the antiulcer activity of sulphasalazine nor stress-induced ulceration is associated with gastric tissue PGE2 increase or decrease, respectively. The protective mechanism may result from the ability of sulphasalazine to inhibit lipoxygenase activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01966585
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  • 9
    Electronic Resource
    Electronic Resource
    Response to "Comment on ‘Mixture model description of the T-, P dependence of the refractive index of water' " [J. Chem. Phys. 115, 7795 (2001)] (2001)
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 115 (2001), S. 7796-7797 
    Details
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: The valid range of the emphasized experimental data and need, in very precise comparisons, to compensate for the very small temperature shifts resulting from revisions in the accepted standard for the International Temperature Scale over the years, are acknowledged. However, it is emphasized that these corrections do not invalidate the approach and that the physical motivation underlying the mixture model analysis leads to physically meaningful fitting parameters; a result not found in any previous treatment. © 2001 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1406530
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  • 10
    Electronic Resource
    Electronic Resource
    Mixture model description of the T-, P dependence of the refractive index of water (2001)
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 114 (2001), S. 3157-3162 
    Details
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: In this paper the temperature/pressure dependence of the refractive index of liquid water is analyzed using the two-state outer-neighbor mixed bonding structural model. So far, this theoretical model has been successful in reproducing, usually within the experimental uncertainty, the temperature/pressure dependence of the density, the viscosity, and the oxygen–oxygen pair correlation functions, in addition to the isothermal compressibility and isotope effects of this important substance. The philosophy of the present paper is to use the high accuracy of refractive index measurements to further test this model. It is shown that a very simple linear dependence with respect to temperature and pressure of the specific refractions LI and LII of the two contributing structural components in this two-state model is sufficient to give better than 5-decimal-point agreement with the experimental refractive index data at low pressures and temperatures between about −10 °C and +70 °C. The maximum in the refractive index between −5 °C and +5 °C is reproduced to an even better precision. Generally better than 4-decimal-point accuracy is achieved for higher pressures, where the experimental data are less accurately known. The pressure dependence considered here also allows the calculation of the isothermal piezo-optic coefficient as a function of temperature, which exhibits a minimum near 50 °C. © 2001 American Institute of Physics.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1063/1.1331571
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