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  • 1
    Electronic Resource
    Electronic Resource
    Mechanism of intragastric tetramethylammonium protection against 40% ethanol injury in rat stomach (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 708-712 
    Details
    ISSN: 1573-2568
    Keywords: nicotine ; ethanol-induced gastric mucosal injury ; tetramethylammonium ; gastric mucus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of tetramethylammonium (TMA), a ganglionic stimulant, on gastric mucosal injury induced by 40% ethanol was examined. In studies I–III, rats were treated with intragastric vehicle or TMA (1 or 10 mg/kg). In study I, 1 hr after the treatment, 40% ethanol was given intragastrically. The length of the linear corpus mucosal lesions was measured unbiasedly with a caliper after another hour. In study II, mean blood pressure was assessed before and after the treatment. In study III, 1 hr after the treatment, gastric mucus and juice volumes, and titratable acid were measured. In study IV, 40% ethanol (10 ml/kg) was administered intragastrically immediately after 0.2 or 1.4 ml of intragastric vehicle treatment. One hour later, gastric lesion score was assessed as in study I. Results show that (1) intragastric TMA dose-dependently protected against 40% ethanol-induced gastric injury; (2) neither dose of intragastric TMA increased mean blood pressure; (3) there was a dose-related increase in gastric mucus secretion for TMA 1 and 10 mg/kg, and a significant increase in gastric juice volume only for TMA 10 mg/kg; and (4) the rats treated with 1.4. ml of vehicle plus 40% ethanol had significantly less injury than those treated with 0.2 ml of vehicle plus 40% ethanol. We conclude that the protective effect of intragastric TMA can be explained by its dose-related effect in enhancing gastric mucus secretion for TMA 1 and 10 mg/kg and the significantly greater increase in gastric juice volume for TMA 10 mg/kg. Even though parenteral TMA is a recognized ganglionic stimulant, the protective effect of intragastric TMA is unlikely to be due to its ganglionic stimulatory property, as neither 1 nor 10 mg/kg intragastric TMA increases mean blood pressure. However, the possibility that intragastric TMA acts as a local stimulant of intramural ganglia cannot be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01316804
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  • 2
    Electronic Resource
    Electronic Resource
    Involvement of α2-Adrenoceptors in mechanism of intragastric nicotine protection against ethanol injury in rat stomach (1993)
    Springer
    Digestive diseases and sciences 38 (1993), S. 713-721 
    Details
    ISSN: 1573-2568
    Keywords: α-adrenoceptors ; prazosin ; yohimbine ; β-adrenoceptors ; metoprolol ; butoxamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To elucidate the role of α- and β-adrenoceptors in the mechanism of intragastric nicotine protection against ethanol-induced gastric mucosal injury, the following studies were performed. At 0.5-hr prior to the injury study, rats were pretreated with: subcutaneous control, prazosin (0.5 mg/kg) or yohimbine (5 mg/kg) to block α1- or α2-adrenoceptors; or intraperitoneal control, metoprolol (2 mg/kg) or butoxamine (4 mg/kg) to block β1- or β2-adrenoceptors, respectively. At 1-hr intervals, rats received intragastric vehicle or nicotine (4 mg/kg) and 40% ethanol (10 ml/kg). Total lengths of the linear gastric corpus mucosal lesions were measured by an unbiased observer using a caliper. In a separate study, 0.5-hr after subcutaneous control or yohimbine (5 mg/kg), rats were treated with intragastric vehicle or nicotine (4 mg/kg). One hour later, gastric mucus volume, gastric juice volume and pH, and titratable acid in the gastric juice were measured. In the rat stomach, the intragastric nicotine protection against 40% ethanol-induced mucosal injury was not blocked by selective α1-(prazosin), β1-(metoprolol), or β2-(butoxamine) adrenoceptor antagonists. The protection was significantly reduced although not completely abolished by selective α2-(yohimbine) adrenoceptor antagonist. Yohimbine also significantly reduced basal and nicotine-stimulated increase in gastric mucus volume. These data suggest that α2-adrenoceptors are involved in the protective effect of intragastric nicotine against 40% ethanol-induced gastric mucosal injury possibly by a mucus-dependent mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01316805
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  • 3
    Electronic Resource
    Electronic Resource
    Intragastric nicotine protects against 40% ethanol-induced gastric injury despite pretreatment with NG-Nitro-l-Arginine methyl ester or adrenal medullectomy in rats (1994)
    Springer
    Digestive diseases and sciences 39 (1994), S. 347-352 
    Details
    ISSN: 1573-2568
    Keywords: nicotine ; ethanol-induced gastric mucosal injury ; NG-nitro-l-arginine methyl ester ; adrenal medullectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We tested the hypotheses that the protective effect of intragastric nicotine against ethanol-induced gastric mucosal injury is dependent on endogenous nitric oxide or peripheral sympathoadrenal mechanisms. Rats were pretreated with NG-nitro-l-arginine methyl ester (3 mg/kg subcutaneous, 1 h prior to study) to block endogenous nitric oxide synthesis or with adrenal medullectomy (three weeks prior to study) to ablate the effect of the adrenal medulla. At 1-h intervals, vehicle or nicotine (4 mg/kg) and 40% ethanol were then given intragastrically. The total lengths of the linear gastric corpus mucosal lesions were measured unbiasedly. The protective effect of intragastric nicotine was not modified by either pretreatment. We conclude that the mechanism mediating intragastric nicotine protection against 40% ethanol-induced gastric mucosal injury is independent of endogenous nitric oxide or the adrenal medulla.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02090207
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  • 4
    Electronic Resource
    Electronic Resource
    Mechanism of intragastric nicotine protection against ethanol-induced gastric injury (1991)
    Springer
    Digestive diseases and sciences 36 (1991), S. 39-46 
    Details
    ISSN: 1573-2568
    Keywords: capsaicin-sensitive afferent sensory nerve fibers ; indomethacin ; gastric mucus ; naloxone ; gastric mucosal blood flow ; nicotine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To elucidate the mechanism of intragastric nicotine protection against ethanol-induced gastric mucosal injury seen in a previous report and in our preliminary study, the following studies were performed. Rats were pretreated with naloxone (8 mg/kg intraperitoneal, 0.5 hr prior to study) to block opiate receptors; or capsaicin (125 mg/kg subcutaneous 10 days prior to study) to denervate the afferent sensory fibers; or indomethacin (2.5 mg/kg intragastric or 5 mg/kg subcutaneous, 1 hr prior to study) to inhibit endogenous prostaglandin synthesis. At 1-hr intervals, nicotine (4 mg/kg) or vehicle and 40% ethanol were then given intragastrically. Total gastric corpus mucosal lesion length was measured unbiasedly. In separate studies, gastric mucosal blood flow (GMBF) was assessed by hydrogen gas clearance before and after intragastric nicotine or vehicle; luminal mucus volume, gastric juice volume, and acid output were measured 1 hr after either intragastric nicotine or vehicle administration. The results showed that the acute protective effect of intragastric nicotine was associated with a significantly larger luminal mucus volume. It was not blocked by naloxone, capsaicin, or indomethacin. There was no increase in GMBF. The larger gastric residual volume did not account for the protection. We conclude that the mechanism mediating nicotine protection is unique and is independent of opiate receptors, capsaicin-sensitife afferent sensory nerve fibers, endogenous prostaglandin generation, or dilution of the injurious agent. The increase in luminal gastric mucus volume may contribute to the protective effect of intragastric nicotine against gastric mucosal injury produced by 40% ethanol.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01300085
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  • 5
    Electronic Resource
    Electronic Resource
    Intragastric nicotine protection against 40% ethanol injury in rat stomach (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 1840-1846 
    Details
    ISSN: 1573-2568
    Keywords: nicotine ; ethanol-induced gastric mucosal injury ; hexamethonium ; mecamylamine ; gastric mucus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intragastric nicotine (4 mg/kg) protects against 40% ethanol-induced gastric mucosal injury and raises mean blood pressure. We postulated that this protective effect was mediated by the ganglionic stimulatory property of nicotine and therefore could be abolished by ganglionic blockers. Rats were pretreated with intraperitoneal hexamethonium (10 mg/kg) or mecamylamine (2 mg/kg) to block peripheral or central autonomic ganglia, respectively. Intragastric vehicle or nicotine (4 mg/kg) was then administered. The total lengths of the linear gastric corpus mucosal lesions induced by intragastric 40% ethanol were measured by an unbiased observer using a caliper. The results showed that both intraperitoneal hexamethonium and mecamylamine pretreatments protected against 40% ethanol-induced gastric mucosal injury. Neither modified the protective effect of intragastric nicotine. The protective effect of hexamethonium and mecamylamine was associated with a significant increase in the volume of gastric mucus and gastric juice. The increase in the volume of gastric content (mucus and juice) was partially responsible for the protective effect of these ganglionic blockers. In a separate experiment, intraperitoneal nicotine (4 mg/kg) also protected against 40% ethanol-induced gastric mucosal injury and raised mean blood pressure. These data indicate that the protection against 40% ethanol-induced gastric mucosal injury is not unique to intragastric nicotine. Such protection can be induced by ganglionic blocking doses of hexamethonium and mecamylamine, or a ganglionic stimulatory dose of intraperitoneally administered nicotine. Whether ganglionic stimulation or blockade plays a role in the mechanism of intragastric nicotine protection, however, remains to be determined. Further studies of the regulation of gastric mucus production and gastric juice volume may shed light on the mechanism of protection afforded by intragastric nicotine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01308077
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  • 6
    Electronic Resource
    Electronic Resource
    Intragastric nicotine protects against 40% ethanol-induced gastric mucosal injury despite pretreatment with propranolol orN-ethylmaleimide in rats (1992)
    Springer
    Digestive diseases and sciences 37 (1992), S. 391-396 
    Details
    ISSN: 1573-2568
    Keywords: nicotine ; ethanol-induced gastric mucosal injury ; propranolol ; N-ethylmaleimide ; β-adrenoceptors ; sulfhydryl compounds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We tested the hypotheses that the protective effect of intragastric nicotine against ethanol-induced gastric mucosal injury is dependent on propranolol- orN-ethylmaleimide-sensitive mechanisms. Propranolol was administered in doses (2 and 20 mg/kg) that provided dose-related blockade of β-adrenoceptors (significant decreases in heart rate).N-Ethylmaleimide was administered in doses that previously had been shown to increase gastric vascular permeability (10 mg/kg) or inhibit gastric mucosal sulfhydryl compounds (50 mg/kg). At 0.5 hr after these or control subcutaneous pretreatments, the rats received intragastric nicotine (4 mg/kg) or vehicle. One hour later 40% ethanol was given intragastrically. The gastric corpus mucosal lesions were recorded by polaroid photographs after another hour, and their areas measured unbiasedly by computerized image analysis. The results showed thatN-ethylmaleimide, but not propranolol, aggravated ethanol-induced gastric mucosal injury. The protective effect of intragastric nicotine was not modified by either pretreatment. We conclude that the mechanism mediating intragastric nicotine protection against 40% ethanol-induced gastric mucosal injury is independent of propranolol- orN-ethylmaleimide-sensitive mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01307733
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of perforated partition plate on mixing characteristics of horizontal stirred vessel (1981)
    Hoboken, NJ : Wiley-Blackwell
    AIChE Journal 27 (1981), S. 599-604 
    Details
    ISSN: 0001-1541
    Keywords: Chemistry ; Chemical Engineering
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: To reduce backmixing in the flow-type horizontal stirred vessel, a perforated partition plate was attached and the effects of shape of plate on the mixing characteristics were studied under various operating conditions. Results were analyzed in terms of mixing models to evaluate the extent of preventing backmixing. It enabled us to estimate the extent of back flow at the perforated partition plate from power consumption.
    Additional Material: 11 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/aic.690270410
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  • 8
    Electronic Resource
    Electronic Resource
    Mechanical control of foaming in a bubble column (1984)
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 26 (1984), S. 702-713 
    Details
    ISSN: 0006-3592
    Keywords: Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: This study was performed to evaluate the effects of the air sparge rate, working liquid volume, liquid feed rate onto the disk, and disk diameter on the foam-breaking performance of foam-breaking apparatus with a rotating disk (FARD) installed in the bubble column. Experimental results showed that the smaller the air sparge rate and working liquid volume were, and the larger the liquid feed rate and disk diameter, the lower the critical disk rotational speed required for reduced foam-breaking. The presence of the effective ranges of the disk diameter and liquid feed rate for foam breaking was also confirmed. Furthermore, the quantitative predictions of the upper limits of the liquid feed rate, foam-breaking regions, and the required foam-breaking power were carried out, based on the results obtained above. Comparison of the FARD with two conventional mechanical foam-breaking spray-type apparati also demonstrated the highest level of the FARD in respect not only to foam-breaking performance but also to power requirements.
    Additional Material: 21 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/bit.260260712
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