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  • Articles: DFG German National Licenses  (7)
  • nicotine  (5)
  • gastric mucosal blood flow  (2)
  • GASTRIC HYPEREMIA  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 36 (1991), S. 39-46 
    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
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  • 2
    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
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  • 3
    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
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  • 4
    ISSN: 1573-2568
    Keywords: somatostatin ; gastric mucosal blood flow ; portal hypertensive gastropathy ; reflectance spectrophotometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Agents which decrease gastric mucosal blood flow (GMBF) are postulated to have beneficial effects in arresting gastrointestinal bleeding in cirrhotic patients with portal hypertension. Our objective was to test the hypothesis that in a dose that significantly lowers wedged hepatic venous pressure (WHVP), a bolus injection of somatostatin will significantly decrease GMBF in patients with portal hypertensive gastropathy (PHG). In this placebo-controlled, double-blind, crossover study, 20 cirrhotic patients with PHG were randomly assigned to receive either somatostatin followed by placebo (Group A) or placebo followed by somatostatin (Group B). Wedged hepatic venous pressure was monitored. GMBF in the antrum and corpus was assessed by reflectance spectrophotometry. Indices of hemoglobin concentration (IHb) and indices of oxygen content (ISO2) were recorded. Nine patients were assigned to Group A, and 11 to Group B. Mild PHG was seen in 16 patients, and severe PHG in 4 patients. Baseline WHVP, IHb, and ISO2 were similar in both treatment groups. Wedged hepatic venous pressure (WHVP) was significantly lowered [median, 17.6%; interquartile range (−27.0, −12.6%); P=0.0008] after a 250-µg bolus injection of somatostatin. This dose of somatostatin significantly reduced IHb both in the antrum [−10.2% (−23.4, 0.4%)] and in the corpus [−5.8% (−16.6, 5.6%)] compared to placebo (P=0.02 and 0.04, respectively). Intravenous bolus injection of 250 µg somatostatin significantly reduces WHVP and GMBF in patients with PHG. Whether this ability to decrease the GMBF in PHG makes somatostatin an effective treatment in acute gastrointestinal bleeding in PHG deserves to be studied.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-2568
    Keywords: ANGIOTENSINOGEN ; ANGIOTENSIN CONVERTING-ENZYME INHIBITOR ; GASTRIC HYPEREMIA ; GROWTH FACTOR
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To assess the mechanism of the effect ofcigarette smoke on ulcer disease we employed a rat modelin which cigarette smoke increases the size of aceticacid-induced gastric ulcer and decreases the hyperemia at the ulcer margin. We postulate thatcigarette smoke increases angiotensin II (avasoconstrictor) in ulcer tissue. Since directmeasurement of angiotensin II in small tissue samples isproblematic, we compared the messenger ribonucleic acid (mRNA)for its precursors (angiotensinogen and renin) in ulcerand normal gastric tissue. We also evaluated the effectof enalapril, which blocks the conversion of angiotensin I to angiotensin II on ulcer size.In the ulcer tissue, cigarette smoke produced asignificant increase in mRNA for angiotensinogen but notfor renin. Enalapril decreased the size of the gastric ulcer in rats exposed to cigarette smoke. Thedata support the possibility that in ulcer tissuecigarette smoke stimulates an angiotensin II-mediatedmechanism, which may in part be responsible for the impairment of ulcer margin hyperemia andaggravation of ulcer size.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 37 (1992), S. 1840-1846 
    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
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  • 7
    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
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