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  • Articles: DFG German National Licenses  (3)
  • 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: 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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  • 3
    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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