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  • Articles: DFG German National Licenses  (6)
  • hydrogen gas clearance  (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
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 36 (1991), S. 727-732 
    ISSN: 1573-2568
    Keywords: colonic blood flow ; laser Doppler flowmetry ; in vivo microscopy ; hydrogen gas clearance ; propidium iodide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hypothesis that a significant reduction in colonic mucosal perfusion, and hence ischemic injury, precedes the development of mucosal ulceration and inflammation is tested in this report. The microcirculatory changes in the rat colonic mucosa within 1 hr of topical exposure to 10% acetic acid were assessed. Colonic mucosal blood flow signals measured by laser Doppler flowmetry were, significantly reduced to 61±8, 52±10, and 37±13% (mean±SEM) of baseline values at 1 min, 4 min, and 10 min after the colonic mucosa was exposed to 10% acetic acid, respectively, but not in controls exposed to saline. After the start of application of 10% acetic acid (for 4 min),in vivo microscopy studies demonstrated that colonic mucosal ischemia (stasis of the red blood cells in the mucosal capillaries) occurred at 9±5 min (mean±SEM). Evidence of endothelial cell death, (failure to exclude a fluorescent dye, propidium iodide, by endothelial cells) developed at 25±10 min (mean±SEM). These findings indicate that within minutes after contact of the colonic mucosa with 10% acetic acid, colonic mucosal ischemia develops, followed shortly by death of endothelial cells. The data do not establish a cause-and-effect relationship between the reductions, in mucosal blood flow and loss of endothelial cell viability in response to acetic acid. Nevertheless, because these events occur at such an early time point, they may play a pathogenetic role in the development of the subsequent inflammatory and ulcerative changes in this animal model of colitis. Further studies to define the potential causal relationships between these parameters are warranted.
    Type of Medium: Electronic Resource
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  • 3
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 40 (1995), S. 1112-1117 
    ISSN: 1573-2568
    Keywords: duodenal mucosal blood flow ; hydrogen gas clearance ; iodoantipyrine autoradiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The hyperemia at the duodenal ulcer margin is important for ulcer healing. We studied the effect of tobacco cigarette smoke on the hyperemia at the margin of mepirizole-induced duodenal ulcer. Duodenal mucosal blood flow values measured by iodo[14C]antipyrine (IAP) autoradiography and hydrogen gas clearance (HGC) were compared. Twenty-four hours after rats were injected with an ulcerogenic dose of mepirizole, they were exposed to tobacco cigarette smoke and duodenal mucosal blood flow was measured by IAP autoradiography. There is a significant correlation between the blood flow measurements by HGC and IAP autoradiography. The hyperemia at the ulcer margin previously demonstrated in our laboratory is absent after exposure of the rats to tobacco cigarette smoke. We speculate that the inhibition of ulcer margin hyperemia could explain the aggravation of duodenal ulcer by tobacco cigarette smoke.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 40 (1995), S. 1118-1124 
    ISSN: 1573-2568
    Keywords: hydrogen gas clearance ; tobacco cigarette smoke ; injury-induced hyperemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the model of gastric mucosal injury induced by 2 mol/liter hypertonic saline in rats, we tested the hypothesis that tobacco cigarette smoke aggravates gastric mucosal lesions by inhibition of injury-induced gastric mucosal hyperemia. Experimental rats were treated with tobacco cigarette smoke or nicotine-free smoke from nontobacco cigarettes, and controls breathed room air. Gastric mucosal blood flow was measured by hydrogen gas clearance before and during the intragastric administration of hypertonic saline. Tobacco cigarette smoke 3 and 18 ml/min, but not nicotine-free smoke, significantly attenuated the hyperemia and aggravated the hypertonic saline-induced lesion in a dose-dependent manner. We then tested the hypothesis that 18 ml/min of tobacco cigarette smoke, and the dose of intravenous nicotine previously shown to block injury-induced hyperemia and aggravate 2 mol/liter saline-induced gastric damage, will also adversely affect gastric lesions induced by acidified aspirin or acidified ethanol. The results confirm that tobacco cigarette smoke and intravenous nicotine indeed aggravate gastric mucosal damage in these two models. Taken together, the data suggest that the inhibition of injury-induced hyperemia by nicotine and tobacco cigarette smoke is an important predictor of their ability to increase the susceptibility of the gastric mucosa to noxious damage. Although limited in their experimental nature, these data provide one plausible explanation for the adverse effect of tobacco cigarette smoke on peptic ulcer disease.
    Type of Medium: Electronic Resource
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