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  • 1
    ISSN: 1432-1106
    Keywords: Key words Coherence ; Entorhinal cortex ; Cortex ; Hippocampus ; Amygdala ; 192 IgG-saporin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Changes in brain electrical activity in response to cholinergic agonists, antagonists, or excitotoxic lesions of the basal forebrain may not be reflective entirely of changes in cholinergic tone, in so far as these interventions also involve noncholinergic neurons. We examined electrocortical activity in rats following bilateral intracerebroventricular administration of 192 IgG-saporin (1.8 µg/ventricle), a selective cholinergic immunotoxin directed to the low-affinity nerve growth factor receptor p75. The immunotoxin resulted in extensive loss of choline acetyl transferase (ChAT) activity in neocortex (80%–84%) and hippocampus (93%), with relative sparing of entorhinal-piriform cortex (42%) and amygdala (28%). Electrocortical activity demonstrated modest increases in 1- to 4-Hz power, decreases in 20- to 44-Hz power, and decreases in 4- to 8-Hz intra- and interhemispheric coherence. Rhythmic slow activity (RSA) occurred robustly in toxin-treated animals during voluntary movement and in response to physostigmine, with no significant differences seen in power and peak frequency in comparison with controls. Physostigmine significantly increased intrahemispheric coherence in lesioned and intact animals, with minor increases seen in interhemispheric coherence. Our study suggests that: (1) electrocortical changes in response to selective cholinergic deafferentation are more modest than those previously reported following excitotoxic lesions; (2) changes in cholinergic tone affect primarily brain electrical transmission within, in contrast to between hemispheres; and (3) a substantial cholinergic reserve remains following administration of 192 IgG-saporin, despite dramatic losses of ChAT in cortex and hippocampus. Persistence of a cholinergically modulated RSA suggests that such activity may be mediated through cholinergic neurons which, because they lack the p75 receptor, remain unaffected by the immunotoxin.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: gastrointestinal blood flow ; gastric motility ; cold water immersion restraint stress ; iodo[14C]antipyrine autoradiography ; hyperemia ; convolution ; Gaussian functions ; gastric ulcers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Cold water immersion restraint (CWIR) is associated with gastric hypercontractility and gastric corpus erosions in the rat. Because the gastric blood flow response to CWIR has not been well defined, we performed the following study. Rats were implanted with force transducers, subjected to CWIR for 2 hr, and then blood flow was determined by the iodo[14C]antipyrine autoradiographic (IAP) technique. When compared to control animals, the CWIR-treated animals displayed foci of gastric corpus hyperemia with a marked and significant increase in blood flow in all layers of the gastric corpus. There was approximately a 100% increase in the mucosa and a 50% increase in the muscularis externa. The hyperemia was not uniform, but rather alternated every 2.1±0.2 mm with regions of low blood flow. Blood flow in the antrum and duodenum was unaffected by CWIR. We conclude that CWIR is associated with alternating regions of high and low blood flow only in the gastric corpus. Reduction of corpus mucosal blood flow might be due to the powerful gastric contractions associated with CWIR.
    Type of Medium: Electronic Resource
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  • 3
    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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  • 4
    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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  • 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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