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Experiments were performed on rats anesthetized with urethane and nembutal. Intrathecal administration of a nitric oxide inhibitor L-NAME (60 mg) into the cerebrospinal fluid of the thoracic spinal cord was followed by a 40-45% decrease in tonic activity of efferent fibers of the abdominal aortic nerves. L-NAME reduced a reflex increase in the rate of efferent impulses, which was induced by tetanic stimulation of afferent C-fibers in the mesenteric nerve. Administration of L-arginine into the cerebrospinal fluid of the spinal cord (80 mg/20 ml) was accompanied a long-term increase in tonic activity of efferent fibers of the abdominal aortic nerves (by 15-20%). These changes reflect a prolonged activating effect of L-arginine on sympathetic structures.

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Although a large body of evidence shows that pretreatment of brain tissue with creatine protects against anoxic injury in vitro, only a couple of papers have investigated creatine protection in vivo, and they yielded conflicting results. We attempted to clarify how creatine may be protective in an in vivo model of global cerebral ischemia (GCI). We administered creatine either before of after GCI. We decided to administer it by intracerebroventricular infusion, to maximize its bioavailability to the brain. Our findings show that creatine is clearly protective in vivo when administered before ischemia. In that case, histological evaluation of damage was consistently improved in all regions examined, and neurological score was better in creatine-treated rats than in controls. When administered after ischemia, histology was improved in the hippocampus, while only a not significant trend toward improvement was observed in the cerebral cortex and in the caudo-putamen. Neurological score was not improved by creatine administration after GCI. Our findings show that creatine administration is protective in vivo. Such protection was clear in the case of pretreatment, and was present, to a lesser degree, when treatment was started after ischemia. Our results should encourage further research in the possible role of creatine therapy in neuroprotection.

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The aim of the present work was to study the location and structural organization of astrocytes in the rat hippocampus, which contain immunoreactive glial fibrillary acid protein (GFAP) after ischemic damage to the brain after intracerebroventricular administration of the neuroprotective agent creatine and without treatment. Light microscopy and immunocytochemical methods were used to study the brains of 26 adult male Sprague-Dawley (Koltushi) rats, some of which were subjected to total cerebral ischemia (12 min) under anesthesia with subsequent reperfusion (seven days). Creatine was given to 11 animals intracerebroventricularly using an osmotic pump (Alzet Osmotic Mini-Pump). The results showed that GFAP-immunoreactive hippocampal astrocytes were concentrated in two main zones (the stratum lacunosum-moleculare of field CA1 and the stratum polymorphae of the dentate fascia). The neuroprotective effect of creatine had the result that moderate ischemic damage to the hippocampus did not lead to changes in the zones containing activated astrocytes. The redistribution of GFAP-positive astrocytes in the post-ischemic period was associated with loss of pyramidal neurons in cytoarchitectonic field CA1. Complete loss of pyramidal neurons in this area of the hippocampus leads to a qualitatively new level of astrocyte activation--proliferation.

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Feeding fogs with meat after a 3-day period of starvation increased hydrochloric acid concentration with subsequent return of the parameter to normal values. Under the same conditions, pepsin concentration decreased and raised up after re-feeding. Histamine administration following the starvation decreased hydrochloric acid concentration with subsequent normalising. In three days after re-feeding and histamine administration, pepsin concentration drooped owing, probably, to a decrease of parietal cell H2-receptor affinity to histamine. Pentagastrin administration after the starvation increased hydrochloric acid concentration. The findings suggest G-cell function inhibition occurring after a 3-day starvation which is important for the stomach mucous membrane protection.

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The aim of this investigation was to study the distribution and structural organization of rat hippocampal astrocytes containing immunoreactive glial fibrillary acidic protein (GFAP) after ischemic damage of the brain in the animals treated with intraventricular infusion of creatine as a neuroprotective drug, and in those which received no treatment. Using the methods of light microscopy and immunocytochemistry, the brain of 26 mature Sprague-Dawley (Koltushi) rats was studied. Some animals were narcotized and subjected to general brain ischemia (lasting for 12 min) followed by a reperfusion (for 7 days). Creatine was infused intraventricularly to 11 animals using an automatic Alzet osmotic minipump. It was found that GFAP-immunoreactive hippocampal astrocytes were concentrated within two major areas (stratum lacunosum-moleculare CA1 and fascia dentata stratum polymorphae). As a result of neuroprotective effect of creatine, moderate ischemic damage of the hippocampus was not followed by the changes in the zones of activated astrocyte localization. Redistribution of GFAP-positive astrocytes in postischemic period was caused by the loss of pyramidal neurons in cytoarchitectonic field CA1. Complete loss of pyramidal neurons in this hippocampal area resulted in a qualitatively new level of astrocyte activation--their proliferation.

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The article presents a mathematic model, which describes regulation of the digestion process. The simulation was based on data on mutual influence of the factors participating in digestion regulation, which were acquired from analysis of over 1200 sources of experimental observations on digestion in dogs published in Russia and abroad, and on own experimental studies. The simulation includes 67 factors and about 400 interactions observed between them. The computer implementation of this simulation demonstrated descriptive coincidence of patterns of the variables respective to the factors of the model with experimental research data; the coincidence was observed in individual patterns and in combined patterns, as well as in coordinated responses in time.

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Acute experiments on anesthetized rats showed that group B nerve fibers of the subphrenic portion of the vagus nerve do not participate in the regulation of gastric secretion. Gastric acid production is mainly controlled by fast C-fibers (2.11 0.09 m/sec), while secretion of pepsinogen and bicarbonates depends on activity of both fast and slow (0.95 0.11 m/sec) C-fibers. Some fast conduction C-fibers stimulating the release of bicarbonates in the stomach are capsaicin-sensitive afferents. The local effect of these afferents depends on cholinergic transmission and most probably it is mediated via its modulation.

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Phosphocreatine can to some extent compensate for the lack of ATP synthesis that is caused in the brain by deprivation of oxygen or glucose. Treatment of in vitro rat hippocampal slices with creatine increases the neuronal store of phosphocreatine. In this way it increases the resistance of the tissue to anoxic or ischemic damage. In in vitro brain slices pretreatment with creatine delays anoxic depolarization (AD) and prevents the irreversible loss of evoked potentials that is caused by transient anoxia, although it seems so far not to be active against milder, not AD-mediated, damage. Although creatine crosses poorly the blood-brain barrier, its administration in vivo at high doses through the intracerebroventricular or the intraperitoneal way causes an increase of cerebral phosphocreatine that has been shown to be of therapeutic value in vitro. Accordingly, preliminary data show that creatine pretreatment decreases ischemic damage in vivo.

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Maximal responses to splanchnic nerve stimulation occurred in rats at the pulse width 0.5-1.0 Ohms regardless of the frequency. Peak constriction of arterioles and venules occurred at a 3-4-sec burst duration and 1-2-sec interval. Adrenergic blockade abolished the vasoconstriction in response to continuous nerve stimulation. However, the responses persisted in high-frequency burst stimulation, suggesting an involvement of non-adrenergic co-transmitter release. Thereupon, an efficient control of microvascular tone can be achieved by grouping the pulses into bursts or by an increase of the burst rate or duration.

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In lumen-perfused stomachs of anaesthetized rat, acid and bicarbonate types of secretion were estimated on the basis of pH/PCO2 measurements. The data obtained reveal that, in anaesthetised rats, pentagastrin and cholinergic input affect acid secretion mainly indirectly via histamine release. Vagal effects on pepsinogen output are mediated partially via indirect histamine pathways. The direct action of pentagastrin, however, predominates. Bicarbonate production is subjected to cholinergic control alone.

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The effects of electrical stimulation of the left splanchnic nerve in 1 s bursts at 4 s intervals at 5-80 Hz or continuously at 1-16 Hz (6 V, 1 ms) on gastric submucosal microvasculature were studied by the reflected light in vivo TV-microscopy. Burst stimulation, like a continuous one, induced frequency-dependent vasoconstrictor responses. Maximal reduction in diameter of both arterioles (by about 90%) and venules (by about 60%) occurred at the same total number of stimuli delivered for 1-min period of nerve stimulation continuously at 16 Hz or in bursts at 80 Hz. In other frequencies used, burst stimulation evoked significantly more pronounced contractile responses of arterioles (but not the venules), which followed by much less pronounced autoregulatory escape and poststimulatory hyperemia as compared to continuous stimulation at the comparable total number of impulses. After alpha-adrenoreceptor blockade, reduced in magnitude and slow developing contractile responses of arterioles persisted to stimulation in bursts rather than continuously suggesting the involvement of nonadrenergic co-transmitters) release. The data obtained show that not only the number of neural pulses but also their bursting pattern may have an informational role in microvascular contractile responses. Bursting pattern of nerve stimulation seems to be more "physiological" than the continuous one.

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Cylindrical segments from mesenteric veins of 8 cats were prepared and mounted in a Krebs-Ringer tissue bath. The oxygenized solution was bubbled with 95% O2 and 5% CO2. For lowered oxygen tension 95% N2 and 5% CO2 was used. Intraluminal pressure was changed between 0-20-0 mm Hg in consecutive cycles at a rate of 0.93-1.33 mm Hg/sec. Outer radii on the upward routes were recorded. Norepinephrine was added in doses of 6 X 10(-8) -6 X 10(-5) M, first in the oxygenized medium then under hypoxic conditions, and then in oxygenized medium again. Maximally relaxed curves were taken with 1.5 X 10(-4) M papaverine at the end of the experiment. Outer radius of relaxed segments at 20 mm Hg intraluminal pressure was 2.03 +/- 0.12 mm which slowly dilated to 2.09-0.12 mm toward the end of the experiment, and reached 2.11 +/- 0.11 mm with papaverine. Maximum active contractions of the outer radii were found at 6 mm Hg intraluminal pressure and with 6 X 10(-5) M norepinephrine in the bath: 23.1 +/- 3.2% in oxygenized, 20.3 +/- 3.4% in hypoxic and 19.0 +/- 3.4% again in oxygenized media. The observations showed that acute hypoxia had no or had only a limited effect on the contraction of the feline mesenteric vein.

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