Impulse flow in sympathetic efferents of the abdominal aortic nerve after intrathecal administration of the substrate and inhibitor of nitric oxide synthase.

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.

Intracerebroventricular administration of creatine protects against damage by global cerebral ischemia in rat.

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.

Structural organization of astrocytes in the rat hippocampus in the post-ischemic period.

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).

[Concentration of hydrochloric acid and pepsin in gastric juice in dogs after starvation and refeeding].

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.

[Structural characteristics of astrocytes from the rat hippocampus in postischemia].

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).

[Mathematical model of the digestion process regulation and its computer presentation].

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.

Role of creatine and phosphocreatine in neuronal protection from anoxic and ischemic damage.

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.

Selective regulation of acid, pepsinogen, and bicarbonate secretion in the stomach by different C-fiber populations of vagus nerve.

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.

[The role of stimulation parameters of sympathetic nerves in regulation of microvessel tone in the rat stomach].

Maximal responses to splanchnic nerve stimulation occurred in rats at the pulse width 0.5-1.0 Ohms regardless of the frequency.

[The role of histamine in vagal and gastrin effects on the secretory function of the rat stomach].

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 pattern-dependent mechanisms of the neural regulation of the microvascular tonus in the rat stomach].

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.

Norepinephrine induced contractions of the feline mesenterial vein under oxygenized and hypoxic conditions in vitro.

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.

[Direct effect of hypoxia on the function of skeletal muscle blood vessels in the cat].

In decentralized skeletal muscles of the cat hindlimbs, pO2 of arterial blood dropped from 105 to 87, 68 and 37 mm Hg in artificial respiration with 18% O2 (slight), 14% O2 (moderate) and 8% O2 (grave hypoxia) mixtures, resp. The slight hypoxia practically did not affect vascular resistance and capacity, distensibility of veins, capillary filtration coefficient and mean capillary hydrostatic pressure. Moderate and grave hypoxia reduced perfusion pressure by 3.

[Direct effect of hypoxia on the functions of the small intestinal vessels of the cat].

In anesthetized cats, artificial ventilation with 18, 14 and 8% O2 mixtures decreased the arterial blood pO2 from 104 to 85, 69 and 38 mm Hg, resp. Resistance of the intestine vessels and their capacity decreased in 14 and 8% O2; the capillary filtration coefficient increased at all levels of hypoxia whereas distensibility of veins and mean capillary hydrostatic pressure practically did not alter. A significant diminishing of constrictor responses of the intestine arterial vessels to noradrenaline only occurred in 8% O2.

[Coefficient of capillary filtration and distensibility of small intestine vessels at various levels of blood flow and venous and perfusion pressure].

In the cat decentralized small intestine perfused with a constant blood volume, the capillary filtration coefficient (CFC) increased from 0.02 to 0.22 ml/min/mm Hg/100 g on increase of the venous pressure from 0 to 18 mm Hg.

[Effect of medullary chemosensitive structures on vascular neurogenic tonus].

In anesthetized cats, blockade of the intermediate chemosensitive area (area "S") of the ventral medulla by means of local cooling to 20-22 degrees C induced drop of arterial blood pressure by 22% as well as of the perfusion pressure in hind-limb skin-muscular and muscular preparations by 24% and 12%, resp. Analogous cooling of the caudal chemosensitive area (area "L") increased the BP by 6% as well as the perfusion pressure. Decentralizing of the hind-limbs prevented the perfusion pressure changes but did not affect the BP shifts.