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D R Gutsaeva

Publications and source records attributed to D R Gutsaeva.

11 recordsLinked to original sources
PubMed2003

Hyperoxic vasoconstriction in the brain is mediated by inactivation of nitric oxide by superoxide anions.

The hypothesis that decreases in brain blood flow during respiration of hyperbaric oxygen result from inactivation of nitric oxide (NO) by superoxide anions (O2(-)) is proposed. Changes in brain blood flow were assessed in conscious rats during respiration of atmospheric air or oxygen at a pressure of 4 atm after dismutation of O2(-) with superoxide dismutase or suppression of NO synthesis with the NO synthase inhibitor L-NAME. I.v. administration of superoxide dismutase increased brain blood flow in rats breathing air but was ineffective after previous inhibition of NO synthase. Hyperbaric oxygenation at 4 atm induced decreases in brain blood flow, though prior superoxide dismutase prevented hyperoxic vasoconstriction and increased brain blood flow in rats breathing hyperbaric oxygen. The vasodilatory effect of superoxide dismutase in hyperbaric oxygenation was not seen in animals given prior doses of the NO synthase inhibitor. These results provide evidence that one mechanism for hyperoxic vasoconstriction in the brain consists of inactivation of NO by superoxide anions, decreasing its basal vasorelaxing action.

Animals↗
PubMed2002

[Hyperoxic vasoconstriction in the brain is realized by inactivation of nitric oxide by superoxide anions].

We tested a hypothesis that the cerebral blood flow (CBF) is reduced at hyperbaric oxygen due to inactivation of nitric oxide (NO) by superoxide anions (O2). In our experiments, the CBF was measured under hyperbaric oxygenation (HBO) 4ATA after inhibition of NO synthesis and inactivation of O2. The CBF was reduced at HBO exposure. Inhibition of NO--synthase type I and III (NOS) by L-NAME in the air caused the same decreasing of the CBF as at 4 ATA HBO. Hyperbaric vasoconstriction was diminished after NOS inhibition. Intravenous injection of superoxide dismutase (CuZn SOD) increased the CBF in the air and HBO exposure. This effect disappeared at preliminary NOS inhibition. These data suggest that inactivation of NO by O2 is a more effective mechanism of HBO vasoconstriction.

Animals↗
PubMed2002

[Cerebral blood flow modulates hyperbaric oxygen induced neurotoxicity by neuronal and endothelial nitric oxide].

The goal of work was to reveal changes in microcirculation of the rat brain and the role of nitric oxide (NO) in development of seizures at hyperbaric oxygen exposure. The Wistar rats with implanted paired platinum electrodes in left and right striatum were used for experiments. The latency of seizures was defined by the EEG, the cerebral blood flow (CBF) was measured by hydrogen clearance. One group of animals was exposed to a 5-ata oxygen, while the others before oxygen treatment were injected with: Nw-nitro-L-arginine methyl ester (L-NAME), blockator of constitutive NO synthase; 7-nitroindozol (7NI), specific inhibitor of neural NO synthase. The latency of seizures was 41 +/- 1.9 min at 5 ata oxygen exposure. CBF was decreased to 10-14% but before seizures it increased to 23 +/- 9%. L-NAME and 7NI prevented development of hyperoxygen hyperemia and onset of seizures. The results indicate occurrence of hyperbaric oxygen changes of the CBF that modulate neurotoxic effects of NO in neurons as well as in cerebral vessels.

Animals↗
PubMed2000

[Involvement of nitrogen oxide in the cerebral vasoconstriction during respiration with high pressure oxygen].

High pressure oxygen evokes a cerebral vasoconstriction and diminishes cerebral blood flow with the aid of mechanisms which are not yet sufficiently studied. We were checking a hypothesis that the hyperbaric oxygen (HBO2) inactivates cerebral nitrogen oxide (NO), interrupts its basal relaxing effect, and evokes a vasoconstriction. In our experiments, HBO2 decreased cerebral blood flow depending on the pressure. Inhibiting the NO-synthase weakened basal vasorelaxation in breathing with atmosphere air and eliminated the vasoconstriction in exposure to the HBO2. Inactivation of O2 prevented the HBO2-induced vasoconstriction. The data obtained reveal that diminishing of cerebral blood flow in HBO is related to the NO inactivation and weakening of its basal vasorelaxing effect. Possible mechanisms of the NO inactivation may involve its reaction with oxygen and superoxide anion which lead to diminishing of the tissue NO concentration and weakening of its vasorelaxing effect.

Anesthesia↗
PubMed1995

[The relationship of the acid-base status of the blood to the electrophoretic mobility of the erythrocytes in liver pathology].

With cholestatic hepatite, the relationship between acid-alkaline condition of blood and electrophoretic mobility of erythrocytes was studied. It is shown that changes in parameters of the individual mobility distribution are translated into reality independently, and are directed to maintain the steadiness of the index middle level. Dependence of this sign on the pH value, hemoglobin content and bicarbonate-ion concentrating in blood, an on partial pressure of oxygen and carbonic gas was discovered. The intravenous infusion of patients with hemodese restored the middle level of cell electrophoretic mobility previously reduced due to liver pathology. Membrane mechanisms controlling stability of erythrocyte electrokinetic characteristics are discussed.

Acid-Base Equilibrium↗
PubMed1995

[The control mechanisms of the electrokinetic properties of human erythrocytes in emotional stress].

A study was made of the influence of psycho-emotional strain, experienced by students when taking examinations, on the erythrocyte electrophoretic mobility (EPM). It has been shown that students under psycho-emotional strain the mean value of EPM remains the same, but changes were observed in the form of EPM distribution, while estimated by asymmetry and excession coefficients. Similar results were obtained when adrenalin was added to the blood.

Educational Measurement↗