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Biomedical subjects

T V Kazueva

Publications and source records attributed to T V Kazueva.

15 recordsLinked to original sources

[Effectiveness of the elimination of lipid peroxidation products in various methods of detoxication therapy of patients with traumatic shock].

The shockogenous trauma is followed by a considerable accumulation of lipid peroxidation products in the patient's organism. The most effective of all the measures used for the detoxication was found to be extracorporal use of the donor spleen which resulted in lower content of lipid peroxidation products in blood plasma immediately after the procedure. The maximum effect was observed 1 hour later and persisted during one day after treatment.

Free Radicals↗

[Preservation of liver mitochondria function in hemorrhage-resistant rats during severe long-term hypotension].

In contrast to the reported data evidencing early impairment of the liver mitochondrial function in the Wiggers model of hemorrhagic shock at the arterial blood pressure 30-40 mm Hg, lasting not over 6 h, a group of hemorrhage-resistant rats was discovered. In these rats, the lifetime was about 20 h, with the blood pressure being the same as indicated above. Rectal temperature decreased to 24-25 degrees C during shock. No substantial disorders were recorded in oxidative phosphorylation and ATPase activity of the mitochondria isolated from the liver in the irreversible stage of shock (70% blood return) or in the terminal state of animals. It is assumed that hypothermia plays the protective role. The conclusion is made that the damage to the mitochondria is not indispensable factor of the development of irreversible shock.

Adenosine Triphosphatases↗

[Energy metabolism in the liver and kidneys of rats during the 1st few days after acute hemorrhage].

A relative stability of the adenylate nucleotide system redox of liver and kidney cells was recorded in rats during the first day after acute hemorrhage (2.5% of body weight) in spite of a severe course of the posthemorrhagic period. Energy metabolism was examined in the state of the decompensation of circulation at a blood pressure of 35-45 mm Hg that progressively fell down after a short-term stabilization at the level of 40-60 mm Hg. Comparison of the results obtained with the reported data warrant conclusion that the magnitude of the critical arterial blood pressure at which the test parameters change lies between 40 and 50mm Hg and can vary in relation to a number of the conditions.

Adenine Nucleotides↗

[Use of gutimin for the treatment of experimental traumatic shock].

The guthymine medication of a severe shock in rats started 10-20 minutes after injury is shown to eliminate energy metabolism disorders in the brain, liver and kidneys. In the brain of the guthamyine treated rats even a somewhat reduced adenosinetriphosphate content was demonstrable. Administration of guthymine together with polyglucin to cats in a torpid phase of the shock did not effect treir survival, but shortened the life-span of the test animals as compared to controls (receiving polyglucin alone). With guthymine addid to polyglucin the lactate and pyruvate concentration in the blood remained unchanged.

Amidines↗

[The state of energy metabolism in the rat liver after a single acute hemorrhage].

A system of adenine nucleotides and redox state of liver cells as well as activities of dehydrogenases of the tricarbonic acid cycle and of cytochrome oxidase in liver cell homogenates were not altered after an acute single hemorrhage in rats even though the process run into the step of circulation decompensation (AP 40 mm Hg).

Acute Disease↗

[Energy metabolism in skeletal muscles in experimental traumatic shock].

Content of ATP and adenylate nucleotides was not markedly altered in rats during a traumatic shock induced by Cannon's procedure involving an impairment of skeletal muscles. Energy potential and content of creatine phosphate were only slightly decreased in these tissues, while the level of lactate and the lactate/pyruvate ratio were increased at the terminal phase.

Adenine Nucleotides↗