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Biomedical subjects

S V Gasteva

Publications and source records attributed to S V Gasteva.

At least 19 recordsLinked to original sources
PubMed1987

[Effect of corticotropin on the rate of 32P-orthophosphate incorporation into the synaptosome phosphoinositides of the ischemic rat brain].

A high rate of 32P turnover in polyphosphoinositides (up to 80% of the total radioactivity) was found in synaptosomes of normal and ischemic rat brain. Corticotropin (ACTH) increases the rate of 32P turnover in polyphosphoinositides of normal synaptosomes and decreases it in ischemic synaptosomes. Depolarization (high KCl concentration in the incubation medium) activates polyphosphoinositide metabolism in normal (by 50%) and ischemic (by 30%) synaptosomes. The combined influence of depolarization and ACTH results in the additive effect. Thus, a stimulating effect of ACTH on phosphoinositide metabolism disturbed in ischemia was recovered during depolarization of ischemic synaptosomes.

Adrenocorticotropic Hormone↗
PubMed1984

[Phospholipids of the subcellular fractions of brain and liver tissues in rats in total oxygen starvation of the body].

The rate of phospholipid turnover in brain subcellular fractions differ from that in the liver tissue. Hypoxia of medium severity (pressure chamber 240 mm Hg) influences neither the content nor the turnover rate of phospholipids in liver subcellular fractions. Meanwhile in brain subcellular fractions, it results in a decreased phospholipid turnover rate. Severe hypoxia (less than 200 mm Hg) leads only to the suppression of the phospholipid turnover rate in the liver, whereas in the brain, it results in the decline of the phospholipid turnover rate as well as in the reduction of phospholipid content. Thus, the well-known concept of the higher brain sensitivity to oxygen deficiency as compared to the liver is exemplified by phospholipid turnover in subcellular fractions.

Animals↗
PubMed1979

[Effect of cerebral blood supply disorders on certain aspects of metabolism].

Bilateral ligation of common carotid arteries sharply decreases volume blood flow and oxygen consumption in the cortex, in diencephalon and midbrain whereas inducing no changes in the cerebellum and medulla oblongata. The same is true for intensity of metabolism of both total and separate fractions of phospholipids. This suggests that the changes of phospholipid metabolism in neural tissue depend on the degree of its blood supply disturbance and duration of the ischemia.

Adenine Nucleotides↗
PubMed1978

[Phospholipid metabolism in the microsomes and cytosol of the brain tissue of normal rats and rats with hypoxic hypoxia].

The content and the intensity of metabolism of various phospholipid groups (phosphatidylcholines, monophosphoinositides, aminophospholipids) was studied in the homogenate, microsomes, and cytozol of the rat brain under normal conditions and in hypoxic hypoxia (240 mm Hg). Phospholipid content per 1 mg of protein was the highest in the microsomes, and the least in the cytozol. However, the total phospholipids of the cytozol had the greatest rate of metabolism of their phosphate groups. Without influencing the phospholipid content, hypoxia depressed the intensity of their metabolism, and this depression proved to be approximately the same in all the tissue preparations under study.

Animals↗
PubMed1977

[Relationship between the phospholipid metabolism of different portions of rat brain and the degree of circulatory disruption in them (following carotid artery ligation)].

Bilateral ligation of common carotid arteries in rats caused a considerable reduction of the blood supply and also a marked fall of phospholipids (PL) metabolism in the hemispheres; in the diencephalon and the midbrain it occurred to a lesser degree; there were no alterations in the blood supply or the PL metabolism in the medulla oblongata and the cerebellum. Dependence of the extent of depression of the PL metabolism on the degree of blood supply disturbances varied in different brain regions. Even 5 hours after the ligation of both carotid arteries there was no restoration of blood supply.

Animals↗
PubMed1975

[Intensity of respiration and the metabolism of phospholipids in isolated brain tissues of rats at various temperatures in the presence of KCN].

The intensity of oxygen consumption, as well as phospholipid metabolism of minced rat brain tissue were studied at different temperature of the incubation media (37 degrees, 32 degrees and 27 degrees C) without cyanide and in the media containing KCN (0.5 and 1.0 mM). As shown, both parameters depended directly upon the incubation temperature within the range of 27 degrees-37 degrees. KCN inhibited both processes, but depression of phospholipid metabolism was more expressed. These data suggest that under conditions of cyanide poisoning phospholipid metabolism depends both on the toxic effect of KCN directly and on the temperature, whose reduction reinforces this effect.

Animals↗