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Biomedical subjects

V I Kulinskiĭ

Publications and source records attributed to V I Kulinskiĭ.

At least 19 recordsLinked to original sources
PubMed2000

[Receptor agonists as perspective neuroprotective agents].

Selective agonists of adenosine A1, GABAa, GABAb, and alpha 2-receptors (inhibitory neurotransmitter analogs) have a high neuroprotective effects (NPE) on two models of complete cerebral ischemia (CI). These NPEs are specific as they are inhibited by selective antagonists and, in addition, the selective alpha 1- and beta-receptor agonists have no NPE. The natural resistance to CI is also associated with A- and alpha 1-receptors. NPE does not result from improved cerebral blood flow. The receptor agonists protect the brain itself. They use a tolerance strategy and hypothermia is an important component, but not the only mechanism of NPE. Unlike most drugs, receptor neuroprotectors (RNP) guard not only a penumbra zone, but the core of ischemia as they are effective in complete global CI. Moreover, RNP-induced delay of irreversible lesions may increase a therapeutical window for using other drugs. RNPs are promising potential drugs in CI.

Adrenergic Agonists↗
PubMed1993

[Protective effect of adenosine in total brain ischemia].

Adenosine has prominent cerebro-protective effect at total brain ischemia. Other nucleotides and nucleosides are less active or have no effect at all. It suggests participation of A-receptors. Adenosine is more effective than 8 other drugs that have protective effect in different models of brain ischemia (nimodipine, gamma-hydroxybutyrate etc).

Adenosine↗
PubMed1990

[The physiological significance of regulation by catecholamines, second messengers and enzyme inducers of glutathione metabolism].

Stress, catecholamines (CA), cAMP and protein-kinase A do not affect superoxide dismutase, catalase, thioredoxin reductase, thiol transferase and glutathione reductase (GR). However, they activate glutathione peroxidase and glutathione transferase (GT) in a number of organs and inhibit renal gamma-glutamyl transferase. Ca2+ ions activate GT through calmodulin. CA were found to stimulate GSH transport from liver to blood and GT phosphorylation by protein kinase C. This suggests a regulation of the GSH metabolism by hormones and a second messenger. This regulation favours metabolism of active O2 substances (including protection from peroxide stress and leukotriene C4 synthesis), supporting of SH-proteins in reduced state, xenobiotics detoxication. GT and GR induction can play an important role in the mechanism of anti-peroxide action of butylhydroxytoluene.

Animals↗
PubMed1990

[The role of inner membrane in the realization of cAMP-dependent activation of mitochondrial enzymes].

It was shown that the increase in the activities of transhydrogenase and NAD(+)-dependent isocitrate dehydrogenase after incubation of mitochondria with cAMP is due to the stimulating effect of cAMP on mitochondria, but not to the increased stability of mitochondria to the incubation procedure. Treatment of mitochondria with trypsin prevents the action of cAMP on the both enzymes. The integrity of the inner mitochondrial membrane is necessary for the manifestation of cAMP effect. Pretreatment of mitochondria with the local anesthetic, lidocaine, prevents the activation of NAD(P)(+)-transhydrogenase and NAD(+)-dependent isocitrate dehydrogenase during subsequent incubation of mitochondria with cAMP. It is concluded that the role of the inner mitochondrial membrane consists in the reception of the cAMP signal for the internal compartment of mitochondria, i.e. for mitoplasts. Peripheral protein(s) on the external side of the inner mitochondrial membrane seems to play a role in cAMP reception.

Animals↗
PubMed1988

[Changes in the sensitivity of the alpha 2- and beta 1-adrenoreactive systems during the intensive cooling of rats acclimatized to cold].

Cold-acclimated rats with an increased resistance against intensive cold, differ from ordinary animals by increased beta 1- and decreased alpha 2-adrenoreactivity in ordinary conditions; their beta 1-adrenoreactive systems preserve sensitivity at intensive cold exposure (up to hypothermia below 25 degrees C), whereas the sensitivity of their alpha 2-adrenoreactive systems declines more rapidly (up to a moderate hypothermia--33-34 degrees C). The data obtained suggest the described shifts to be important for essential increase in general resistance against acute intensive cold exposure in rats.

Acclimatization↗
PubMed1986

[Regulation of mitochondrial transhydrogenase activity by catecholamines].

Administration of catecholamines to rats or their addition to liver and heart homogenates activates (by 30-50%) mitochondrial transhydrogenase in the direction of hydride-ion transfer NADPH----NAD+ via beta-adrenoreceptors and cAMP. Glucagon administration also increases by 48% the transhydrogenase activity of liver mitochondria. cAMP (1 microM) incubated with both liver homogenates and mitochondria exerts an independent activating effect on transhydrogenase. The effect of cAMP is specific and is expressed as an increase of V. The integrity of mitochondrial membranes is crucial for the manifestation of cAMP effect. Possible mechanisms of cAMP action on the transhydrogenase activity and the significance of this regulation for mitochondrial energetics are discussed.

Adrenergic alpha-Agonists↗
PubMed1986

[Protective effect of adrenergic alpha 2-receptor agonists in hypoxic hypoxia].

The antihypoxic effect of alpha 2-adrenoceptor agonists was studied by two different approaches: reproduction of the effect by a number of alpha 2-agonists and its blockade with selective antagonists. The data obtained suggest that alpha 2-adrenoceptor agonists increase the survival and the lifespan of mice in all the models of acute hypoxic hypoxia under study. A close correlation between antihypoxic action of alpha 2-adrenoceptor agonists and their anticalorigenic effect was established (r = +0.87; P less than 0.01).

Adrenergic alpha-Agonists↗
PubMed1985

[Submitochondrial distribution of cAMP during incubation with rat liver mitochondria].

Labeled cAMP incubated with rat liver mitochondria penetrates not only through outer mitochondrial membranes, but also into mitoplasts, where it is accumulated mainly in the matrix. Damage of mitochondrial membranes caused by single freezing-thawing treatment promotes no influx, but efflux of cAMP from mitoplasts. cAMP molecules penetrate inside mitochondria largely in an unchanged state in all submitochondrial fractions, as was demonstrated by the TLC method. cAMP transport into mitochondria can serve as a reason for: 1) stimulation of mitochondrial function by hormones whose effects are realized through activation of cytoplasmic adenylate cyclase and by extramitochondrial (cytosolic) cAMP; 2) existence of cAMP-dependent protein kinase and cAMP-phosphodiesterase in mitochondria.

Animals↗
PubMed1985

[Effect of serotonin on proliferating and resting cells in culture].

The influence of exogenous serotonin on cell division of L929 and L-41 cell strains has been investigated under various conditions of cell growth in culture (the incubation either in 10% serum medium without changing the medium, or in the medium with 0.5% serum). The data obtained show that serotonin in physiological concentration (10(-7) M) stimulates proliferation of resting cells. In proliferating cells, compared to resting ones, the sensitivity to exogenous amine appeared statistically non-significant. Exogenous serotonin is suggested to be a proliferating stimulus for resting cells.

Animals↗
PubMed1984

[Regulation of purified NAD-isocitrate dehydrogenase from the pig heart by calcium ions and cAMP-dependent protein kinase].

Different cAMP-dependent protein kinases do not phosphorylate homogeneous NAD-isocitrate dehydrogenase (ICDH) and do not change its activity. Ca2+ (3 X 10(-7) = 10(-3) M) activates the enzyme throughout the process of purification including homogeneous enzyme by decreasing the KM for isocitrate. The calmodulin inhibitor trifluoperazine does not change ICDH activation.

Animals↗