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Biomedical subjects

A L Azin

Publications and source records attributed to A L Azin.

At least 19 recordsLinked to original sources
PubMed2004

[Possibilites to improve the cerebral venous tonus in patients suffering of accelerated ageing in blood circulation system by the nonmedicamentousal sympathocorrection method].

The aim of the study was to evaluate the effectiveness of the transdermal electro impulses directed on ganglions stellatum in order to prevent the accelerated ageing and improve the cerebral venous flow. Using by the angioscanning method it was been found the phenomenon of ectasia in venae jugularis int. in patients suffering of accelerated ageing in 100% cases. The normalization of venous diameter after the treatment by electrical impulses has been found in 31-55% of cases.

Adult↗
PubMed2002

[Decrease of reactivity of cerebral arteries at late stages of life].

The reactivity of cerebral arteries have been examined in three groups of patients (young, middle and adult ages). The medium meanings of the blood flow velocity (V) and the pulsativity index (Pi) were registrated in MCA and PCA under hypercapnia, hyperventilation and light stimulation. It was revealed that the reactivity of cerebral arteries in middle and especially in adult groups was decreased.

Adolescent↗
PubMed1990

[Effects of tumor necrosis factor on the tonus of cerebral arteries].

It was determined that tumor necrosis factor (TNF) is capable of decreasing the local brain's blood flow on 45.6% (in the concentration of 6 micrograms/kg); to make a spasm of the pial arteries on 39.6%. In vitro experiments TNF increased the amplitude of the rhythmical and the tonic contractions of the brain's arteries smooth muscles (3.6 X 10(-8) M). The direct action of the TNF in the vascular wall is endothelium-dependent.

Animals↗
PubMed1989

[Effect of atriopeptin on the adrenergic mechanism regulating blood vessel tonus].

The direct action of atriopeptin on the cell regulation mechanism of the smooth muscle in isolated segments of the portal vein, aorta, pancreatic and cerebral arteries have been studied. It was found that atriopeptin induce the direct relaxation of the smooth muscle in the main vessels only (aorta, portal vein). In the cerebral and pancreatic arteries atriopeptin stops norepinephrine-induced contractions. The data obtained show that the action of the atriopeptin is mediated by Na+-K+ pump activation of smooth muscle cells and restricts vasoconstriction of catecholamine effect.

Adrenergic Fibers↗
PubMed1989

[The reactivity and functional heterogeneity of the cerebral arteries].

The reactivity and functional heterogeneity of cerebral arteries are maintained by the participation of the endothelium in the regulation of the smooth muscles and by the influence of vasoactive peptides upon the neurotransmitter mechanisms. The initial level of the basal tone plays a major role, too.

Animals↗
PubMed1989

[Mechanisms of the regulation of the blood supply of the aortic wall].

The monoamine-induced contraction as well as the ATP- and hypoxia-induced relaxation of the smooth muscles were recorded in isolated aortal paravasal arteries. The data obtained show that the muscles of paravasal arteries represent a regulation mechanism of the aorta wall blood supply.

Adult↗
PubMed1988

[Mechanism of the effect of atriopeptin on regional blood flow].

Atriopeptin exerts a direct regulatory vasodilating effect on the mechanism of the regional blood flow maintenance. Under preliminary activation of vascular tone the atrial factor can produce the smooth muscle relaxation. Atriopeptin II is the most active among the three types of atriopeptin, atriopeptin III is the least active.

Animals↗
PubMed1982

[Oxygen, carbon dioxide and calcium control of the mechanisms of relaxation in the cerebral artery smooth musculature].

The direct action of the hypoxic (PO2 60-20 mm Hg) and hypercapnic (PCO2 50-60 mm Hg) solutions on isolated strips of human cerebral arteries was studied. Verapamil, sodium nitroprusside, manganese, dichlordiphenyltrichlomethylmethan inhibited the hypoxic and hypercapnic relaxation. The data obtained suggest that lowering of PO2 or raising of PCO2 decrease the membrane calcium transport and increase the activity of the cellular calcium pump.

Calcium↗
PubMed1981

[Role of pH in the mechanism of action of CO2 on the smooth musculature of cerebral arteries].

It has been discovered on isolated strips of the internal carotid artery of man that changes in extracellular pH influence the effects of hypercapnia that manifest in relaxation of smooth muscles. However, under conditions of pH stabilization within the range of 7.3--7.4 the direct action of hypercapnia was unchanged. Acetazolamide, the blocker of the intracellular carboanhydrase activity, inhibited the effects of hypercapnia. It is inferred that changes in the intracellular H+ are of the greatest importance in the action mode of CO2 on smooth muscles of the vessels, whereas changes in the extracellular pH have but a modulating effect.

Acetazolamide↗
PubMed1981

[Role of extracellular pO2 and pCO2 in membrane mechanisms regulating cerebral artery smooth muscle].

The O2 insufficiency and excessive CO2 relaxed the brain arteries smooth muscles abolishing their spontaneous electrical and contractile activity. The hypoxia effects were potentiated in the hypopotassium milieu and weakened in the hyperpotassium and hyposodium solutions. Hypercapnic responses insignificantly both in hypo- and hyperpotassium solutions whereas hyposodium one enhanced them. A decrease of the extracellular PO2 seems to reduce the excitability of membranes and to inhibit the active transport of Na+ and K+. CO2 appears to exert no considerable effect on the active transport processes but to interfere in the intracellular mechanisms of Ca2+ regulation.

Animals↗
PubMed1977

[Activation mechanisms of the contractile cells of cerebral arteries and veins].

In isolated strips of internal carotid artery and middle cerebral artery in humans, spontaneous electric and contractile activities were revealed. Low (35 degrees C) and high (40--41 degrees C) temperatures inhibited the development of spontaneous contractions. Under depolarization of the cells' membranes by potassium ions, no development of spontaneous electric or contractile waves occurred, while contractions of the tonic type were observed in arterial preparations. No spontaneous contractions were found in the cerebral veins.

Acetylcholine↗