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Biomedical subjects

A V Samoĭlenko

Publications and source records attributed to A V Samoĭlenko.

At least 19 recordsLinked to original sources
PubMed1990

[The organic macro- and microhemodynamics and the systemic circulation under the combined action of hypoxia and hypothermia].

In regimen of the constant blood flow perfusion of shank and small intestine of cat combined effect of hypoxia (10% O2 in N2) and hypothermia (about 30 degrees C) involved a decrease in precapillary resistance, an increase in capillary filtration coefficient in both vascular regions, an increase in postcapillary resistance and in mean capillary pressure in the intestine, and their decrease in the shank. In hypothermia, the hypoxic stimulus induced insignificant shifts in all the parameters under study in both organs. Dependence of hypoxic changes of macro- and microhemodynamics on the activity of adrenergic receptors in the cooled organism was studied on decentralized shank of cat. After cooling of cat and blockade of alpha-adrenoreceptors hypoxic hypoxia caused much greater reduction of precapillary resistance of shank, more striking (by 3 times) increase of capillary filtration coefficient and the increase of capillary pressure and postcapillary resistance in contrast with their decrease to hypoxia under hypothermia before alpha-blockade. Beta-adrenoreceptor blockade had no influence on the changes of the resistance and exchange function of skeletal muscle (shank) blood vessels evoked by hypoxia under cooling. Systemic arterial pressure are diminished during hypoxia under the normothermic conditions of animals. Such kind shifts caused especially by the decreasing of the total peripheral resistance; cardiac output are small raised in this situation. But combined influence of hypoxia and hypothermia evoked the pressor shifts of the systemic arterial pressure because of less decrease of total peripheral resistance and more remarkable rise of cardiac output. Hypoxic stimulus caused both in normothermia and hypothermia conditions caused the rising of venous return.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[The dependence of the hemodynamic shifts in the systemic arterial and venous vascular beds on the degree of change in the arterial pressure under the action of vasoactive substances].

The participation of hemodynamic parameters in formation of systemic pressor displacement due to action of norepinephrine and angiotensin was shown in acute experiments in cats. An arterial pressure rise by 15 +/- 2% and 25 +/- 3% depended on total peripheral resistance and cardiac output enhancement. The maximal arterial pressure rise only depended on total peripheral resistance increase. The reduction of venous return resulted from a decrease of the blood flow in v. cava posterior whereas the blood stream in v. cava anterior increased. Depressor actions of acetylcholine and histamine were enhanced owing to a fall in the vessels resistance.

Acetylcholine↗
PubMed1987

[Effect of the thoracic pumping function on venous return in chronic experiments].

In cats with implanted ultrasonic transducers, interrelationships between phasic oscillations of the blood flow in posterior v. cava due to the chest sucking function and changes of intrapleural pressure, were studied. Linear dependence of shifts of these parameters was only observed in an increased pressure and respective drop in venous blood flow. The dependence was absent in drop of the pressure and increase of venous blood flow. The ratio of the intrapleural pressure shift to magnitude of phasic changes of the blood flow in the posterior v. cava (the pumping coefficient) is suggested for estimation of effect of the chest sucking function upon the venous outflow and for relative estimation of rigidity of the vascular bed's venous portion.

Animals↗
PubMed1987

[Changes in systemic hemodynamics during exposure of the cooled body to hypoxia].

In cats with normal body temperature, hypoxia (10% O2 in nitrogen) induced depressor shifts of the arterial pressure due to a drop of the general peripheral resistance, whereas in cooling of the organism to +30 degrees C a slight increase of the arterial pressure occurred. Hypothermia was found to reduce the degree of increase in the venous return in response to a hypoxic stimulus.

Animals↗
PubMed1986

[Systemic hemodynamic shifts in the arterial and venous portions of the vascular bed in hypoxia].

A reduction of total peripheral resistance is of a major importance for depressor shifts of arterial pressure in moderate hypoxia. The hypoxic stimulus induces a deficiency of increment in cardiac output shifts as compared with venous return. An increment of venous return and cardiac output suggests that the compensation for the depressor shifts induced with the lack of O2 in air and blood, occurs on account of flow induces of the circulation system.

Animals↗
PubMed1983

[Study of the role of the venous return in pressor changes in the systemic hemodynamics by the means of the automatic regulation of its value].

Feed-back experiments with catecholamine-induced pressor changes of arterial pressure (AP) aided to study possible contribution of the venous return changes in cats. Preliminary recorded changes were reproduced with the aid of electronic control of perfusion pump connected with extracorporeal reservoir and venous portion of vascular bed. The reproduced changes of venous return corresponded to those occurring under action of catecholamines. The same maximal increase of AP (by 50%) could be obtained by means of increasing the venous return either by 1/6 with adrenaline (A) or by 1/10 with noradrenaline (NA). Maintaining of the increased AP involves to a greater extent participation of the above parameters in systemic shifts; in response to A 1/2 and in response to NA 1/3 of the pressor response can be maintained by an increase in the venous return. The quantitative contribution of the vascular component (total peripheral resistance) to pressor shifts of AP under the catecholamines action is greater than that of the cardiac component, particularly in response to NA.

Animals↗
PubMed1981

[Blood flow in the inferior vena cava measured by a Doppler ultrasound flowmeter in chronic experiments on cats].

Supercound Doppler's transducers indwelled in the cat v. cava posterior revealed that the higher blood flow values in chronic experiments as compared to acute ones were due to the effect of the chest suction action on the blood flow. The phasic changes of the venous blood flow occurring at resting and under various effects were related to respiration and heart activity, the respiratory component being more obvious than the cardiac one. A significant correlation existed between the mean value of the blood flow in the v. cava posterior and the respiratory changes of the blood flow amplitude.

Animals↗
PubMed1980

[Changes in systemic hemodynamics caused by intra-arterial and intravenous autoperfusion of small blood volumes].

Changes of general peripheral resistance in response to autoperfusion both prior to and after blockade of alpha- and beta-adrenoreceptors depended on its initial level: at a relatively low initial value autoperfusion increased the vascular resistance whereas at high value decreased it. During maximal shifts of hemodynamic parameters the venous return prevailed over the cardiac output. The pressor effect was practically unrelated to the way of blood administration.

Animals↗
PubMed1979

[Adrenergic mechanisms of changes in the resistance and volume vessels of the small intestine in the presence of a reduced volume of circulating blood].

In humorally isolated small intestine, the 10--20%--decrease in the perfusing blood volume against the background of augmented vascular resistance of the small intestine, induces different shifts of the latter's vascular capacitance. At the blockade of small intestine's beta--adrenoreceptors the decrease does not practically tell on the character of shifts in the intestine's resistance and capacitance while the blockade of alpha--adrenoreceptors abolishes the augmentation of these parameters.

Animals↗
PubMed1979

[Hemodynamic structure of pressor reactions to vasoactive substances].

In cats, similar changes of the blood pressure had different hemodynamic structures under the influence of catecholamines or angiotensin. Adrenalin was able to evoke a pressor response by means to either caridac or vascular factor. In the former case, the increase in the cardiac output was induced both by an increasing blood flow towards the heart and by an additive outflow of the blood from the minor to the major circulation; in the latter case, the increase in the general peripheral resistance entailed a decrease in the cardiac output in spite of the augmentation of the venous return which determined a delay of the blood in the minor circulation. The latter variant of interrelationships among hemodynamic parameters can occur under the influence of noradrenaline as well. A combined similarly rendered participation of the cardiac and the vascular factors in the increasing the blood pressure occurs under the influence of angiotensin and sometimes of noradrenaline. The participation of cardiac output in the pressor response may depend on hemodynamic shifts in the minor circulation which either limit or facilitate, or leave unchanged the rate of increment of the cardiac output.

Angiotensin II↗