Biomedical subjects

V F Sagach

Publications and source records attributed to V F Sagach.

At least 73 records · Page 4Linked to original sources

PubMedDate not supplied

[Relese of Ca2+ from mitochondria after mitochondrial membrane depolarisation].

With the aid of specific inhibitors of Ca(2+)-uniporter (ruthenium red) and mitochondrial permeability transition pore, PTP (cyclosporine A) it is shown that PTP opening takes place after loading the rat liver mitochondria with calcium and depolarisation of mitochondrial membrane with protonophore (carbonyl cyanide m-chlorophenyl hydrazone, CCCP), and the pore opening accounts for accelerated efflux of calcium from mitochondrial matrix as well as availability of "rapid" component of two-exponential kinetic curve of Ca(2+)-efflux. An analysis of kinetic data of Ca2+ transport after membrane depolarisation also confirms our earlier observations that time frame of the pore open state is restricted, and membrane integrity is restored before all the calcium load is delivered into incubation medium. The absence of additivity between the shares of Ca(2+)-uniporter and PTP in Ca(2+)-transport is observed, and conclusion is made that partial share of PTP in calcium transport is not a constant, but a variable constituent which is diminished to zero as soon as the Ca(2+)-uniporter activity reaches its maximum after the abolition of membrane potential with CCCP. Based on some observations, it is supposed also that PTP inactivation takes place during calcium translocation across the mitochondrial membrane, which could account for limited release of Ca2+ from mitochondrial matrix through the pore itself as well as relatively narrow limits of the pore open state in comparison with time scale of complete cation release from depolarised mitochondria.

Animals↗

PubMedDate not supplied

[Age-related characteristics of the role of the endothelium in the response of vascular smooth muscles to hormones. The role of ultrastructural changes].

The experiments performed on isolated preparations of femoral artery and aorta of the mature and old rats as well as on those of coronary arteries of adult and old subjects failed to reveal direct participation of endothelium in the realization of insulin and vasopressin effects on the smooth muscles of the vessels studied. However, the endothelium modulated their influence on the vessels in the mature age. The lack of modulating effect of the endothelium in old age may be a result of its structural changes and thickening of a hemato-cellular barrier of the vessel wall observed by electron microscopy.

Adult↗

PubMedDate not supplied

[The role of prostaglandins in the development of cardio- and hemodynamic disorders in postischemic shock].

Experiments on anaesthetized dogs have shown, that reperfusion of ischemized tissues is accompanied by significant increase in thromboxane A2 (Tx A2) and prostacyclin (PG I2) blood level and by development of pronounced cardiovascular insufficiency. Preliminary blockade of prostaglandins biosynthesis prevent an increase of TbA2 and PG12 blood level, postreperfusion disturbances of central and regional circulation develop later and are less pronounced. Therefore, endogenic prostaglandins take part in the development of post ischemic shock reaction, influencing chiefly the venous vessels and blood return to heart.

Animals↗

PubMedDate not supplied

[Study of cardio- and hemodynamic reactions to administration of GABA into the neuronal structures of the ventrolateral area of the medulla oblongata of cats].

The data obtained in acute experiments on cats have indicated that the most GABA-sensitive injected neuronal structures in the ventrolateral medulla appear to be located in the vicinity to the roots of the XII cranial nerves. GABA injected into these structures just rostrally to the roots induced hypotensive reactions due to heart rate and myocardial contractile activity decrease, besides inhibition of sympathetic vasoconstrictor influences. GABA injected into the neuronal structures in the caudal ventrolateral medulla induced hypertensive reactions, to a large extent due to increase in heart rate and contractile activity of myocardium.

Animals↗

PubMedDate not supplied

[Various mechanisms of circulatory failure in septic shock].

The main parameters of hemodynamic and myocardial contractile activity, transcapillary fluid and proteins exchange have been studied in healthy and infected anaesthetized dogs with source of purulent infection during septic shock development. Besides, blood gas tension, pH and toxicity of blood and lymph are determined as well. It is shown that damage of microcirculation promoting tissue hypoxia and endogenous intoxication, is responsible for the initiation of decompensating disturbance of circulation at pus process generalization.

Animals↗

PubMedDate not supplied

[The role of the thrombocyte-activating factor in the development of circulatory disorders in the postischemic shock reaction].

Experiments carried out on anesthetized dogs have shown that reperfusion of long-ischemized leg tissues is accompanied by a significant decrease of the cardiac output and myocardial contractility. Restriction of the venous return to the heart is important in the cardiac output decrease due to an increase of venous compliance and blood pooling on the peripheral circulation. The preliminary blockade of platelet-activating factor (PAF) receptors decreases degree of the cardio- and hemodynamic disturbances after reperfusion of ischemized tissues and prevents development of pulmonary hypertension. Similarity of the postreperfusion central and peripheral hemodynamic disturbances and animal responses to injection of the exogenous PAF as well as the presence of the protective effect of PAF-receptor antagonist BNo. 52021 permit concluding, that PAF takes part in the development of postischemic shock reaction and its receptor blockade can be used to prevent postreperfusion hemodynamic disorders.

Animals↗

PubMedDate not supplied

[Changes in the effects of verapamil in sensitized dogs].

The cardiovascular effects of verapamil were studied on anesthetized dogs with the intact chest, control ones and those sensitized with horse serum. Verapamil dose inducing the minimal cardio- and hemodynamic effects in the sensitized dogs was 2-3 times less that used in the controls. In addition, in contrast to the control dogs, the sensitized dogs exhibited the cardiotoxic effects of verapamil-a disorder of atrioventricular conductivity and a deterioration of the cardiac muscle relaxation. The cardiovascular effects of verapamil are modified by sensitization of the organism by heterologous serum proteins.

Animals↗

PubMedDate not supplied

[Effect of hyperthermia on the cardio- and hemodynamics and acid-base balance of the blood in dogs].

The effect of severe hyperthermia on the circulatory function was studied in dogs. Arterial pressure was maintained at the normal level, cardiac output increased at the core temperature of about 40 degrees C. An abrupt fall of the arterial pressure and cardiac output was observed at the rectal temperature of about 41 degrees C. The results suggest that a decrease in the cardiac output during severe hyperthermia is due to the fall of the central venous pressure and to the increase of the vascular compliance.

Acid-Base Equilibrium↗

PubMedDate not supplied

[Effect of indomethacin on the development of cardiac and hemodynamic disorders in shock of immune origin].

Blockade of biosynthesis of prostaglandins (indomethacin) was shown to decrease significantly disorders of cardio- and hemodynamics after immune heart damages (intracoronary anticardiac serum injections) in experimental anesthetized dogs. A positive effect of indomethacin was produced by blockade of the first part (0-15 min) of capacity vessels dilation reaction (blood deposition), subsequent decrease of venous return limit and fall of heart output. Indomethacin potentiated constriction of coronary vessels.

Animals↗

PubMedDate not supplied

[Shifts in the parameters of cardio- and hemodynamics and their correction using liposomes in the process of the development of septic shock].

The interdependence between changes in central cardiac hemodynamics and regional blood flow has been studied in dogs with experimental septic shock. Possible correction of the above damages by direct delivery of liposomes to tissues of the septic focus has been investigated. It has been found that vascular insufficiency is primary in the genesis of decompensated circulatory disturbances, with its progress leading to the inhibition of pump and contractility cardiac functions. Regional subcutaneous administration of liposomes in developing septic shock prevents the onset of cardiovascular disturbances.

Animals↗

PubMedDate not supplied

[Cardio- and hemodynamics of dogs during the development of postischemic shock reaction].

Experiments on dogs have shown that tension of peripheral capacitive vessels decreased and development of the blood deposition reaction in the venous part of the vascular bed occurred immediately after beginning of long-ischemized tissue perfusion. This leads to limitation of venous blood return to the heart, decrease of the cardiac output and development of the system hypotension. Lowering in the perfusion coronary pressure induced limitation of the coronary blood flow and inhibition of the myocardial contractility. Indicated constriction of resistive vessels and dilatation of the capacitive ones may be due to an increase of the prostacyclin and thromboxane A2 blood levels. Described disturbances achieved their maximum 3 hours later and were accompanied by arterial hypoxemia, metabolic acidosis and hypercapnia.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied