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Biomedical subjects

Iu B Koloskov

Publications and source records attributed to Iu B Koloskov.

At least 19 recordsLinked to original sources

[Soluble guanyl cyclase of blood platelets and heart of rats with experimental myocardial ischemia].

The activity of soluble guanylate cyclase (GC) and its regulation in the platelets and heart of normal rats and rats with experimental acute myocardial ischemia provoked by coronary ligation was examined. There was a synchronous reduction in platelet and heart GC activity immediately following 15 minutes after surgery along with a drastically marked drop in genuine baseline activity (with Mg2+) to 19 and 40% in the platelets and heart (both ischemic and intact areas), respectively. Following 24 hours, GC activity insignificantly rose (up to 35.5%) in the platelets with Mg2+, that with Mn2+ remained unchanged; in the ischemic area it decreased much more (to 30%), whereas in the intact area it partially restored (up to 70%). The stimulating effect of DTT on platelet GC activity 15 minutes after the surgery drastically rose (from 2.8 to 8), then returning to normal 24 hours later. The findings show an enhancement in free radical processes typical of ischemia and indicate their high response of platelet GC at the earliest stages. Sodium nitroprusside-induced activation of myocardial GC diminished in the ischemic area in 15 minutes and virtually lacked in 24 hours. There was a less pronounced decrease in GC activation in the intact area. It is suggested that lower enzymatic activatibility is associated with heme loss. The absence of sodium nitroprusside-induced stimulation of platelet GC both in health and in the abnormality under question may be due to primary heme enzymatic deficiency.

Acute Disease

[Cardiac guanylate cyclase in rats with ischemic damage to the myocardium].

The activity of soluble guanylate cyclase (GC) of rat heart and the regulatory activity of dithiothreitol (DTT) and sodium nitroprusside under ischemic myocardium damage caused by ligation of left coronary artery has been investigated. After coronary occlusion the GC activity in the presence of Mn2+ or Mg2+ decreases both in ischemic and in intact zones (40% from normal) in 15 min, in 24 h it more diminishes (up to 30%) in the ischemic zone, in intact zone it partially normalizes (up to 70%). The stimulatory effect of DTT on the GC activity in studied heart zones doesn't differ from control. The activation of GC by nitroprusside in ischemic zone decreases in 15 min, it is practically absent in 24 h. The decrease of GC activation in intact zone is less expressed. It is suggested that the reduction of GC activation by sodium nitroprusside is due to the loss of the heme by the enzyme during ischemia.

Animals

[Use of hyperbaric oxygenation in the therapy of experimental hypothyroidism].

In animal experiments on rabbits the effect of hyperbaric oxygen was studied on the functional state of the myocardium, the cardiac resistance to induced peroxide lipid oxidation, the structural and functional changes in the thyroid gland and the state of microcirculation in the conditions of experimentally induced hypothyrosis. It was demonstrated that hyperbaric oxygen has a favourable effect on the state of myocardium and microcirculation.

Animals

[Changes in the balance of biogenic monoamines and their metabolites in the organs of rats with oxygen-induced epilepsy].

The content of some biogenic monoamines and their metabolites in rat brain and heart in different periods of oxygen epilepsia was studied using high performance liquid chromatography with electrochemical detection. It was shown that already at the 5th minute of exposure to oxygen adrenaline, DOPA and some noradrenaline metabolites disappeared in the brain and noradrenaline level reduced. At this period in rat heart the reduction of catecholamine content was the most distinct and serotonin level was unchanged. At the beginning of convulsive period the modifications of biogenic amines content were nonparallel in brain regions: in the heart the reduction of catecholamine level went on, especially in right ventricle. In the terminal phase of oxygen epilepsia brain biogenic amines increased, however, not up to normal meaning, heart catecholamines at this period were at the same level as at the beginning of the convulsive period.

Animals

[Kinetics of the oxidative deamination reaction in the preconvulsive period of oxygen-induced epilepsy].

Kinetic parameters of monoamine oxidative deamination in compensatory and preconvulsive periods of oxygen epilepsia were studied. It was shown that in rat brain MAO's affinity for serotonin reduced from the 5th minute of exposure to hyperbaric oxygen and went on reducing on the 15th minute. In rat heart the affinity of MAO for serotonin firstly decreased and then returned to normal meaning. Dopamine deamination in rat brain in compensatory period of epilepsia was activated and then was inhibited. In rat heart from the 5th minute of exposure to oxygen dopamine and 2-phenylethylamine deamination was blocked. Tyramine deamination in preconvulsive period of epilepsia changed in a complex manner. It is concluded that the kinetic parameters of monoamine deamination change in the initial phases of exposure to hyperbaric oxygen, and the most distinct modifications take place in rat heart, but not in rat brain.

Animals

[Reaction of deamination of monoamines in the brain and heart of rats under the toxic action of hyperbaric oxygenation].

Kinetic parameters of monoamine deamination processes in the rat brain and heart after hyperbaric oxygenation (HBO) in toxic conditions (6 ata) were studied. HBO was shown to cause a substantial reduction in MAO affinity to serotonin in the brain, but not in the heart. Contrastingly, MAO affinity to dopamine was found to decrease in the heart, but not in the brain in response to HBO. Differences of tyramine and 2-phenylethylamine deamination in the rat brain and heart were also reciprocal following toxic HBO. In the initial phase of seizure episode MAO activity in the brain and heart was also different. Distinct mechanisms of adaptation to toxic oxygen in the central nervous system and cardiovascular system are discussed.

Animals

[Effect of benzamide derivatives on convulsions induced by the toxic action of oxygen in rats].

The reversible MAO-A inhibitor moclobemide (5 mg/kg) was shown to prevent seizures in rats during exposure to toxic oxygen (6 ata). Benzamide derivatives increased the latent period of oxygen seizures and decreased the lethality following hyperbaric oxygenation. The range of anti-MAO activity of moclobemide and clorgyline in the rat brain and heart after toxic oxygenation was studied. It was distinct from those in control animals. Clorgyline was found to be more active in inhibiting MAO during toxic oxygenation in the heart and moclobemide-in the brain. The possibility is shown to prevent oxygen seizures not only with irreversible MAO-A inhibitors (clorgyline), but also with reversible ones (moclobemide).

Animals

[Contractile function and antioxidative system of the myocardium of the intact rabbit during hyperbaric oxygenation].

Daily exposures of rabbits to the HBO (2 ata, 1 hr) enhanced activity of glutathione-peroxidase for all 28 days of exposure. Other parameters of the antioxidative defence and the contractile function remained unchanged. The 2.5-ata oxygenation sharply reduced the activity of antioxidative enzymes, the antioxidative activity of lipids, and the tissue resistance against the induced peroxide oxidation of lipids. The heart contractile function was obviously worsened. Sites of necrosis appeared in the myocardium tissue. Increase in oxygenation seems to lead to changes of adaptation of the antioxidative system, but the exhaustion of the latter's power reserves potentiates the toxic effect of hyperoxia.

Animals

[Superoxide dismutase inhibition as a prerequisite for disordered myocardial function under oxygen loading].

Changes in the contractility of rabbit myocardium following administration of diethyl dithiocarbamate were studied to determine the role of superoxide dismutase (SOD) in cardiac support function. It was observed that in healthy rabbits, a 50% decrease in the left ventricle SOD level induced by the inhibitor was not followed by any considerable disturbances in myocardial contractility as determined without additional stimulation and load. HBO sessions caused appreciable disorders in heart contractility which could be partly prevented by SOD administration. In rabbits with adrenaline-induced heart lesions, depression of myocardial contractility induced by the inhibitor alone or in combination with intensive oxygenation was also observed.

Animals

[Effect of guanyl nucleotides and hyperbaric oxygenation on the adenylate cyclase activity of the heart in rabbits with myocardial hypertrophy].

The authors studied the role of guanyl nucleotides and hyperbaric oxygenation (HBO) in desensitization and resensitization of adenylate cyclase of the heart during hypertrophy which was induced by aorta stenosing. The basal activity of the enzyme and the rate of its activation with adrenaline and guanyl nucleotides were discovered to be reduced. In the presence of guanyl nucleotides, HBO gave rise to the recovery of enzyme sensitivity to the hormone. The data obtained indicate that during myocardial hypertrophy, guanyl nucleotides participate both in densensitization of adenylate cyclase to hormonal exposure and in the enzyme resensitization during HBO therapy.

Adenylyl Cyclases

[Effect of hyperbaric oxygenation on the cyclic nucleotide and catecholamine content, energy and carbohydrate metabolism and on cardiac contractile function in acute focal myocardial ischemia].

Two hours after the ligation of the descending branch of the left coronary artery in rabbits the contractile function of the heart decreased, concentration of phosphocreatine, ATP, glycogen dropped, and the content of lactic acid in the ischaemic and intact areas of the left ventricle elevated. Two-hour ischaemia of the myocardium was accompanied by increase of the cAMP and decrease of cGMP levels in the ischaemic and intact areas. Hyperbaric oxygenation (HBO, 2 at. abs, 1 h) started 30-40 min after coronary occlusion led to partial restoration of the cardiac contractility function, improvement of the energy and carbohydrate metabolism in the ischaemic and intact areas of the left ventricle and prevented cardiac fibrillation. It is surmised that favourable action of HBO on the functional state of the heart in its acute focal ischaemia is related not only to the antihypoxic effect but also to the rearrangement of the system of neurohormonal control of the heart.

Animals

[Patholphysiological aspects of hyperbaric oxygenation exposure on the heart in compensatory hypertrophy].

Chronic interrupted effect of hyperbaric oxygenation applied for 4 weeks reduces the rate of the development of myocardial hypertrophy in rabbits and is thus conducive to stabilization of myocardial contractile function on a sufficiently high level and increases the reliability of the circulation system in emergency situations. In the dangerous stage of compensatory cardiac hyperfunctions, hyperbaric oxygenation protects the myocardium from destructive changes and activates bionergetic processes, whereas in the stage of marked hypertrophy it inhibits the development of cardiosclerosis. Hyperbaric oxygenation prevents the development of functional isolation of the hypertrophied myocardium from the neurohormonal effects and contributes to the preservation of the reserve capacity of the neuroeffector mechanisms of heart regulations.

Acetylcholine

[Effect of hyperbaric oxygenation on several functional and morphologic properties of the heart and catecholamine metabolism in the presence of compensatory myocardial hypertrophy].

Rabbits subjected to hyperbaric oxygenation (HBO) for one month following ascending aorta stenosis developed less distinct hypertrophy and signs of myocardial dystrophy with a more distinct enhancement of the left ventricular contractility than animals with aortic stenosis kept under normal pressure. In rabbits with heart hypertrophy developing under HBO the increasing adaptive capacity of the myocardium was accompanied by an elevation in functional reserve of the sympathetic regulation apparatus. Apparently HBO aided the development of the optimum cardiac adaptation to a high afterload.

Animals

[Soluble guanylate cyclase from rat platelets during experimental myocardial ischemia].

Activity of soluble guanylate cyclase and regulation of the enzyme were studied in thrombocytes of intact rats and under conditions of acute myocardial ischemia caused by ligation of left coronary artery. Distinct decrease in the enzymatic activity was detected already within 15 min after the operation: down to 19% and 46%, in presence of Mg2+ and Mn2+, respectively, as compared with control values. Within 24 hrs of the ischemia the guanylate cyclase activity was slightly increased up to 33.5% in Mg2(+)-containing mixture and was unaltered (46%) in presence of Mn2+. Considerable activation of the enzyme by 2.10(-4) M dithiotreitol (from 288% to 790%, respectively) was observed after 15 min of myocardial ischemia with subsequent normalization (down to 340%) within 24 hrs. The data obtained suggest elevation of free-radical reactions, specific for myocardial ischemia, as well as high sensitivity of guanylate cyclase in thrombocytes to these reactions beginning from the early steps of the disease. Absence of the sodium nitroprusside stimulating effect on rat thrombocyte guanylate cyclase, found under conditions of both normal state and myocardial ischemia, may be due to initial hemdeficiency of the enzyme.

Animals

[Effect of ischemia and postischemic reperfusion on some mechanisms of regulation, rhythmogenesis, and contractile function of the heart in rats].

Isolated rat hearts were perfused with Krebs' solution after Langendorff's method. Decrease of the perfusion rate from 8.8 to 2.2 ml/min for 40 minutes led to inhibition of the contractile and rhythmic function of the heart and its reactivity to isoproterenol (IP) and acetyl choline (AC), drop in the intensity of lipid peroxidation appraised according to malonyl dialdehyde (MDA) level, and reduction of noradrenaline (NA) concentration in the myocardium in maintenance of the cAMP level. Forty-minute postischemic reperfusion normalized cardiac function, caused further diminution of the heart reactive properties to IP and AC, activated lipid peroxidation, reduced the NA concentration, and maintained a normal MDA level. The effect of ischemia and reperfusion on the regulatory mechanisms, rhythmogenesis, and contractile function of the heart is discussed.

Animals

[Effect of hyperbaric oxygenation on paramagnetic centers in the rabbit myocardium during experimental myocardial infarction].

Changes in paramagnetic centres (PC) concentration in rabbit's myocardial muscle were studied under experimental myocardial infarction during 168 hours by means of ESR-spectroscopy. PC characterized by ESR signal with g = 3.0 was found. It was shown that hyperbaric oxygenation did not affect PC content in the infarction zone, and resulted in an increase of PC concentration with g = 1.94 and g = 2.0 in the intact myocardial zone.

Animals