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Biomedical subjects

E A Demurov

Publications and source records attributed to E A Demurov.

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

Changes in the properties of plasma fibronectin in Shigella-induced endotoxaemia and the responses to hyperbaric oxygenation and indomethacin.

In rabbits, Shigella endotoxin causes hypoxaemia, metabolic acidosis, and hypocapnia. These changes are more marked at a dose of 1 mg kg-1 than with one of 0.5 mg kg-1 body weight. The endotoxin also reduces the plasma level and heparin-binding activity of fibronectin (FN). During convalescence, FN activity recovers at a slower rate than its level. Hyperbaric oxygenation (HBO; 2 atm for 1 h) normalizes blood gas composition and acid-base and electrolyte balance, improves the clinical picture of endotoxaemia, enhances FN activity and, to a lesser degree, its concentration, and lowers mortality. Indomethacin (IN) (5 mg kg-1 orally) has a similar action. When HBO and IN are used in combination, there is no enhancement of the therapeutic effect and mortality increases.

Animals

[Substantiation and use of a new method of transorganic oxygen preservation of the kidneys].

A new method has been developed for effective normobaric transorganic oxygen preservation of the kidneys. According to this method, oxygen is insufflated simultaneously through an artery, a vein and a ureter. A portable autonomously-operated device has been developed and used successfully for its clinical application. In experimental conditions, transorganic oxygen preservation ensures viability of the preserved kidney for up to 48 hours, with immediate post-transplantation recovery of renal function, and for 72 hours, with delayed functional recovery. The success of transorganic oxygen preservation was controlled by cellular metabolism assessment. Changes in adenylic acid components, lactic acid and lipid peroxidation products were measured in renal tissue. In clinical conditions, the outcome of transplantation could be predicted with high probability on the basis of intraoperative transplant hemodynamic studies. Two groups of patients were compared: 43 patients to whom a cadaver kidney, preserved by transorganic oxygenation for up to 52 hours, was transplanted, and recipients of contralateral kidneys, obtained from the same donors and preserved in Eurocollins solution for not more than 26 hours without perfusion. Preservation by transorganic oxygenation was shown to be preferable when clinical results were analysed.

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

[Structural changes in the lungs induced by different levels of hyperbaric oxygenation].

Morphological and ultrastructural changes in the lungs of 30 rabbits placed into the altitude chamber with 100% O2 and the pressure of 2, 2.5, 3 and 4 ata for 60 min daily during 1, 2 and 3 weeks have been studied. Morphological changes in the lungs were shown to depend on the degree and duration of oxygen pressure. 2 ata for 60 min daily during two weeks or 2.5 ata for 60 min daily during one week were considered to be safe regimens of hyperbaric oxygenation. Microcirculatory disorders and dystrophic changes of the aero-hematogenic barrier (AHB), its increased permeability, the development of intraalveolar and interstitial edema are observed in the lungs at a higher pressure of 3 or 4 ata. The endothelium and type I alveolocytes are more sensible to high doses of hyperbaric oxygenation. Hydropic degeneration and exfoliation of cells from the basilar membrane are gradually increasing. Type II alveolocytes are more stable to the destructive action of hyperbaric oxygenation. Greater dystrophic changes in other AHB elements are associated with the hypertrophy of mitochondria and lamellar bodies. The described AHB changes are more expressed in atelectasis areas.

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 combined use of hyperbaric oxygenation and alpha-tocopherol on the contractile function and various components of the antioxidant system of the heart after adrenaline lesioning].

A session of hyperbaric oxygenation (HBO) at 2.5 at. abs. conducted for one hour in rabbits with adrenalin heart affection (AHA) immediately after adrenalin administration prevented a decrease in the cardiac contractile function usually developing within two hours after AHA. On the third day of the follow up, rabbits with AHA receiving daily HBO displayed a decrease in the pump and contractile functions as well as in superoxide dismutase (SOD) activity and the antioxidant activity (AOA) of the left ventricle lipids. Combination of HBO sessions with the intra-muscular administration of alpha-tocopherol (50 mg/kg) made the decrease in SOD activity less pronounced and prevented both the fall in lipid AOA and the depression of the heart contractile and pump functions on the third day following AHA. It is suggested that the combined use of HBO and substances increasing the potency of the cell antioxidation system may become one of the principles of reducing HBO side effects and of expanding the potentialities of HBO in treating ischemic and adrenergic heart impairments.

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