Publications by authors named "Gilinskiĭ M"

To determine the effect of ischemic preconditioning upon myocardial serotonin and 5-hydroxyindolacetic acid (5-HIAA) dynamic in myocardial ischemia and reperfusion. 28 male Wistar rats anesthetized with urethane were randomly divided into 2 groups. In the control group (n = 13) rats were subjected to 30 min coronary occlusion and subsequent 120 min reperfusion.

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We studied the dynamics of interstitial serotonin during local myocardial ischemia under conditions of ischemic preconditioning in Wistar rats. Ischemic preconditioning increased serotonin content in the dialysate (p=0.003).

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Nitric oxide (NO) is synthesized from arginine (ARG) by NO synthase (NOS). Asymmetric dimethylarginine (ADMA), a competitive inhibitor of NOS, participates in the endogenous regulation of NO synthesis. The main amount of ADMA is enzymatically degraded by dimethylarginine dimethylaminohydrolase (DDAH) widely expressed in renal tissue.

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Experiments on rats showed that blockade of norepinephrine reuptake in the early reperfusion period after focal myocardial ischemia aggravates myocardial injury and abolishes the protective effect of ischemic preconditioning.

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We implanted under urethane narcosis microdialysis probes into myocardium of Wistar rats. In experimental group we used ischemic preconditioning. After this left descending coronary artery was occluded for 60 minutes and then reperfused for 60 min.

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To determine the effect of uptake 1 inhibition in reperfusion after myocardial ischcmia upon noradrenalin dynamic and myocardial infarction size, 14 male Wistar rats anesthetized with urethane were randomly divided into 2 groups and subjected to 30 min coronary occlusion and subsequent 120 min reperfusion. In control group (n = 7) 1 ml of Ringer's solution was administered intravenously at the beginning of reperfusion. In experimental group (n = 7) instead of Ringer's solution 0.

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A brief preceding ischemia-reperfusion can reduce infarct size; this is known as ischemic preconditioning. During myocardial ischemia, massive norepinephrine is released from the cardiac sympathetic nerve terminals, reflecting the sympathetic nerve injury, and producing myocardial damage. However norepinephrine participates in myocardial protection during ischemia since its depletion in nerve terminals prevents ischemic preconditioning, and exogenous norepinephrine mimics ischemic preconditioning.

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Aim Of The Study: To determine the effects of two-staged ischemic preconditioning on myocardial noradrenaline in prolonged ischemia and reperfusion.

Methods: Thirty-two male Wistar rats anesthetised with urethane randomly divided into 2 groups: group 1 (ischemic preconditioning group, n = 16), and group 2 (control, n = 16). Myocardial interstitial noradrenaline levels were measured using a microdialysis technique.

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Pathophysiology of asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of NO synthase, has been a subject of intensive research activity during last years. The ways of ADMA synthesis and degradation were studied. It was suggested that ADMA plays a considerable role in the realization of so called "Arginine paradox".

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Background: Ischemic preconditioning improves myocardium survival during test ischemia and removes the start of massive norepinephrine (NE) release from sympathetic terminals into the myocardial interstitium. We studied the influence of long and relatively short occlusions on NE release during test occlusion. The possibility has been studied to provoke NE release by local tyramine application on the background of ischemia.

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NISAG rats with stress-induced arterial hypertension are characterized by hyperactivity of the sympathoadrenal system under rest conditions and during stress exposure.

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We report here the results obtained from comparative analysis of learning and the dynamics of extinction of a conditioned passive avoidance response in mice with genetic knockout of monoamine oxidase A (MAO A) and the progenitor line C3H. Mice of both lines acquired the conditioned passive avoidance reaction efficiently. Mice with genetic knockout of MAO A were characterized by prolonged retention of reproduction of the memory trace, as compared with rapid extinction in C3H mice.

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The passive avoidance learning and memory trace retention in mice lacking monoamine oxidase A (MAO A) and control C3H strain were analyzed. It is shown that mice of both strains were well the passive avoidance learners. A delay of the memory trace extinction was found in lacking MAO A mice as compared with control C3H strain.

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The effects of the NO donor sodium nitroprusside and the NO synthase blocker L-omega-N-nitroarginine (LNA) on body temperature, hypothalamic monoamines, and plasma corticosterone in conditions of cooling were studied in Male Wistar rats. Reductions in body temperature on cooling, both after administration of sodium nitroprusside and LNA, were no different from those seen without treatment. The basal corticosterone level after treatment with sodium nitroprusside increased from 5.

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Experiments were performed on knockout Tg8 mice lacking monoamine oxidase A gene that plays a major role in dopamine catabolism. The study by the method of high-performance liquid chromatography revealed considerable regional differences in the contents of dopamine and its metabolite dihydroxyphenylacetic acid in brain structures of these animals. Tg8 mice differed from the parent C3H/HeJ strain by low level of dihydroxyphenylacetic acid in the striatum, midbrain, hypothalamus, and hippocampus and high concentration of dopamine in the striatum.

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Effects of NO-synthase inhibitor N(omega)-nitro-L-arginine (LNA) and donor sodium nitroprusside (SNP) on alteration in body temperature, plasma corticosterone level and hypothalamic monoamines in response to cold exposure, were studied. Drop of the body temperature in cold exposure in rats treated with LNA or SNP was the same as in the control group. Administration of SNP (2 mg/kg i.

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Evaluation of a local activity of the sympathetic system on the basis of norepinephrine (NE) level in the blood of myocardial vessels depends on at least three processes: NE release by sympathetic neurons, its reuptake and spillover of NE into the blood. The relations between these processes are different in various organs. Direct investigations of changes in the myocardial NE level under the effect of reuptake blockade by desmethylimipramine (DMI) were performed after appearance of the microdialysis technology.

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Fast cooling involving the dynamic activity of the skin cold receptors seems to establish a condition for changes in catecholamine concentration at a lesser decrease of body temperature as compared with slow cooling.

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The adaptive characteristics of the body, including the specific features of increased cold resistance upon repeated exposures to cold, are determined not only by the properties of thermogenic structures themselves, but largely depend on the contribution of the central mechanisms which control the processes of habituation and mobilization of functions. The experiments revealed an increase in cold resistance in rats after preexposure to cold. Immobilization stress prior to training cold significantly decreased rapid cold resistance in the animals, but increased the training effect of the first cooling.

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A level of myocardial norepinephrine (NE) is considered as one of the meaningful parameters in the estimation of myocardium functioning. Long lasting changes of myocardial NE appear to be not only a sequence of pathologic processes in myocardium, but could also be a factor responsible for some diseases. An improved microdialysis sampling technique with HPLC-ED analysis was developed to measure in vivo NE content in a rat myocardial interstitium.

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Blood plasma adrenalin and noradrenaline were measured during correction of acquired mitral defect under conditions of hypothermia without perfusion. Superficial ether anesthesia combined with morphine in a dose of up to 1 mg/kg and droperidol in a dose of up to 0.1 mg/kg did not fully block the sympathoadrenal reaction to cooling.

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Rats bred from Wistar stock for predisposition to catalepsy differed from nonselected animals in the level of brain catecholamines. Most of the brain structures of cataleptic rats (frontal cortex, caudate nucleus, amygdala, n. accumbens, hippocampus, diencephalon and midbrain) had a lower content of norepinephrine, dopamine and DOPAC than the control Wistar groups.

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The article deals with the results of experimental study of adaptation reactions in mild craniocerebral trauma (MCCT) combined with acute alcoholic intoxication on the basis of appraisal of the dynamics of endocrine and neuromediator shifts. A stress character of these shifts was revealed. Acute alcoholic intoxication levelled the stress reaction occurring in MCCT.

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