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A A Miasnikov

Publications and source records attributed to A A Miasnikov.

At least 19 recordsLinked to original sources
PubMed2002

[Current problems in prophylaxis and treatment of acute decompression disease of mild degree].

The authors discuss the causes leading to the rise of acute decompression illness in the amateur skin-divers. They include the insufficient training of most skin-drivers in the basis of diving physiology and medicine, the underwater dipping without consideration of individual sensitivity to decompression illness and nitrogen narcotic action, disorders in decompression regimens, non-observance of behavior rules after dipping, use of air transport immediately after dipping. The case of delayed treatment of decompression illness is described. The data concerning the possibility of chronic decompression illness formation due to the action of asymptomatic decompression gasformation and acute decompression illness of mild degree are presented. The authors propose the system of measures that would help to decrease the incidence of disease and to make the treatment of decompression illness more effective.

Acute Disease↗
PubMed2002

[Effectiveness of endovideosurgical technology in diagnosis and treatment of patient with hemoblastoses].

Results of using endovideosurgical technology for diagnosis and treatment of hematological diseases in 123 patients are described. It was shown that laparoscopy is highly effective parallel with ultrasound examination and tomography in a complex diagnostic program. Using the developed diagnostic algorithm was shown to be very expedient for making primary diagnosis, recurrent diseases and control of the effectiveness of chemotherapy. Endovideosurgical interventions were shown to be less invasive and safe in hematological patients. Laparoscopy is an alternative to diagnostic laparotomy which is often used in this group of patients.

Adult↗
PubMed2001

Atropine-sensitive and -insensitive components of the somatosensory evoked potential.

The evoked potential in primary somatosensory cortex changes with time. Short puffs of air administered to the nose of awake, quietly resting adult rats elicited potentials that could be altered by one of several treatments (saline, atropine methyl nitrate or atropine sulfate). The change produced by blocking muscarinic receptors in the central nervous system with atropine sulfate (100 mg/kg) was the largest, but control substances also altered the potential, suggesting that the gradual changes observed in the evoked potential 30 min after intraperitoneal injection may also be affected by factors such as the stress associated with injection itself and the blockade of peripheral muscarinic receptors. The changes observed in the evoked potential when central cholinergic receptors are blocked include a large shift towards positivity in the early components (between 18 and 64 ms with maxima at 20 and 47 ms) and a similarly significant shift towards negativity in the later components (between 90 and 208 ms with maxima at 115 and 157 ms). The actual changes observed during inactivation of central muscarinic receptors suggest that the role of acetylcholine during arousal is more than to simply bias the cortex towards greater excitability. Rather, the muscarinic receptors on inhibitory interneurons or on the dendritic terminals of pyramidal cells in superficial layers of cortex enhance the first intracortical synaptic events but reduce the population response at later times during the first 250 ms following a tactile stimulus.

Acetylcholine↗
PubMed2001

Rapid differential conditioning of the somatosensory evoked potential by changed patterns of brief innocuous tactile stimuli in waking rats is altered by atropine sulfate.

Air puffs delivered to the nose of an awake, lightly restrained rat every 15 s produced evoked potentials that changed gradually over time so that the averaged response to the last 40 stimuli was measurably different from the first 40. This habituation-like paradigm increased the size of an early component of the potential in several places. When measured with respect to the time of stimulus onset (there was a 21.6 ms delay in the time of arrival of the stimulus maximum at the nose), one of the largest increases occurred 46 ms later (39 ms latency to onset, and 55 ms latency to offset). As well, a late component of the waveform became more positive, showing a maximum between 156 and 185 ms (133 ms latency to onset, and more than 250 ms latency to offset). Changing the pattern but not the number of stimuli accelerated the rate of this positive shift with a maximum at 37 ms (21 ms latency to onset, and 42 ms latency to offset), but did not affect the rate of change in the late component. This effect of altering the temporal pattern of the stimuli was blocked by systemic injections of atropine sulfate, a blocker of central muscarinic receptors, whereas, neither saline injections nor atropine methyl nitrate injections (an atropine analog that does not cross the blood-brain barrier) could produce these changes. These observations suggest that the adaptive changes of the somatosensory evoked potential induced by novel patterns intercalated in otherwise monotonous repetitive somatic stimuli depend upon central muscarinic mechanisms.

Acetylcholine↗
PubMed2001

Muscarinic dependence of nucleus basalis induced conditioned receptive field plasticity.

Receptive field (RF) plasticity in primary auditory cortex of adult animals, specifically selective increased response to a tonal conditioned stimulus (CS) relative to other frequencies, can be induced both by behavioral conditioning and by pairing a tone with stimulation of the nucleus basalis (NB). This study determined whether cortical muscarinic receptors are necessary for NB-induced RF plasticity. Single units in layers II-IV were studied in Urethane anesthetized adult rats. The cortex was perfused with saline or saline+atropine sulfate. Conditioning, 30 trials of pairing a tone with NB stimulation, produced a significant CS-specific response increase (n=8). Local atropine blocked NB-induced RF plasticity, actually resulting in CS-specific response decrease (n=6). Therefore, NB-induced RF plasticity requires engagement of muscarinic receptors in auditory cortex.

Acetylcholine↗
PubMed2000

The design and application of three speaker-based stimulating devices for cutaneous stimulation in anesthetized and awake animals.

Those wishing to study neuronal plasticity in sensory systems are confronted by the need to deliver equivalent stimuli to the organism at time intervals separated by hours, days or months. This problem is particularly acute in the somatosensory system where delivering an equivalent stimulus generally requires a second physical contact with the same point on a geometrically complex surface. This requirement is difficult to fulfill. We have designed two stimulators that avoid or minimize the importance of this requirement by obviating the need for the stimulator to be at a fixed distance from the skin. As well, we have redesigned a system for whisker stimulation originally proposed by Simons. The first stimulator is appropriate for experiments in anesthetized animals; the surface to be stimulated is immersed in water warmed to body temperature and the tactile stimulus is generated as an hydraulic pulse. The second uses a high velocity pulse of air shaped so that it can be transmitted significant distances without attenuation. The redesign of the Simons' vibrissa stimulator provides larger amplitude displacements and lower controlling voltages more readily generated by equipment normally found in laboratories. We also described the design of a chamber for restricting the awake rat during chronic study and the electrodes used for recording and for delivery of drugs in awake animals held in such a chamber.

Air Pressure↗
PubMed1999

Evidence for homeostatic adjustments of rat somatosensory cortical neurons to changes in extracellular acetylcholine concentrations produced by iontophoretic administration of acetylcholine and by systemic diisopropylfluorophosphate treatment.

We describe the responses of single units in the awake (24 cells) or urethane-anesthetized (37 cells) rat somatosensory cortex during repeated iontophoretic pulses (1.0 s, 85 nA) of acetylcholine, both before and after systemic treatment with the irreversible acetylcholinesterase inhibitor diisopropylfluorophosphate (i.p., 0.3-0.5 LD50). The time-course of the response to acetylcholine pulses differed among cortical neurons but was characteristic for a given cell. Different time-courses included monophasic excitatory or inhibitory responses, biphasic (excitatory-inhibitory, inhibitory-excitatory, excitatory-excitatory, and inhibitory-inhibitory), and triphasic (excitatory-excitatory-inhibitory, inhibitory-inhibitory-excitatory, and inhibitory-excitatory-inhibitory) responses. Although the sign and time-course of the individual responses remained consistent, their magnitude fluctuated across time; most cells exhibited either an initial increase or decrease in response magnitude followed by oscillations in magnitude that diminished with time, gradually approaching the original size. The time-course of the characteristic response to an acetylcholine pulse appeared to determine direction and rate of change in response magnitude with successive pulses of acetylcholine. Diisopropylfluorophosphate treatment, given 1 h after beginning repeated acetylcholine pulses, often resulted in a gradual increase in spontaneous activity to a slightly higher but stable level. Superimposed on this change in background activity, the oscillations in the response amplitude reappeared and then subsided in a pattern similar to the decay seen prior to diisopropylfluorophosphate treatment. Our results suggest that dynamic, homeostatic mechanisms control neuronal excitability by adjusting the balance between excitatory and inhibitory influences within the cortical circuitry and that these mechanisms are engaged by prolonged increases in extracellular acetylcholine levels caused by repeated pulses of acetylcholine and by acetylcholinesterase inhibition. However, this ability of neurons in the cortical neuronal network to rapidly adjust to changes in extracellular levels of acetylcholine questions the potential efficacy of therapeutic treatments designed to increase ambient levels of acetylcholine as a treatment for Alzheimer's disease or to enhance mechanisms of learning and memory.

Acetylcholine↗
PubMed1999

Temporally structured impulse activity in spontaneously discharging somatosensory cortical neurons in the awake cat: recognition and quantitative description of four different patterns of bursts, post-recording GFAP immunohistology and computer reconstruction of the studied cortical surface.

We elaborated two methods used in two previous publications [J. Martinson, H.H. Webster, A.A. Myasnikov, R.W. Dykes, Recognition of temporally structured activity in spontaneously discharging neurons in the somatosensory cortex in waking cats, Brain Res. 750 (1997) 129-140 [16]; H.H. Webster, I. Salimi, A.A. Myasnikov, R.W. Dykes. The effects of peripheral deafferentation on spontaneously bursting neurons in the somatosensory cortex of waking cats, Brain Res. 750 (1997) 109-121 [21]]: (A) a procedure for detecting and classifying brief epochs of high-frequency extracellular impulse activity (bursts) recorded chronically in the somatosensory cortex of the awake cat, and (B) a modification of an immunohistochemical technique [L.A. Bevento, L.B. McCleary. An immunochemical method for marking microelectrode tracks following single-unit recordings in long surviving, awake monkeys, J. Neurosci. Meth. 41 (1992) 199-204 [5]] for visualization of electrode tracks and electrolytic lesions around the tip of tungsten-in-glass microelectrodes [D.M.D. Landis, The early reactions of non-neuronal cells to brain injury, Annu. Rev. Neurosci. 17 (1994) 133-151 [15]] weeks after lesions were made in cortex. The burst recognition and classification method uses an interval threshold to determine the beginning and end of one epoch [M. Armstrong-James, K. Fox, Effects of ionophoresed noradrenaline on spontaneous activity of neurons in rat primary somatosensory cortex, J. Physiol. (London), 335 (1983) 427-447 [3]] in the original sequence of interspike intervals (ISIs) to segregate and analyze separately a burst. The threshold is based on the duration of the shortest modal ISI found in the autocorrelogram [J. Martinson, H.H. Webster, A.A. Myasnikov, R.W. Dykes, Recognition of temporally structured activity in spontaneously discharging neurons in the somatosensory cortex in waking cats, Brain Res. 750 (1997) 129-140 [16]]. The technique allowed recognition of bursts with several distinctive patterns: (i) an initial, longer ISI followed by progressively shorter ones; (ii) an initially shorter ISI followed by progressively longer ones; (iii) patterns where the intermediate ISI could be either longer or shorter than surrounding ones; and (iv) consecutive ISIs of relatively equal duration. Among the cells discharging in bursts with equal ISIs, the technique allows recognition of cells generating only short (up to three to five intervals) bursts, and others generating mixtures of a short and long (up to six or more intervals) bursts. Finally, frequency distributions of the probability of encountering bursts having intervals of a stated length is described. The visualization of tracks from chronic recording experiments is important for relating neuronal function to a specific cytoarchitectural region and a specific cortical layer. Several modifications of the procedure of immunostaining for GFAP allows identification of recording sites in clearer relationship to the cytoarchitectonic details of cat somatosensory cortex.

Animals↗
PubMed1999

[Structural changes in the parenchymatous organs in animals in venous gas embolism of varying intensity and acute decompression disease].

Structural changes in tissues of liver, kidneys and lungs were studied in guinea pigs in post-decompressive gas venous embolism of high and low intensity. In moderate gas venous embolism cells of the organs studied display cytoplasm vacuolization due to the rupture of inner mitochondrial membrane and appearance of single rounded spheroidal structure with homogeneous contents situated near the cell nuclei that were thought to reflect formation of gas bubble within the cell. Possible pathogenetic mechanisms of formation of chronic decompressive disorders in asymptomatic gas formation are discussed.

Acute Disease↗
PubMed1999

[Human resistance to decompression sickness and nonspecific methods of its elevation].

The object of this study was the dependence of decompression sickness (DCS) tolerance determined by the intensity of venous gas embolism on functioning of the cardiovascular and respiratory systems, and micro-circulation which predetermine wash-out of an indifferent gas. Efficiency of nonspecific methods, e.g. hypercapnic training, hyperbaric oxygenation, exposures to pulse current to enhance human tolerance to DCS was experimentally substantiated.

Adult↗
PubMed1998

Effects of D-AP5 and NMDA microiontophoresis on associative learning in the barrel cortex of awake rats.

Experiments involving single-unit recordings and microiontophoresis were carried out in the barrel cortex of awake, adult rats subjected to whisker pairing, an associative learning paradigm where deflections of the recorded neuron's principle vibrissa (S2) are repeatedly paired with those of a non-adjacent one (S1). Whisker pairing with a 300 ms interstimulus interval was applied to 61 cells. In 23 cases, there was no other manipulation whereas in the remaining 38, pairing occurred in the presence of one of three pharmacological agents previously shown to modulate learning, receptive field plasticity and long-term potentiation: N-methyl-D-aspartic acid (NMDA) (n=8), the NMDA receptor antagonist AP5 (n=17) or the nitric oxide synthase inhibitor L-nitro-arginine-N-methyl-ester (L-NAME) (n=13). Non-associative (unpaired) experiments (n=14) and delivery of pharmacological agents without pairing (n=14) served as controls. Changes in neuronal responsiveness to S1 following one of these procedures were calculated and adjusted relative to changes in the responses to S2. On average, whisker pairing alone yielded a 7% increase in the responses to S1. This enhancement differed significantly from the 17% decrease obtained in the non-associative control condition and could not be attributed to variations in the state of the animals because analysis of the cervical and facial muscle electromyograms revealed that periods of increased muscular activity, reflecting heightened arousal, were infrequent (less than 4% of a complete experiment on average) and occurred randomly. The enhancement of the responses to S1 was further increased when whisker pairing was performed in the presence of L-NAME (27%) or NMDA (35%) whereas AP5 reduced it to 1%. During the delivery period, NMDA enhanced both neuronal excitability and responsiveness to S1 whereas AP5 depressed them. However, the effects of both substances disappeared immediately after administration had ended. L-NAME did not affect the level of ongoing activity and responses to S1 significantly. From these data, we concluded that, since the changes in the responses to S1 lasted longer than the periods of both whisker pairing and drug delivery, they were not residual excitatory or inhibitory drug effects on neuronal excitability. Thus, our results indicate that, relative to the unpaired controls, whisker pairing led to a 24% increase in the responsiveness of barrel cortex neurons to peripheral stimulation and that these changes were modulated by the local application of pharmacological agents that act upon NMDA receptors and pathways involving nitric oxide. We can infer that somatosensory cerebral cortex is one site where plasticity emerges following whisker pairing.

2-Amino-5-phosphonovalerate↗
PubMed1998

Blockade of cholinergic receptors in rat barrel cortex prevents long-term changes in the evoked potential during sensory preconditioning.

We offer evidence that acetylcholine (ACh) is involved in the emergence of functional neuronal plasticity induced by whisker pairing. Evoked potentials were recorded within the barrel cortex of awake, adult rats before, during, and after one of five paradigms. In the pairing procedure, each of 50 deflections of a whisker (S1) was followed 150 ms later by the deflection of a second whisker (S2). The explicitly unpaired control procedure differed by the lack of contiguity and contingency between the stimulation of S1 and S2. In the three remaining groups, pairing was performed 30 min after an intraperitoneal injection of either 0.5 ml of saline (150 mM NaCl), 100 mg/kg of atropine methyl nitrate (0.5 ml of AMN in saline), or 100 mg/kg of atropine sulfate (0.5 ml of ATS in saline). Changes in responsiveness to S1 were compared with, and adjusted by, changes in responsiveness to stimulation of S2. Changes in potentials evoked by S1 were interpreted as a change in neuronal excitability occurring when the first innocuous stimulus systematically predicted the appearance of the second innocuous stimulus. When whisker pairing was performed alone or in the presence of either saline or AMN (a blocker of muscarinic cholinoreceptors that does not cross the blood-brain barrier, BBB), responses to S1 increased, whereas, in the presence of ATS (blocker of muscarinic cholinoreceptors that does cross the BBB) or following the explicitly unpaired control, they decreased. The effects of saline, AMN, and ATS on the evoked potential without vibrissae pairing were opposite to those observed when these substances were injected and pairing occurred. Analysis of the behavioral state of the animal showed that the changes observed in the evoked potential could not be attributed to changes in behavioral state. The changes in responsiveness to S1 induced by whisker pairing were independent of neuronal excitability, did not occur in the absence of contingency and contiguity between S1 and S2, were blocked by the muscarinic receptor antagonist ATS, but not by blockade of muscarinic modulation of normal synaptic transmission. Thus activation of muscarinic cholinoreceptors within the CNS were a necessary condition for this form of neuronal plasticity.

Animals↗
PubMed1998

[Total irradiation of the liver in treating patients with lymphogranulomatosis].

AIM: The study of efficiency of radiation in specific affection of the liver in lymphogranulomatosis (LGM). MATERIALS AND METHODS: 212 LGM patients were examined for hepatic lesions using x-ray, radiological, cytochemical and histological investigations of the biopsies. Coagulation, alkaline phosphatase, copper and ceruloplasmin in the serum were measured to evaluation the disease activity. All the patients received polychemotherapy (PCT). Irradiation of the liver in the total focal dose 36-44 Gy was performed in confirmed involvement of the liver as adjuvant to PCT. RESULTS: Specific liver lesions were detected in 6.1% of patients at primary examination and in 15.6%--at follow-up. Liver lesions occurred most frequently in mixed-cell variant of LGM and lymphoid depletion. Eradication of liver lesion after PCT was achieved in 15.4%. Subsequent radiation produced a complete remission in 100% of patients with diffuse and 80% of patients with large-focal liver lesion. In detection of liver involvement at the time of LGM progression eradication and remission were achieved in 70 and 50% of patients, respectively. From 30% of patients with liver lesions resistant to PCT and radiation, 15% had stable disease. The survival did not depend on eradication of liver lesion. CONCLUSION: In involvement of the liver its radiation is indicated for all the patients with new-onset LGM. In the recurrence, liver radiation is recommended for those in whom the liver is the only extranodal lesion.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

[Late complications of combined therapy of lymphogranulomatosis].

Basing on the results of follow-up of 212 lymphogranulomatosis patients in long-term remission, the authors have identified most frequent and serious complications. Contribution of different treatment components to development of these complications is specified. Signs of mono- and polyorganic lesions due to combined therapy are described, recommendations on the follow-up and prevention of the complications are provided.

Adult↗
PubMed1996

[A method for evaluating the safety of decompression regimens for divers].

The authors offer a way of estimation of safety modes of decompression, based on definition of intensity of venous gas embolism (VGE) at each decompression and account of probability of illness of divers in series of tests. Intensity of VGE was determined with the help of ultrasonic gas bubbles Doppler radar. Comparative safety of standard modes of decompression of divers of the Navy was estimated, and also the modes, designed in accordance with mathematical model of decompression, offered by I. A. Voĭtsekhovich (1990), were done. The results testify, that use of ultrasonic radar for estimation of intensity of VGE at decompression and account of average and maximum probability of decompression illness in series of tests of modes permit to receive the comparative characteristic of safety of modes at small number of decompressions.

Adult↗
PubMed1996

[The functional status of the cardiovascular system in the late period after the combined therapy of patients with lymphogranulomatosis].

The study included 127 patients with lymphogranulomatosis confirmed histologically. The patients were exposed to total or subtotal irradiation of lymph nodes and 6 cycles of polychemotherapy (COPP). Before the treatment and once a year after it all the patients were examined for defects in the cardiovascular function. Radiation pericarditis was found in 0.79% of the patients, acute coronary death occurred in 3 (2.8%) patients. At 3-11-year follow-up persistent changes in the cardiovascular parameters were noted only in older patients or those with cardiovascular disorders at the moment of the therapy. The authors think that feasibility of cardiac damage in lymphogranulomatosis patients is exaggerated and that reduction of radiation dose and COPP intensity is not valid in patients under 40.

Adult↗
PubMed1995

[The microvascular permeability of the skin and mesentery in rats adapting to hypoxia].

Changes of the rat skin and mesenteric microvascular permeability for Na-fluorescine were studied during adaptation to intermittent hypobaric hypoxia. The data obtained revealed that the microvascular permeability increased on the 10 th day after the hypoxia and decreased within 25 days of hte adaptation to the hypoxia in both areas under study.

Adaptation, Physiological↗