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Biomedical subjects

V A Voronin

Publications and source records attributed to V A Voronin.

At least 19 recordsLinked to original sources
PubMed1995

[An anamnestic method for studying the cause-effect connections between the status of public health and manufacturing, ecological and social factors].

The authors elaborated a medical and ecologic questionnaire for specific history. The questionnaire was applied to express-evaluation of public health state and environmental factors in the certain settlement. The health state was proved to be influenced significantly by occupational conditions, hardiness and intensity of work, psychologic climate. The most hazardous environmental factors are: unsatisfactory quality of drinkable water, air pollution and traffic noise. The lifestyle of the population examined is strongly associated with bad habits (smoking, short sleep, alcohol abuse).

Ecology↗
PubMed1994

Role of non-quantal acetylcholine release in surplus polarization of mouse diaphragm fibres at the endplate zone.

1. In mouse diaphragm, with intact cholinesterase (ChE), the mean value of the resting membrane potential was significantly higher (-84.8 +/- 0.3 mV; mean +/- S.E.M.) at the endplate zone than in the extrajunctional area of the muscle fibres (-82.5 +/- 0.3 mV) at 22 degrees C. 2. This hyperpolarization of about 2-3 mV at the endplate zone was abolished within 5 min by 1 x 10(-6) M ouabain, indicating that it might be caused by an electrogenic Na(+)-K+ pump. (+)-Tubocurarine (TC; 1 x 10(-5) M) had no effect on this hyperpolarization after bath application for 10-20 min. 3. Short-term denervation (4 h), a slight increase of Mg2+ in the bath of from 1 to 4 mM and application of a Ca(2+)-free solution for 60 min also led to the disappearance of the surplus polarization. All of these factors are known to eliminate TC-induced hyperpolarization in anti-ChE-treated muscles (H-effect), which is considered to be a correlate of non-quantal acetylcholine (ACh) leakage. 4. The time courses of the decline of the H-effect and surplus polarization after denervation were identical. 5. In short-term denervated muscles with intact ChE, the surplus polarization was restored by 5 x 10(-8) M ACh, which simulates the H-effect in anti-ChE-treated muscles. The presence of 1 x 10(-6) M ouabain either prevented or abolished the effect of the bath-applied ACh.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

The effect of non-quantal acetylcholine release on quantal miniature currents at mouse diaphragm.

1. The amplitude and exponential decay time constant of miniature endplate currents (MEPCs) were measured in mouse diaphragms treated with anti-cholinesterase under conditions known to modulate non-quantal acetylcholine (ACh) release. 2. Anti-cholinesterase prolonged MEPC decay and the extent of this initial prolongation was not influenced by non-quantal release. When non-quantal release was present, the decays of MEPCs became increasingly faster over several hours. This increased decay did not occur in the absence of non-quantal release. 3. Potentiation of the non-quantal release by zero Mg2+ and 1 x 10(-5) M choline, on the other hand, led to acceleration of MEPC shortening. 4. Increase of temperature from 15 to 26 degrees C and the presence of the desensitization-promoting drug proadifen (5 x 10(-6) M) accelerated the rate of MEPC shortening. 5. These observations are consistent with increased receptor desensitization due to non-quantal release. Repetitive binding of ACh to postsynaptic receptors which prolongs the time course of MEPC in anti-cholinesterase-treated endplates leads to progressive desensitization in the presence of non-quantal release and to the subsequent shortening of the quantal responses.

Acetylcholine↗
PubMed1991

Kinetic differences in the effect of calcium on quantal and non-quantal acetylcholine release at the murine diaphragm.

The effects of Ca2+ withdrawal on non-quantal, evoked quantal and spontaneous quantal release of acetylcholine (ACh) from the motor nerve terminals were studied with standard intracellular recording techniques. Anticholinesterase-treated mouse diaphragms were used. In a Ca2(+)-free solution all forms of ACh release decreased, but with different kinetics. As expected, evoked quantal release declined to zero within a few minutes. Spontaneous quantal release, i.e. the frequency of the miniature end-plate potentials (MEPPs), decreased to 15% of the control within 20 min after calcium withdrawal. The slowest decay was that of non-quantal release which declined very slowly and reached zero after 45-50 min. Following Ca2+ re-admission, both quantal types of ACh release were rapidly restored (evoked in 10 min, spontaneous in 20 min). However, recovery of non-quantal release did not occur until after 50 to 60 min.

Acetylcholine↗
PubMed1991

The dependence of non-quantal acetylcholine release on the choline-uptake system in the mouse diaphragm.

The time course of local end-plate hyperpolarization after d-tubocurarine application measured by an intracellular microelectrode was followed in vitro in anticholinesterase-treated mouse diaphragm pinned to the bottom of the perfusion chamber. The d-tubocurarine-induced hyperpolarization, which served as an indicator of non-quantal acetylcholine release, started to decline from 6 mV after 1 h and was negligible after 3 h in continuously perfused preparations. This decline was slowed down by 10 mumol l-1 choline and almost completely prevented by long-term nerve stimulation with a frequency of 3 Hz. The rapid decrease of the d-tubocurarine-induced hyperpolarization was observed within 10-15 min after the application of 1 mumol l-1 hemicholinium-3 and substitution of lithium for sodium. Both these procedures inhibit the fast choline uptake into nerve terminals. Our data suggest that the amount of available acetylcholine for non-quantal release is proportional to the rate of its synthesis and to the number of available carriers in the nerve terminals. Some of our observations might also be explained by postulating that the choline-uptake system as such is responsible for the non-quantal release.

Acetylcholine↗
PubMed1991

[The role of a spasm of the coronary arteries in the pathogenesis of acute myocardial infarct and in the development of sudden coronary death].

Based on the clinical experience and clinicoanatomic correlations, the authors suggest the role of hemorrhage and rupture of atherosclerotic patches in the pathogenesis of sudden coronary death. Proceeding from long-term follow-up studies of patients suffering from CHD, the necessity is substantiated of the regular use of beta-adrenoblockers which significantly reduce the rate of sudden death both in the acute and chronic phases of CHD, particularly in patients with a history of myocardial infarction. Taking into consideration the multifactorial nature of the pathogenesis of acute occlusion of coronary arteries, it is suggested that in addition to the preventive administration of beta-adrenoblockers, thrombolytic agents in combination with antiaggregation remedies and calcium antagonists should be prescribed, especially in cases of arterial pressure rises.

Aged↗
PubMed1991

[Minimal pulmonary regurgitation (pulsed Doppler echocardiography findings) in the absence of pulmonary valve defect].

A diastolic turbulent flow of pulmonary regurgitation with the maximum velocity of no more than 1.5 m/sec and prevalence in the exit portion of the right ventricle up to 17 mm was detected in 36 patients with cardiac and pulmonary diseases and apparently healthy individuals without organic pulmonary valve lesion and diastolic localization at the respective site, by using pulsed Doppler echocardiography. The highest diastolic transpulmonary pressure gradient estimated by a modified Bernulli's equation was no more than 9 mm Hg (within the range of normal values for diastolic pulmonary artery-right ventricle pressure gradient). Asymptomatic subclinical pulmonary regurgitation of physiological and functional nature without substantial hemodynamic significance which has been detected in these patients cannot be regarded as a manifestation of pulmonary valve defect.

Adult↗
PubMed1990

[The effect of "nonquantal" acetylcholine on miniature end-plate currents in the mouse].

The development of postsynaptic potentiation (PSP) and desensitization (DS) under the nonquantal secretion (NS) of acetylcholine (ACh) was studied using characteristics of miniature end-plate currents (MEPCs) in mice diaphragm muscle. The H-effect (the measure of the NS level) fell to zero during 3 hours after acetylcholinesterase (AChE) inhibition by armine at 20 degrees C. The MEPCs decay time constant (tau) decreased in parallel with the H-effect, though there was no reduction of the MEPCs amplitude in this case; tau did not change when NS was absent (early denervation). The maximal prolongation of tau after AChE inhibition was the same both in innervated (NS was normal) and denervated (NS was absent) muscle. The reduction of tau accelerated with the temperature rise and occurred after AChE inhibition by neostigmine. There was no changes in tau when AChE was active. It is suggested that nonquantal ACh decreases tau due to the DS development. NS induces no significant PSP after the AChE inhibition, but can do it later according to DS development, so that signs of DS may partially be masked by PSP.

Acetylcholine↗
PubMed1989

[Study of the effect of arterial hypertension on the status of left- ventricular myocardium based on thallium-201 scintigraphic data].

Functional relationship was examined between the parameters of myocardial perfusion, left ventricular myocardial mass, and complications developed in patients with coronary heart diseases concomitant with arterial hypertension. Examination was made of 102 patients with various natural history of arterial hypertension, of whom 53 had concomitant angina pectoris, myocardial infarction, congestive heart failure, sudden death, or rhythm disturbances. As "perfusion deficiency" progressed, the patients with complicated natural history of arterial hypertension were found to increase in number with higher left ventricular myocardial mass index. In patients with arterial hypertension, the critical hypertrophy phase in which the index of left ventricular myocardial mass was 110-120 gm2 was demonstrated to be followed by myocardial perfusion deficiency. If the myocardial mass index is 90 g/m2, it means a phase of compensatory hypertrophy, which shows higher myocardial perfusion.

Adult↗