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L A Gnatiuk

Publications and source records attributed to L A Gnatiuk.

10 recordsLinked to original sources
PubMed1989

[Function-structural features of cardiac adaptation to static physical loads].

The cardiovascular system of 70 white rats was studied during adaptation to the physical static load by means of functional and morphometric techniques. The physical static loads induced variations of adaptive changes of the myocardium: right ventricle hypertrophy was mainly responsible for the cardiac mass increase in 47.1% of rats; 31.4% of the hearts revealed an equal proportional hypertrophy of both ventricles; the predominants increase of the left ventricle mass was found in 17.2% of the animals; no changes were found in 4.3%. The various adaptive rearrangements of the myocardium led to individual peculiarities of the cardiac rhythm regulation.

Adaptation, Physiological↗
PubMed1989

[Adaptive changes in sections of the myocardium of experimental animals undergoing physical loading of a static nature].

Adaptation of the parts of myocardium of 18 white rats to the physical static loadings during two months have been studied by means of morphometric and histological methods. Physical loadings cause hyperfunction and hypertrophy of all chambers of the heart with a predominant hypertrophy of the right ventricle, right auricle and dilatation of these cavities. The heterogeneous changes of the myocardium were found on the organic level.

Adaptation, Physiological↗
PubMed1985

[Adaptation of the heart of the experimental animal to physical loading (morphometric characteristics)].

Physical loadings produce in experimental animals various adaptive rearrangements in the cardiac muscle parts. Peculiar changes in the parts of the hyperfunctioning myocardium essentially depends on the character of physical strains. Static physical loadings produce an increase of the cardiac mass with a predominant hypertrophy of the right ventricle and dilatation of its cavity in most rats. Under swimming--in half of the observations the cardiac hypetrophy occurs mainly at the expense of analogous structural rearrangement in the left ventricle.

Adaptation, Physiological↗
PubMed1983

[Organometric evaluation of heart changes during systematic physical exercise].

Hearts from 23 athletes who had died of traumas were investigated using a morphometric approach that involves external and internal macro-changes measurement, plani-and gravimetry, histostereometry, and morpho-statistical treatment. Hypertrophic heart was found in all the cases, while the ratios between quantitative parameters of individual heart muscle departments, as well as nuclear-cytoplasmatic and stromal-parenchymatous relationships and myocardial blood supply were within normal range. It was demonstrated that only a certain portion of myocardial muscular cells, responsible for intensified operation, became hypertrophic in response to systematic exercise.

Adult↗
PubMed1980

[Morphometric study of the hypertrophied heart].

Diagnostic potentials of morphometric methods in studies of right-ventricle and left-ventricle hypertrophy of the heart were analysed. Different cardiometric methods were found to give dissimilar information on the quantitative changes in parts of the hypertrophic heart. Composite morphometry using the methods of individual weighing, external-internal, planimetric-weight, and histometric determinations followed by their mathematical treatment was found to reveal the dynamics of the quantitative parameters of hyperfunctioning heart parts most objectively.

Cardiomegaly↗
PubMedDate not supplied

[Secretory activity of atrial cardiomyocytes in adrenaline myocardiodystrophy].

Ultrastructure of atrial cardiomyocytes in adrenalin myocardiodystrophy was studied in white rat experiments. Morphometrically, there was a reduced number of mitochondria and secretory granules in the atrial muscular cells, space characteristics of cardiomyocytes and their nuclei increased. The above rearrangement of the atrial cardiomyocytes indicates that adrenalin myocardiodystrophy is associated with a decline in synthetic and secretory function of the test cardiac muscular cells.

Animals↗