[Thromboembolic complications in children].

An analysis was made of 2093 autopsies of children aged 0-14 years. Thromboembolic complications (TEC) were detected in 6.68% of the victims who had died from acute infections, chronic inflammatory diseases, congenital malformations.

[Neuro-ultrasonography in the assessment of perinatal lesions of the brain in high-risk children at birth and at 3 months of age].

As many as 135 children belonging to the group at high risk underwent neurosonography to assess the neuropsychic status in the early neonatal period and at an age of three months. A high rate of perinatal brain injuries was established as was a close relationship between the gestation age of the child, on the one hand and the character and intensity of the injury, on the other one. It has been revealed that the combination of deep immaturity and severe ante-intranatal hypoxia predetermines almost 100% injury of the brain structures, bringing about the formation of organic pathology and impairment of the psychoneurologic development of these children by the age of 3 months.

[Vascular component of the fibrinolytic system of blood (plasminogen activator of vascular wall) in patients with duodenal ulcer with a history of hemorrhagic complications].

It has been established that patients with duodenal ulcer complicated by hemorrhage in the past are characterized by the low response of the fibrinolytic system (FS) to two different exposures--local venous occlusion and administration of the sympathomimetic alupent. The rate of plasminogen the lower limit of normal in almost 2/3 of patients with activator release (RPAR) from vascular depots was under hemorrhages and in 1/4 of those with uncomplicated duodenal ulcer. The low RPAR was coupled with hereditary aggravation and hyperplasia of the parietal glandulocytes of the stomach.

[Changes in the myofibrillary apparatus of the heart in early postnatal ontogenesis of rats in conditions of high altitude and physical exertion].

During postnatal development of rats under high-altitude conditions, the cardiac mass was enlarged as a result of cellular and intracellular hyperplastic processes. Under additional physical exercise the enlargement of the myocardial mass in high-altitude conditions resulted from the hypertrophy of muscle cells, i.e.

[Effect of riboxine on myocardial metabolism in conditions of altitude hypoxia].

Riboxine stimulates activation of redox biosynthetic processes and raises aerobic production of energy in rat myocardium. Under pressure chamber hypoxia corresponding to the altitude 6000 m, riboxine promotes the correction of metabolic acidosis, normalization of the ultrastructure of cardiomyocytes and more balanced development of heart hypertrophy.

[Quantitative analysis of the mitochondrial ultrastructure of cardiomyocytes in rats adapting to altitude hypoxia].

A study was made of the quantitative characteristics of mitochondria of the myofibrillar, perinuclear and subsarcolemmal zones of cardiomyocytes during long-term adaptation of rats to an "altitude" of 9000 m in a pressure chamber. The data are presented on the role played by hypertrophic and hyperplastic processes occurring in the mitochondrial apparatus in supporting viability of cardiac cells at high altitude.

[Intensity of RNA synthesis and the DNA content in the myocardium of newborn rats during adaptation to altitude hypoxia].

Newborn rats were exposed to staged adaptation to altitude hypoxia in a pressure chamber at an atmospheric pressure corresponding to an altitude from 2000 to 9000 m. The time course of changes in the synthesis of RNA and DNA by the nuclei of muscle and connective tissue cells of the heart were studied by light autoradiography with the use of 3H-5-uridine and 3H-thymidine. In the course of early postnatal ontogenesis adaptation to altitude hypoxia was demonstrated to be accompanied by the intensified synthesis of nucleic acids by muscle and non-muscle cells of the heart, which is regarded as a compensatory-adaptation reaction of the myocardium to hyperfunction under the test experimental conditions.

[Ultrastructural bases of myocardial metabolic disorders under physical loads in alpine adaptation].

Ultrastructural and metabolic manifestations of adaptation mechanisms of myocardium of white rats were studied in highlands (Tuya-Ashu pass, 3200 meter above sea level) upon treatment with dosed physical loading. The development of processes of myocardial adaptation to highland hypoxia was found to be step-wise and manifested by the development of destructive and compensatory-adaptative processes. Physical loads in the early period of adaptation resulted in destruction and loss of mitochondria and other intracellular organelles.

[Functional morphology of myocardial ultrastructure during prolonged adaptation to pressure chamber hypoxia].

The myocardium of the right and left heart ventricles of rats was studied during 2.5-month adaptation to high-pressure chamber hypoxia (at an altitude of 6000 m). During varying time of rats' adaptation to hypoxia, destructive and compensatory-adaptive processes in the cardiomyocytes were seen concurrently.

[Structural changes in the rat myocardium in the process of adaptation to high-altitude hypoxia].

Changes in the weight of diverse parts of the heart, in cross-sectional area of myocytes and vascularization of the myocardium were studied in rat experiments under altitude hypoxia (3200 m above the sea level) during adaptation of the animals to hypoxia. Morphologically, the compensatory and adaptive reactions of the rat to hypoxia were shown by its increases weight at the expense of hypertrophy of the right ventricular myocardium. Vascularization of the myocardium augmented synchronously to its growing hypertrophy.