[Structural and functional changes in the histohematic barrier of the rat myocardium in the postischemic period]. / Strukturno-funktsional'nye izmeneiia gistogematicheskogo bar'era miokarda krys v postishemicheskom periode.

The aim of this study was to examine the myocardial histohematic barriers during the rehabilitation period after a cardiac arrest for 10 min. The electron histochemical analysis was applied to evaluate the permeability of histohematic barriers, to assess their ultrastructure and calcium localization. During 24 hours post resuscitation the destructive and compensatory-adaptive changes were found in the microcirculatory bed, accompanied by a pericapillary space edema, selective elevation of sarcolemmal permeability and calcium redistribution in cardiomyocytes. The structural and functional disturbances of histohematic barriers following the total ischemia are important factors of myocardial reperfusion lesions and of cardiodepression.

[Age differences in the post-reperfusion recovery of structure of the human myocardium]. / Vozrastnye osobennosti postreperfuzionnogo vosstanovleniia struktury miokarda cheloveka.

The ultrastructure of myocardium was studied in children and adults with congenital heart defects 1 hour after intraoperational cardiac arrest followed by reperfusion. It was established that the intensity of adaptation reactions which provide the structural homeostasis, is progressively reduced with age resulting in gradual depletion of compensatory reserves. The presence of preoperational compensatory-adaptive reserve in children defines the possibility and adequacy of post-ischemic myocardial regeneration and restoration of its contractile function. The depletion of compensatory reserves in adults is one of the main reasons for development of post-reperfusion myocardial injury and of its plastic insufficiency.

[Change in the permeability of cardiomyocyte sarcolemma after short-term total ischemia]. / Izmenenie pronitsaemosti sarkolemmy kardiomiotsitov posle kratkovremennoi total'noi ishemii.

Total ischemia (10 min) was produced in experimental rats by compression of the vascular band at the heart base. Sarcolemma permeability was studied with electron-microscopic tracer lantan at the height of ischemia and during 24 hours after resuscitation. It was established that reperfusion induces derangement of glycocalix and elevation of permeability of sarcolemma basal membrane. Plasmatic membrane in most cardiomyocytes was intact. This is an important factor of reversibility of myocardial lesion reperfusion.

[Ultrastructural features of heart insufficiency and its correction during the post-asphyxia period]. / Ul'trastrukturnye priznaki serdechnoi nedostatochnosti i ee korrektsiia v postasfiksicheskom periode.

The ultrastructure of myocardium was studied in the experiments on rats during 24 hours after 6-min mechanical asphyxia with following clinical death. It has been established that the contractile cardiac apparatus of myocytes lesions on the intracellular edema background is the main while energy production process impairs insignificantly. The effectiveness of anti-hypoxia, membrane stability and protease inhibiting preparations for prevention of postresuscitation myocardium lesion was examined. The contrykal protective action, suppressing the proteolytic ferment hyperactivity was determined.

[Structural basis of functional heart failure during the postresuscitation period]. / Strukturnye osnovy funktsional'noi nedostatochnosti serdtsa v postreanimatsionnom periode.

Light and electron microscopic study of the myocardium of dogs two weeks after clinical death caused by the loss of blood was carried out and showed that the structural bases of the myocardium contractile function insufficiency during the postresuscitation period included the damage of the contractile apparatus of cardiomyocytes (microlysis and fragmentation of myofibrils, deformation of Z-bands, relaxation of sacromeres) and marked lysis of the sacrotubular system leading to the violation of the excitation-contraction coupling. Cardiomyocyte damages are associated with changes in the microcirculatory channel causing the worsening of transcapillary exchange that provides the tissue homeostasis.

[Morphologic changes in the myocardium following acute blood loss and subsequent resuscitation]. / Morfologicheskie izmeneniia v miokarde posle ostroi krovopoteri s posleduiushchei reanimatsiei.

An electron microscopic investigation on reparative regeneration of the myocardium has been performed in dogs survived after clinical death resulted from loss of blood. Some regenerative processes already begin on the first hours after reanimation and they proceed on the background of certain distrophic and destructive changes. On the 3d-7th days of the restorative period, the intracellular regeneration of cardiomyocytes increases considerably; it is demonstrated by newly formed myofilaments in the foci of myofibrillar lysis, increasing content of small mitochondria, hyperplasia of the granular endoplasmic reticulum. Simultaneously, a great number of secondary lysosomes is forming; as a result, the cells are releasing themselves from the substances formed after decomposition and decay of some organelles. Myelin-like bodies are observed to be pushed out of the cardiomyocytes into the intercellular space. In fact, by the end of the second week after total ischemia the structure of the cardiac muscle is fully normalized. T-system of cardiomyocytes is the one which is the slowest to restore.

[Stereologic analysis of myocardial ultrastructure during the postresuscitation period]. / Stereologicheskii analiz ul'trastruktury miokarda v postreanimatsionnom periode.

The myocardium of dogs which suffered the 5-minute clinical death was subjected to ultrastructural stereologic examination. It was found that the T system density volume in cardiac myocytes was drastically reduced because of the massive destruction of its tubules. The regeneration of the T system was slow in progress. The mitochondrial density volume was discovered to be reduced 6 hours after the resuscitation. The myocardial ultrastructure virtually returned to normal by the end of the second week of the postresuscitation period.