[Structural and functional changes in the histohematic barrier of the rat myocardium in the postischemic period].

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.

[Age differences in the post-reperfusion recovery of structure of the human myocardium].

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.

[Change in the permeability of cardiomyocyte sarcolemma after short-term total ischemia].

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.

[Ultrastructural features of heart insufficiency and its correction during the post-asphyxia period].

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.

[Structural basis of functional heart failure during the postresuscitation period].

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.