Protective effect of transplantation of neonatal liver cell nuclei on the model of acute toxic hepatitis.

We present the results of comparative analysis of functional and morphological changes in the liver of animals with experimental CCl(4)-induced hepatitis under conditions of transplantation of neonatal liver cells and nuclei. It was found that transplantation of neonatal liver cell nuclei in acute toxic hepatitis provides better functional and structural state of the target organ.

Evaluation of myocardial energy parameters during simulation of epinephrine damage under conditions of cell transplantation.

The effects of transplantation of xenogenic neonatal heart cells on energy processes were studied in rat myocardium during the early period of epinephrine injury. Transplantation promoted a less pronounced ATP hydrolys to adenosine monophosphate and inorganic phosphate, a higher level of creatine phosphate, pyruvate, lactate, retention and activation of myocardial enzymes involved in energy metabolism.

Transplantation of xenogenic cardiomyocytes in experimental epinephrine-induced damage to myocardium: enzyme activity and morphological parameters.

We studied the effect of xenogenic neonatal cardiomyocytes on enzymatic processes in rat myocardium under conditions of epinephrine-induced damage. It was found that transplantation of the cell preparation restricts the zone of suppressed enzyme activity in the myocardium and promotes its recovery. Less pronounced metabolic disturbances corresponded to less pronounced morphological changes in the myocardium.

[Endothelial dysfunction in patients with angina pectoris of functional classes II and III].

Hemostatic parameters and the diameter of the brachial artery were studied in patients with functional classes II and III angina on exertion before and after an ischemic test. A multivariate statistical analysis was used to determine the significant parameters that distinguish vascular endothelial function in these patients. At the same time it was established that endothelial dysfunction in patients with varying angina pectoris is determined by different predictors of thrombocytic-vascular hemostasis.