[The subcellular pathophysiology of heart failure due to toxic-allergic myocarditis and the action of refracterin on intracardiac hemodynamics and the functional state of the 3 subcellular cardiomyocyte systems responsible for the act of contraction-relaxation].
It is shown that cardiotropic drug refracterin promotes recovery of cardiac contraction and relaxation, their coordination destroyed in cardiac failure (CF) caused by 10-day toxico-allergic myocarditis (TAM). Pumping capacity of the heart returns to normal after normalization of functional activity of three systems of cardiomyocyte responsible for contraction-relaxation: contractile proteins, energy supply and calcium transport. The key process is refracterin-related reestablishment of normal content and proportion of adenyl nucleotides and creatininephosphate and regulation role of phosphorylation and energy of metabolic processes in the cells and their interaction. Thus, refracterin effectiveness lies in its ability to interfere in intracellular metabolic processes in the myocardium, to reestablish normal homeostasis of the systems responsible for contraction-relaxation function and eventually to remove left ventricular cardiac dysfunction.
Karsanov
N V
NV
Sukoian
G V
GV
Dzhibgashvili
I K
IK
Tatulashvili
D R
DR
Gorelishvili
I I
II
Guchua
E I
EI
D000113:Acetyldigoxins / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D002317:Cardiovascular Agents / Q000494:pharmacology* / Q000627:therapeutic use; D003574:Cytochrome c Group / Q000494:pharmacology* / Q000627:therapeutic use; D004338:Drug Combinations; D004353:Drug Evaluation, Preclinical; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006333:Heart Failure / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D009124:Muscle Proteins / Q000187:drug effects / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects* / Q000502:physiology; D009205:Myocarditis / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure*; D010099:Oxyfedrine / Q000494:pharmacology* / Q000627:therapeutic use; D011817:Rabbits; D013997:Time Factors
D000113:Acetyldigoxins; D002317:Cardiovascular Agents; D003574:Cytochrome c Group; D004338:Drug Combinations; D009124:Muscle Proteins; D010099:Oxyfedrine; D002118:Calcium