[The action of a number of cardiac glycosides on an isolated system of myocardial contractile proteins in heart failure due to toxic-allergic myocarditis. The molecular mechanism].
Experiments conducted on an isolated contractile apparatus, myocardial fibers (MF) in cardiac insufficiency (CI) caused by toxico-allergic myocarditis of 10 days duration (TAM10dd) showed that cardiac glycosides (CG), beta-acetyldigoxin (beta AD), beta-methyldigoxin, and strophanthin K (SK) increase the capacity of the actomyosin ensemble (AME) for generation of force, hydrolization, and economic use of the free energy of ATP hydrolysis. The mechanism of the effect of these CG in the phase of contraction differs from that of their effect on the AE of a normal myocardium. For instance, in severe CI induced by TAM10dd beta AD, in distinction from its action on the AME of a normal myocardium, can increase contractility economy, particularly in the phase of highest energy capacity, the phase of force generation, and exceed the level encountered in normal conditions, it also increases significantly the rate and reduces the time of MF relaxation as in the case of MF of a normal heart.
Karsanov
N V
NV
Republican Research Center of Medical Biophysics, Tbilisi, Georgia.
Sukoian
G V
GV
Karsanov
V N
VN
Tatulashvili
D R
DR
Kipshidze
N N
NN
D000818:Animals; D002301:Cardiac Glycosides / Q000494:pharmacology*; D004734:Energy Metabolism / Q000187:drug effects; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006333:Heart Failure / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D009124:Muscle Proteins / Q000187:drug effects* / Q000502:physiology; D009200:Myocardial Contraction / Q000187:drug effects; D009205:Myocarditis / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D011817:Rabbits; D013997:Time Factors
D002301:Cardiac Glycosides; D009124:Muscle Proteins