Role of actin and myosin in the mechanism of the decrease of myocardial contractility and efficiency of energy transformation by myocardial myofibrils in chronic heart failure in humans.

Experiments with hybrid myocardial fibers showed that abnormalities of actin (basic protein of fine sarcomer threads) are responsible for reduced contraction rate, decreased developed force, and low efficiency of cardiomyocyte contraction in chronic heart failure caused by dilatation and ischemic cardiomyopathies and infective allergic myocarditis. Wastefulness of the contractile process in cardiomyocyte under conditions of pronounced energy deficit play a key role in progression of chronic heart failure. Hence, actin hypothesis of reduced contractile activity of myocardial contractile protein system in acute heart failure transforms into the actomyosin concept in chronic heart failure.

[Disruption of chemomechanical coupling in cardiomyocyte myofibrils in L-tyroxine toxicosis and athyreosis].

Skin assay of dog myocardial fibers showed alterations in free energy of ATP hydrolysis correlated distinctly with the rate of activity generated by the fiber (r = 0.87; P < 0.01).

[The uncoupling of the functioning of the force generation and ATP hydrolysis centers in the myocardial myofibrils in experimental informational disease].

Active and rigor force generation under the effect of electrostatic charge, the temperature and pCa, was significantly decreased in informational experimental disease. Other significant changes on the molecular level occurred in cardiomyocyte contractile apparatus in conditions of experimental informational disease.

Superprecipitation of hybrid actomyosin containing pathologic actin from failing hearts of adults and infants.

Superprecipitation (SP) of artificial actomyosin, obtained by hybridization of Straub actin from the human myocardium with myosin of normal animal hearts was studied. Actin was prepared from the myocardium of persons who died of congestive heart failure and various non-cardiac diseases, as well as of infants whose death resulted from toxic pneumonia complicated or not with heart failure. It was shown that, in the control hybrid actomyosin, the substitution of normal Straub actin by that from the failing heart resulted in decrease of both the rate and extent of SP.