[Subcellular basis of disorders of the contractile capacity of the heart in L-thyroxine-induced thyrotoxicosis].

In experiments on dogs, the authors examined the functional activity of three cardiomyocyte systems responsible for contraction-relaxation (the systems of contractile proteins, calcium transport and energy supply) in the dynamics of L-thyroxine-induced toxicosis. A fall in the capacity of the contractile protein system to generate energy and to perform was shown to play the leading role in decrease of myocardial reserve forces and reduction in cardiac contractility. There was a drop in the intensity of calcium transport through the membranes of the sarcoplasmic reticulum and mitochondria and a deficiency of the direct energy source for contraction only in the late period of the disease.

Inosine effect on high-energy phosphate content, mechanical activity of glycerinated fiber bundles, morphology and microcirculation in myocardium in toxi-allergic and allergic myocarditis.

It has been shown in experiments on rabbits on rabbits that in AM and TAM 80 mg/kg of inosine increase the total content of adenylic system nucleotides to the normal level and 160 mg/kg of inosine exceeds it. At the same time in the case of 80 mg/kg, ATP content is considerably increased and ADP is normalized while with 160 mg/kg ATP content becomes normal and ADP exceeds the normal level significantly. MGFB contractility returns to normal.