[Metabolic stability of the protein-synthesizing system of the myocardium in compensatory cardiac hyperfunction in actinomycin D block of RNA synthesis].
Under conditions of complete actinomycin block in rat heart muscle an inhibition of protein synthesis and dissociation of myocardial polyribosome structures were observed (half-life was equal to 6.5 hrs). In compensatory hyperfunction of heart muscle, caused by stenosis of aorta, the inhibitory effect of actinomycin D on the protein synthesis was manifested earlier than in control and was exhibited more distinctly. In myocardium under compensatory hyperfunction of heart muscle the protein synthesis was decreased by 50% within 4 hrs after administration of actinomycin into animals and it was completely inhibited within 10 hrs after the antibiotic administration. The alteration in stability of polyritobosomes under compensatory hyperfunction of heart muscle was specific for myocardium and was not observed in liver tissue.
D000222:Adaptation, Physiological; D000818:Animals; D001012:Aorta, Abdominal; D002250:Carbon Radioisotopes; D003584:Cytological Techniques; D003609:Dactinomycin / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects; D006331:Heart Diseases / Q000378:metabolism*; D006984:Hypertrophy; D007700:Kinetics; D008026:Ligation; D008099:Liver / Q000166:cytology / Q000378:metabolism; D008297:Male; D009124:Muscle Proteins / Q000096:biosynthesis*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism*; D011132:Polyribosomes / Q000378:metabolism; D012313:RNA / Q000037:antagonists & inhibitors*; D051381:Rats; D013997:Time Factors
D002250:Carbon Radioisotopes; D009124:Muscle Proteins; D003609:Dactinomycin; D012313:RNA
Metabolicheskaia stabil'nost' beloksinteziruiushcheĭ sistemy miokarda pri kompensatornoĭ giperfunktsii serdtsa v usloviiakh bloka sinteza RNK aktinomitsinom D