[Role of stationary activation of glycolysis in the heart during compensatory hyperfunction and aging].
Stationary stimulation of glycolysis was observed in rat heart muscle which produced the compensatory hyperfunction after aorta coarctation. The general character of alterations in energy balance of the hypertrophic heart muscle corresponded to the rearrangements, which occurred during ageing; therefore the coarctation of aorta caused more distinct stimulation of glycolysis in old animals than in young ones. Stimulation of glycolysis in ;the hypertrophic heart muscle was carried out via phosphofructokinase activation as G-PPK was increased by 87% during the heart compensatory hyperfunction. Stimulation of glycolysis, which developed at the beginning of the heart compensatory hyperfunction and continued up to its final steps, was apparently the adaptational mechanism providing the additional intake of ATP into the contractile apparatus, and so this stimulation prevented the decrease of oxygen consumption, produced in the hypertrophic heart muscle.
D000244:Adenosine Diphosphate / Q000032:analysis; D000249:Adenosine Monophosphate / Q000032:analysis; D000255:Adenosine Triphosphate / Q000032:analysis; D000375:Aging; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D003401:Creatine / Q000032:analysis; D005635:Fructosediphosphates / Q000032:analysis; D005636:Fructosephosphates / Q000032:analysis; D006019:Glycolysis; D007773:Lactates / Q000032:analysis; D009206:Myocardium / Q000378:metabolism*; D010725:Phosphocreatine / Q000032:analysis; D010732:Phosphofructokinase-1 / Q000378:metabolism; D051381:Rats
D005635:Fructosediphosphates; D005636:Fructosephosphates; D007773:Lactates; D010725:Phosphocreatine; D000249:Adenosine Monophosphate; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D010732:Phosphofructokinase-1; D003401:Creatine
Rol' statsionarnoĭ aktivatsii glikoliza v serdtse pri kompensatornoĭ giperfunktsii i starenii.