[Glucose-6-phosphate dehydrogenase of neurogenically damaged heart].
Neurogenic damage of the myocardium by electrostimulation of the aortic arch led to deficiency of tissue noradrenaline (the sympathetic nervous system mediator). Simultaneously there was a marked rise of the glucose-6-phosphate dehydrogenase activity. Preliminary administration of the RNA synthesis inhibitor--actinomycin D--fully prevented the increase of this enzyme activity in the myocardium produced by its neurogenic damage. The data obtained testified to the acceleration of induction of this enzyme in the myocardium in case of its neurogenic damage, this correlating with the change of tissue noradrenaline balance.
D000818:Animals; D009202:Cardiomyopathies / Q000188:drug therapy / Q000201:enzymology*; D003609:Dactinomycin / Q000627:therapeutic use; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism*; D006321:Heart / Q000294:innervation*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats
D003609:Dactinomycin; D005954:Glucosephosphate Dehydrogenase; D009638:Norepinephrine
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