Novikova N A
Biull Eksp Biol Med. 1978 Sep;86(9):297-8.
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.
通过电刺激主动脉弓对心肌造成的神经源性损伤导致组织去甲肾上腺素（交感神经系统介质）缺乏。同时，葡萄糖-6-磷酸脱氢酶活性显著升高。预先给予RNA合成抑制剂——放线菌素D——可完全阻止神经源性损伤所致心肌中该酶活性的增加。所获数据证明，在心肌发生神经源性损伤时该酶的诱导加速，这与组织去甲肾上腺素平衡的变化相关。
