NEURONS OF INTRAMURAL GANGLIA OF THE HEART IN ITS HYPERFUNCTION AND HYPERTROPHY

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Abstract
The neurons of intramural neural ganglia in compensatory hyperfunction of the heart produced by experimental aortic stenosis in dogs and rabbits have been studied by neurohistological and histochemical methods. In the process of continuous hyperfunction, the neurons of the heart pass through the same 3 stages as does the contractile myocardium, namely: the damage stage, the stage of relatively stable hyperfunction and the stage of gradual exhaustion. At the damage stage the neurons are on the verge of exhaustion, some of them being really destroyed. The essential feature of this stage consists in an almost complete disappearance of the Nissl substance and specific cholinesterase. At the 2nd stage of the compensatory process the content of the Nissl substance and acetylcholinesterase in the neuroplasm is restored and the mass of the neuron is augmented. The function of the cell is distributed within this augmented neuronal mass and the intensity of function of cellular structures becomes normal. The adaptational process ensuring the transition of neurons to the stage of a relatively stable hyperfunction may be effected owing to the increased capacity of the apparatus of RNA and protein synthesis, i. e. the genetic apparatus of the cell. The increase of the genetic apparatus capacity of the neuron is morphologically expressed by augmentation of the nuclear mass and appearance of several nucleoli in a single nucleus. At the 3rd stage of the compensatory process, along with hypertrophy of the neurons, augmentation of the nucleus and increase of the number of nucleoli, sclerosis of neural ganglia at the expense of proliferation of the intermediate connective tissue and capsular elements have been observed.