Abstract

This study was carried out with the purpose of investigating the functional significance and the role of neuroepithelial bodies (NEB) in the regulation of respiration in hypoxia. 22 mongrel dogs of 17-23 kg. in body weight were used as experimental animals. The animals were anesthetized with intravenous injections of sodium pentobarbital (30 mg/kg). The carotid and aortic chemoreceptors of one dog (the recipient) were denervated. By means of a cross circulation technique, the cerebral circulation of the recipient dog was separated from its systemic circulation and was perfused via the vertebral and internal carotid arteries with blood from the common carotid artery of a donor dog. 0n the breathing of the normoxic and hypoxic gast mixtures by the recipient animal, its respiratory parameters and systemic arterial blod pressure were recorded. At the end of each experimental phase, Pa02, PaCO2 and pHa were determined in blood samples obtained from the vertebral and femoral arteries. 0n the breathing of the hypoxic gas mixture (7% 02-93% N2) by the recipient dog (cerebral normoxia-systemic hypoxia), tidal volume (VT), respiratory frequency [f(min-1)] and ventilation minute volume (VE) were significantly increased to 27.6 %, 32% and 30.1 %, respectively, of the normoxic values as 100. These respiratory responses were followed by and apneic phase. Following biiateral vagotomy in the chemoreceptor-denervated recipient dog, the respiratory responses to hypoxia were diminished. The hypoxic stage was again followed by an apneic phase. Upon the induction of cerebral hypoxia-systemic hypoxia in the recipient animal, significant diminutions in VT were accompanied by a significant increase in [f(min-1)] when compared wtih the control normoxic values. An apneic phase again followed this last experimental stage. ln conclusion, the results of the present study suggest that in cerebral normoxic-sytemic hypoxic phase the increase in respiratory activity of peripheral chemorecteptor-denervated dogs may be attributed to the effect of facilitatory impulses from the NEB, transmitted to respiratory centers via the vagal fiber. In cerebral hypoxia, on the other hand, the decrease in neuronal activity of the centers may overcome the effects of the facilitatory impulses from the NEB.

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