An Analysis of Rate and Amplitude of Breathing

Abstract

Gaseous mixtures of low oxygen content following double vagotomy in the dog produced an augmentation of tidal air with little or no change in rate of breathing. After carotid gland denervation and section of the pulmonary branches of the vagus nerve, which leaves the chemically sensitive aortic nerve endings intact, the effects of anoxemia are similar, but not as great as those following double cervical vagotomy. With the vagus nerves intact and the carotid glands denervated, anoxemia augmented respiratory rhythm with little or no change in tidal air. Frequently the amplitude of breathing diminished. (See Figs.)

Such results indicate that peripheral chemical stimulation at the carotid gland and at the endings of the aortic nerve contribute importantly to the control of depth of breathing, and that the vagus nerves contribute importantly to the control of rate of breathing. While a differentiation of rate and depth of breathing appears to have been demonstrated, it is not suggested that rate and amplitude control occur exclusively through these 3 channels of nervous influence, for breathing can be accelerated after double cervical vagotomy, and amplitude can be augmented by stimulation of cutaneous sensory nerves.

In some individuals anoxemia produced a greater change in rate of breathing than in amplitude. In others the reverse occurred. In those dogs in which the rate control was developed at the expense of amplitude control, anoxemia produced the same increase in rate after denervation of the carotid gland, and the same small change in amplitude after double vagotomy with carotid gland innervation intact. In those dogs, in which amplitude control was developed at the expense of rate control, anoxemia produced the same large increase in depth of breathing after double vagotomy, and the same small increase in rate after carotid gland denervation with the vagus nerves intact.