MECHANISM OF THE RESPIRATORY CENTER ESTIMATED FROM CHANGES IN VAGAL EFFERENT RESPIRATORY DISCHARGES BY VAGAL AFFERENT STIMULATION AND LESION

• Published in: Journal of The Showa Medical Association Vol. 44; no. 1; pp. 1 - 9
• Main Authors: SEGAWA, Katsumi, TAKESHIGE, Chifuyu
• Format: Journal Article
• Language: English; Japanese
• Published: The Showa University Society 1984
• ISSN: 0037-4342; 2185-0976
• DOI: 10.14930/jsma1939.44.1

The effect of vagal unit discharges appearing in the finely desected central end of the cervical vagus nerve and respiration were recorded simultaneously on an oscilloscope in urethane anesthetized rabbits. Some neurons on one side of the severed vagal nerve continuously discharged, with an almost constant frequency. These kinds of discharges changed and became periodic, increasing firing rates during inspiration and decreasing during expiration, and new discharges appeared concomitantly with inspiration or expiration after the other side of the vagus was severed, or when cold-blocked with chlorethyl. Such periodic discharges once again became continuous, and newly-appeared discharges were extinguished by low frequency stimulation of the other side of the vaqus. The continuous discharges were inhibited by high f requeny afferent stimulation of the desected same side vaqus nerve. Central respiratory mechanisms were proposed as following by these vagal respiratory discharges : 1) Two kinds of inspiratory (IC1 and IC2) and expiratory (EC1 and EC2) centers exist in the respiratory center. 2) EC2 and IC2 caused expiratory and inspiratory discharges in the vagus eenters respectively, under abolishment of vagal afferent impulses. 3) IC1and EC1converged in some neurons in the vagal center and caused continuous vagal discharging. Vagal afferent nerves inhibited IC1, which inhibited EC1, therefore, IC1excitability is enhanced under the absence of vagal afferent impulses, increasing the firing rate of vagal continuous discharges during inspiration, and increased IC1excitability enhances the inhibitory effect on EC1, decreasing firing rate in continuous discharge during expiration. Wyss's observation that a different respiratory effect was induced by different stimuli frequencies of the vagal nerve can be explained by the above and following: 1) IC1is inhibited by high frequency vagal afferent stimulation and, hence, the inhibitory effect of IC1on the expiratory center subsides. As a result, expiration was induced by high frequency vagal stimulation. 2) EC2is inhibited by low frequency vagal afferent stimulation and, hence, the reciprocal inhibitory effect of EC2on IC1disappeared. As a result, inspiration was induced by low frequency vagal stimulation.