THE INTERACTION OF CENTRAL AND PERIPHERAL CHEMICAL CONTROL OF BREATHING

Abstract

Repeated withdrawal of known chemo-reflex support to the respiratory center (bilateral reversible cold blocking of Hering''s nerve after double vagotomy and permanent sinus collapse in chloralosed dogs) during various respiratory states yielded data and conclusions as follows. During eupneic breathing of atmospheric air or O2 rich air, chemoceptive nerve block usually reduced the vol. of pul-monar'' ventilation. The reduction was smaller with an O2 rich mixture than with a mixture containing but slightly less O2 than room air. Reasons were presented for concluding that both CO2 and O2 pressures prevailing during eupnea are sources of reflexogenic respiratory support. Apnea produced by overventilation with room air was markedly prolonged by chemoceptive nerve block. This effect was much greater than the reduction of breathing by chemoceptive block during eupnea. The chemoceptors exert an important tonic stimulation of breathing and they are particularly responsive to O2 lack occurring at the end of apnea. Repeated withdrawal of reflexogenic support during progressive hypercapnia caused a diminishing absolute reduction in breathing which disappeared at 5-6% CO2 in the inspired air. Hyperpnea of high grade hypercapnia is purely centrogenic. The peculiar absence of reflexogenic stimulation could not be explained by central paralysis, for pulmonary ventilation continued to increase with increasing CO2 well above the 6% level. In view of the linear relation of chemoceptor discharge to CO2 pres-sure, and of the progressively increasing centrogenic activity in these expts., increasing CO2 exerts an increasing central blocking action on the signals which it sets up in the chemoceptors. Conversely, diminishing pressures are thought to diminish the central blocking action of CO2 and, thereby, potentiate the signals arising in the chemoceptors. This relationship will explain the stimulating action of low CO2 pressures obtaining during eupnea, and at the end of exptl. apneas. Repeated chemoceptive nerve blocks during progressively increasing hypooxic hyperpnea produced progressively increasing reduction of breathing, vigorous breathing being finally converted to apnea. Hyperpnea of high grade O2 deficiency is purely reflexogenic. In view of the abrupt resumption of hyperpnea on chemoceptive deblock and of the suddenly increased frequency of breathing on vagal deblock, central depression or paralysis was but a minor factor in the reduction of the centrogenic component and progressive hypocapnia and alkalinization from several causes was a major factor in the diminishing centrogenic component. It is further proposed that the progressively increasing hypocapnia leads to a progressively increasing potentiation of the reflexogenic signals, thereby assuring an increasing dominance of the reflexogenic component. Prolonged apneas resulting from maintained withdrawal of chemoceptive support during hypooxic hyperpnea, frequently gave way to renewed breathing attributed to re-accumulation within the center of acid derived from its own acid metabolism and to increasing acidemia. Granting that a localized acidity of the chemoceptors is the stimulating influence producing a general alkalinization of the body during hypooxia, the basic physiological chemical control of breathing (acid excess and O2 deficiency) is again broadly interpretable in terms of the reaction theory. Not only is the activity of the center and of the chemoceptors explained but the changing relations of centrogenic and reflexogenic breathing during varying intensities of hypercapnia and O2 deficiency are accounted for as well.