Journal of Applied Physiology, Vol 49, Issue 3 497-505, Copyright © 1980 by American Physiological Society
Brain hypoxia and control of breathing: neuromechanical control
R. W. Chapman, T. V. Santiago and N. H. Edelman
The effects of graded brain hypoxia on respiratory cycle timing, the lung
inflation reflex, and respiratory compensation for an inspiratory
flow-resistive load were studied in unanesthetized goats. Two models,
inhalation and CO and acute reduction of brain blood flow (BBF) were used
to produce comparable levels of brain hypoxia. The lung inflation reflex
was assessed as the ratio of inspiratory time of an occluded breath to that
of the preceding spontaneous breath (TIoccl/TIspont). Compensation for
flow-resistive loading was assessed as the effect of the load upon the
airway occlusion pressure response to rebreathing CO2 (delta P 0.1/delta
PCO2). Major findings were 1) severe brain hypoxia (HbCO of 60% or BBF of
42%) caused tachypnea due to a 50% or more reduction of expiratory time but
only a 20% or less reduction of inspiratory time; 2) moderate
carboxyhemoglobinemia (HbCO of 25-30%) enhanced TIoccl/TIspont from 1.5 +/-
0.1 at control to 2.1 +/- 0.1, while severe brain hypoxia (HbCO of 60% and
BBF of 42%) reduced the ratio to 1.0 +/- 0.2; and 3) compensation for a
flow-resistive load, manifested by increases of delta P 0.1/delta PCO2 of
75-300% in the control state, was abolished at HbCO of 45-50% and BBF of
60%. The data suggest that in unanesthetized animals brain hypoxia elicits
tachypnea largely by an effect on the expiratory phase of the bulbopontine
timing mechanism. The observed enhancement of the lung inflation reflex and
abolition of flow-resistive load compensation are best explained by hypoxic
depression of higher than brain stem neural function.
