Journal of Applied Physiology, Vol 66, Issue 1 51-56, Copyright © 1989 by American Physiological Society
Brain hypoxia preferentially stimulates genioglossal EMG responses to CO2
D. A. Hutt, R. A. Parisi, T. V. Santiago and N. H. Edelman
Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick 08903-0019.
Although the dominant respiratory response to hypoxia is stimulation of
breathing via the peripheral chemoreflex, brain hypoxia may inhibit
respiration. We studied the effects of two levels of brain hypoxia without
carotid body stimulation, produced by inhalation of CO, on ventilatory (VI)
and genioglossal (EMGgg) and diaphragmatic (EMGdi) responses to CO2
rebreathing in awake, unanesthetized goats. Neither delta VI/delta PCO2 nor
VI at a PCO2 of 60 Torr was significantly different between the three
conditions studied (0%, 25%, and 50% carboxyhemoglobin, HbCO). There were
also no significant changes in delta EMGdi/delta PCO2 or EMGdi at a PCO2 of
60 Torr during progressive brain hypoxia. In contrast, delta EMGgg/delta
PCO2 and EMGgg at a PCO2 of 60 Torr were significantly increased at 50%
HbCO compared with either normoxia or 25% HbCO (P less than 0.05). The PCO2
threshold at which inspiratory EMGgg appeared was also decreased at 50%
HbCO (45.6 +/- 2.6 Torr) compared with normoxia (55.0 +/- 1.4 Torr, P less
than 0.02) or 25% HbCO (53.4 +/- 1.6 Torr, P less than 0.02). We conclude
that moderate brain hypoxia (50% HbCO) in awake, unanesthetized animals
results in disproportionate augmentation of EMGgg relative to EMGdi during
CO2 rebreathing. This finding is most likely due to hypoxic cortical
depression with consequent withdrawal of tonic inhibition of hypoglossal
inspiratory activity.
