Abstract
Oxygen consumption, arterial blood ph, CO2 tension and O2 saturation were determined in pontile decerebrate cats with normal respiration and apneustic respiration and in medullary cats with rhythmic respiration. Respiratory acidosis is observed regularly during apneustic respiration. In medullary animals, respiratory acidosis also occurs if the respiration is slow or shallow. The O2 consumption is not changed and a reasonable arterial blood O2 saturation is maintained. This is probably attributable to the fact that these animals are breathing oxygen-rich mixtures. Ten per cent CO2 inhalation increases the amplitude of the inspiratory spasm and accelerates the apneustic cycle. This response persists after carotid denervation. Stimulation of the carotid chemoceptors with intracarotid injection of sodium cyanide also accelerates the apneustic cycle. It is concluded that although the afferent impulses from the carotid receptors can modify the activity of the apneustic center, they are not to be considered essential for the production of the apneusis. The underlying mechanism for the cycling in apneustic respiration is not clear from the present study. It appears that this cycling is probably not related to the low O2 tension but rather to the increased CO2 tension in the arterial blood.