Correlative contribution of carotid and aortic afferences to the ventilatory chemosensory drive in steady-state normoxia and to the ventilatory chemoreflexes induced by transient hypoxia.

The contributions of the peripheral arterial chemoreceptors to the tonic and phasic reflex ventilatory regulation were studied in spontaneously breathing pentobarbitone anesthetized adult cats. The chemosensory drive during eucapnic normoxia was inferred from the transient ventilatory effects induced by anesthetic blockade of the buffer nerves. Aortic nerves block did not modify ventilation. Carotid nerves block provoked transient ventilatory depression, decreasing VT by 46% and fR by 26%, followed by recovery to steady-state values in VT, fR and PETCO2. Changes in PETCO2 were correlated with those in VT, but not with those in fR. The ventilatory effects of blocking a given carotid nerve were more intense when the contralateral carotid nerve was already blocked. This effect may be an expression of hypoadditive interactions between carotid nerves inputs with respect to chemosensory drive of ventilation. Analysis of the dose-response curves for the ventilatory reflexes evoked by NaCN i.v., before and after blockade of the buffer nerves, revealed major contributions of the carotid nerves, with small contributions of the aortic nerves to the those responses to high doses of NaCN. The contributions of each carotid nerve to the tonic chemosensory drive and to the phasic ventilatory chemoreflexes were highly correlated (rs = 0.90; p less than 0.01). We propose that a family of modulatory functions may describe the effects exerted by the peripheral arterial chemoreceptors upon the tonic ventilatory drive in normoxia and the phasic reflex responses evoked by hypoxia. While the carotid nerves mediated modulation is evident in normoxia, that provided by both aortic nerves is only expressed during pronounced hypoxia.