THE CAROTID-BODY IN THE MOTOR-NEURON RESPONSE TO PROTRIPTYLINE

Protriptyline (PRT) has been shown to preferentially stimulate upper a irway inspiratory motorneurons relative to phrenic activity in hyperox ic hypercapnia in the decerebrate cat via a carotid body-independent m echanism. Since previous studies indicated that carotid body stimulati on results in preferential activation of upper airway respiratory musc les during both hypercapnia and hypoxemia, we hypothesized that if PRT preferentially stimulated upper airway motorneurons, the mechanism of action might involve the carotid body. We investigated the effect of PRT on carotid body function by comparing the electrical activity of t he hypoglossal (HYP) with that of the phrenic (PHR) nerve in carotid s inus nerve intact (CSNI) and CSN-sectioned (CSNX) anesthetized rats, b efore and after PRT (0.5 mg/kg i.v.), during 100% O2, 15% O2 (N2 balan ce), and 4% CO2 (O2 balance) administration. The moving time average ( MTA) peak inspiratory electroneurogram activities of both the HYP and PHR nerves increased an equivalent amount after PRT injection during h yperoxia, in both CSNI and CSNX rats. During hypoxia, the HYP activity increased significantly more than the PHR activity only in CSNI rats after PRT injection. During hyperoxic hypercapnia, HYP MTAs increased a similar amount in the CSNI and CSNX rats. We conclude that the HYP a nd PHR respiratory motorneuron pool responses to PRT depend on the blo od gas status at the time of drug administration.