THE EFFECTS OF KETAMINE ON RENAL SYMPATHETIC-NERVE ACTIVITY AND PHRENIC-NERVE ACTIVITY IN RABBITS (WITH VAGOTOMY) WITH AND WITHOUT AFFERENTINPUTS FROM PERIPHERAL RECEPTORS

One reason for the reported conflicting results of the effect of ketam ine on hemodynamics and respiration may be variations in afferent inpu ts from peripheral receptors to the central nervous system. In order t o evaluate unmasked direct effects of ketamine on sympathetic nerve an d phrenic nerve outflow, totally deafferented (involving vagus, sinus nerve, aortic depressor nerve) rabbits (n = 18), rabbits with vagotomy (n = 21), and neuraxis-intact rabbits (n = 6) were used in this study . The animals were anesthetized with urethane and mechanically ventila ted. Ketamine 0.5, 1, or 2 mg/kg was injected intravenously and mean a rterial pressure (MAP), heart rate (HR), and integrated renal sympathe tic nerve and phrenic nerve activity (IRSNA, IPNA) were recorded befor e, and 1, 2, 3, 5, and 10 min after injection. MAP and IRSNA were sign ificantly decreased, even by the smallest dose of ketamine, in the tot ally deafferented group. IPNA was decreased by the largest dose of ket amine only in the totally deafferented group. On the other hand, spont aneous respiratory frequency was decreased in the totally deafferented and vagotomy groups, but more so in the totally deafferented group. I n the neuraxis-intact group, the only significant change with the larg est dose of ketamine, 2 mg/kg was a slight increase in HR. We conclude that ketamine can suppress vasomotor and respiratory centers directly , and that the suppression is counterbalanced by afferent inputs from peripheral receptors.