These data indicate that propofol has a direct depressant effect on dorsal horn neuronal responses to noxious stimulation, with little or no indirect supraspinal effect.

Purpose: The auditory evoked potential (AEP) has been proposed as a method to determine depth of anesthesia, as AEPs are generated in the thalamus and cerebral cortex. Because general anesthesia, in part, relies on anesthetic action in the spinal cord, we hypothesized that isoflurane would have indirect depressant effects on the AEP because of its action in the spinal cord. Methods: Six goats were anesthetized with isoflurane and the jugular veins and carotid arteries isolated to permit cerebral bypass and differential delivery of isoflurane to the head and torso. The AEPs were determined by delivering binaural clicks at 9Hz, and measuring the evoked response from electrodes placed in the skull and scalp. Isoflurane was maintained at 0.8% in the head while the torso isoflurane was alternated between 0.3% and 1.3%, and the AEP determined at each torso concentration. Restflts: At isoflurane 0.3% delivered to the torso, the peak-to-trough amplitude of the mid-latency AEP waves designated as N 14/P24 was 0.337 ___ 0.185/aV and the N36 wave amplitude was 0. I I 5 _ 0.054 pV. When torso isoflurane was 1.3%, these waves decreased to 0.297 ___ 0.186 luV and 0.066 _ 0.037/aV, respectively (P < 0.05). The latency of the N I4 wave increased slightly (from 13.7 ___ 2.6 msec to 14.4 __. 2.8 msec, P < 0.05) but the latencies of the other waves were unchanged. Condusions: Isoflurane action in the spinal cord indirectly alters the AEP, however, the effect is small. These data suggest that isoflurane can depress the transmission of afferent information from the spinal cord to thalamus, midbrain and cerebral cortex.Objecfif : Le potentiel 6voqu~ auditif (PEA) a ~t~ propos~ pour d&erminer la profondeur de l'anesth&ie, puisque les PEA sont g~n&& dans le thalamus et le cortex c&6bral. Comme l'anesth&ie g6n~rale d~pend, en partie, de raction de l'anesth&ique sur la moelle ~pini&e, nous avons 6mis l'hypoth&e que l'isoflurane avait des effets d~pressifs indirects sur les PEA, puisqu'il agit sur la moelle ~pini&e. M&hode : Six ch~vres ont re~u une anesth&ie ~ l'isoflurane, et les veines jugulaires ainsi que les art&es carotides ont 6t~ isol~es pour permettre la d&ivation c&~brale et l'administration diff&entielle d'isoflui'ane ~ la t&e et au thorax. Les PEA ont ~t~ d6termin& par l'administration de clicks biauraux de 9 l-lz et les r~ponses mesur6es au moyen d'61ectrodes plac6es sur le crane et le cuir chevelu, l'isoflurane a ~t6 maintenu ~ 0,8 % au niveau c&~bral mais alternait entre 0,3 ~ et 1,3 % au thorax et les PEA ~taient d&ermin~s pour chaque nouvelle concentration. l~a~u]tats : Sous une concentration d'isoflurane ~ 0,3 % administr~ au thorax, l'amplitude de la cr&e ~ la base des ondes PEA de latence moyenne, d&ign6es comme N 141P24, ~tait de 0,337 ___ 0,185/JV et l'amplitude de l'onde N36 ~tait de 0, I I 5 ---0,054 I./V. Quand la concentration d'isoflurane thoracique ~tait ~ 1,3 %, ces ondes ont diminu~ ~, 0,297 ___ 0, 186/./V et ~ 0,066 _ 0,037/JV, respectivement. (P < 0,05). La latence de l'onde N 14 a augment6 l~g&ement (de 13...