Purpose: To determine the effects of ketamine and pentobarbital on noradrenaline release from the medial prefrontal cortex. Methods: In 14 male Wistar rats, a microdialysis probe with a 2 mm long semipermeable membrane was implanted in the medial prefrontal cortex. The dialysis probe was perfused at a rate of I pl-min-' with an artificial cerebrospinal fluid solution. The rats were randomly allocated to two groups: ketamine (group K, n--7) and pentobarbital (group P, n =7). Each rat was subsequently given 0 (saline), I, 10 and 100 mg'kg -I ketamine ip in group K, and 0 (saline), 0.5, 5 and 50 mgkg-' pentobarbital ip in group P. Sixty minutes elapsed between administration. Results: Noradrenaline release after 100 mg.kg-' ketamine increased by 7.7 • 2.0 (SEM) pg-collection t compared with 2.7 ___ 0.7, 3.3 _+ 1.0 and 4.2 _ 0.8 pg.collection-' after saline, I and 10 mg'kg-' ketamine, repectively (P < 0.05). Noradrenaline release did not change after pentobarbital Conclusion: This study suggests the ketamine and pentobarbital have different effects on noradrenergic neurons in the medial prefrontal cortex. The stimulating effect of ketamine on noradrenaline release from the cortex might contribute to unique clinical features of ketamine anesthesia.Objeetif: D&erminer les effets de la k6tamine et du pentobarbital sur la lib&ation de noradr~naline par le cortex m~dial prefrontal. M(:thode : On a implant~ dans le cortex m~dial prefrontal de 14 rats males Wistar une sonde pour microdialyse avec une membrane semi-permeable de 2 mm de long. La sonde a ~t~ irrigu& avec une solution de liquide c~phalo-rachidien artificiel ~ un d~bit de I pl.min-'. Les rats ont ~t~ r~partis au hasard en deux groupes : k~ta-mine (groupe K, n = 7) et pentobarbital (groupe P, n = 7). On a ensuite administr~ ~ chaque animal 0 (solution R~ttltats 9 La lib&ation de noradr~naline apt& 100 mg'kg-' de k&amine a augment~ de 7,7 • 2,0 (erreur type) pg-collection ~ comparativement ~ 2,7 • 0,7 ; 3,3 _+ 1,0 et 4,2 _+ 0,8 pg.collection-' apt& la solution sal6e, I et 10 mg'kg-' de k&amine, respectivement (P < 0,05). La lib&ation de noradr~naline n'a pas chang& apr~s I'administration de pentobarbital. Conclusion : Cette &ude a montr~ que la k&amine et le pentobarbital ont des effets diff&ents sur les neurones noradr~nergiques dans le cortex m~dial prefrontal. I'effet stimulant de la k&amine sur la lib&ation de noradr& naline par le cortex peut jouer un r61e dans le tableau clinique de I'anesth&ie avec k~tamine.

These data suggest that different clinical profiles observed with these two classes of sedatives may result from changes in noradrenaline release from the medial prefrontal cortex.

Purpose: To study the effects of sevoflurane and isoflurane on noradrenaline release from the rat preoptic area (POA).Method: Sixteen male Wistar rats were studied. A microdialysis probe with a 2 mm long semipermeable membrane was implanted in the POA. Dialysates were collected at intervals often minutes. After obtaining five control samples for 50 rain, 30 rain inhalation of 3% sevoflurane or 1.8% isoflurane was performed. After cessation of the inhalation, five more samples were obtained for 50 rain as recovery phase. Noradrenaline (NA) concentration in the dialysates was measured by high pressure liquid chromatography with an electrochemical detector.Results: Both sevoflurane and isoflurane caused marked increases in NA release from the rat POA (sevoflurane 233% at 20 rain, isoflurane 357% at ten minutes after the start of inhalation). The marked NA releases were also observed during the emergence from sevoflurane and isoflurane anesthesia (sevoflurane 269% at 20 rain, isoflurane 368% at ten minutes in the recovery phase).Conclusion: This study suggests that enhanced release of NA in the POA during sevoflurane and isoflurane may explain the excitatory phase observed during the peri-anesthetic period with these agents. Objectif : Etudier les effets du s&oflurane et de I'isoflurane sur la lib&ation de noradr4naline en provenance de I'aire pr4optique du rat (APO). M~tbode

We have investigated the effect of clonidine on ketamine-induced norepinephrine release from the medial prefrontal cortex in rats using microdialysis. Twenty-one male Wistar rats weighing 200-300 g were allocated randomly to one of four groups: i.p. injection of ketamine 100 mg kg-1 with clonidine 0 (saline: group C0, n = 6), 3 (group C3, n = 5), 30 (group C30, n = 5) and 300 micrograms kg-1 (group C300, n = 5). As reported previously, ketamine increases norepinephrine release. In groups C0 and C3, marked increases in norepinephrine release were observed with maximum values of mean 483 (SEM 55)% and 412 (53)% compared with basal values, respectively. Although significant increases in norepinephrine release were also observed (276 (43)%) in group C30, they were significantly lower than those in groups C0 and C3 (P < 0.01 and P < 0.05, respectively). In group C300, there was a significant reduction in norepinephrine release (62 (13)%) compared with basal and the three other groups (P < 0.01). This inhibitory effect of clonidine on norepinephrine may be related to reduction in undesirable emergence reactions after ketamine anaesthesia.

No abstract