(P < 0.001), pentobarbitone: 27,8% (P = 0,014), mdthohexitone: 24.9% (P = 0,013), propofol: 21,6% (P = 0,006The belief that sub-hypnotic doses of barbiturate agents enhance pain, perception has been a tenet of anaesthetic practice for >30 yr. In 1960, Dundee ~ used tibial pressure analgesimetry to demonstrate a reduction in nociceptive threshold (NT) in humans following low doses of thiopentone or pentobarbitone. Since then, similar actions of barbiturates have been demonstrated in both human 2 and CAN J ANAESTH 1995 / 42:6 / pp 532-40

These findings support further investigation into the role of levetiracetam in the prevention of anesthetic-induced excitability.

Enhanced hippocampal synaptic transmission after exposure to subanesthetic concentrations of pentobarbital persists during drug washout. This finding may help to explain why some patients experience excitation and enhanced pain during emergence from anesthesia.

No abstract

Purpose: To seek behavioural, reflexive and histochemical evidence of long-lasting changes in nociceptive stimulus transmission induced by exposure to doses of pentobarbital that induce nocifensive hyperreflexia.Methods: Nocifensive hyperreflexia was induced in 12 rats with 30 mg·kg -1 pentobarbital ip. Reflex latency times for withdrawal of the hind paw from noxious radiant heat were measured with an automated electronic timer. Subjective responses to noxious stimulation (licking or biting of the stimulated hindpaw) and the level of sedation were recorded. Histological sections of lumbar spinal cord were stained for immunoreactivity of the immediateearly-gene (IEG), c-fos, in three rats that received repeated threshold noxious radiant heat stimulation during the period of nocifensive hyperreflexia induced by 30 mg·kg -1 pentobarbital ip.Results: Reflex withdrawal latency decreased by 32 ± 8% of control values (P < 0.001) following pentobarbital injection and returned to control values 120 min after drug injection. Once fully alert, pentobarbital-treated animals did not show any increase in nociceptive behaviour relative to saline-injected controls (P = 0.41). Sustained noxious stimulation to the hindpaw in halothane-anesthetized animals was associated with an increase in c-fos immunoreactivity in the dorsal horn of the lumbar spinal cord ipsilateral to the stimulation (P < 0.001). Threshold stimulation in the pentobarbital-treated animals was not associated with any increase in c-fos expression.Conclusions: During pentobarbital-induced hyperreflexia, rats did not show any reflexive, behavioural, or histochemical evidence of long-lasting enhancement of nocifensive signal transmission. The results are consistent with previous observations that, in the absence of tissue injury, nocifensive hyperreflexia induced by barbiturates is a short-lived pharmacological effect.Objectif : Découvrir les manifestations comportementales, réflexes et histochimiques de modifications persistantes de la transmission d'un stimulus nociceptif induit par l'exposition à des doses de pentobarbital qui provoquent une surréflectivité défensive.Méthode : La surréflectivité défensive a été induite chez 12 rats avec 30 mg·kg -1 de pentobarbital ip. Les temps de latence réflexe nécessaire au retrait de la patte arrière d'une source de chaleur radiante ont été mesurés avec un chronomètre électronique automatisé. Les réponses subjectives à la stimulation désagréable (lécher ou mordre la patte stimulée) et le niveau de sédation ont été enregistrés. Des sections histologiques de la moelle épinière lombaire ont été colorées pour vérifier l'immunoréactivité du gène précoce immédiat (GPI), c-fos, chez trois rats qui ont reçu une stimulation liminale nocive répétée de chaleur radiante pendant la période de surréflectivité défensive induite par les 30 mg·kg -1 de pentobarbital ip.Résultats : Le temps de latence réflexe a baissé de 32 ± 8 % par rapport aux valeurs témoins (P < 0,001) après l'injection de pentobarbital et est revenu aux valeurs témoins 1...