Koh Shingu

Naloxone does not Antagonize the Anesthetic‐Induced Depression of Nociceptor‐Driven Spinal Cord Response in Spinal Cats

The effects of several anesthetics on spinal cord nociceptive neural mechanisms and their interactions with the opiate antagonist, naloxone, were studied in acute, spinal cord transected cats. Intra‐arterial injection of bradykinin was used as the noxious test stimulus. Spontaneous activity and the neural response induced by bradykinin were recorded by the multi‐unit activity technique in the lateral funiculus of the spinal cord. Naloxone, 0.1 or 2.0 mg/kg i.v., had little effect on the bradykinin‐induced response, but enhanced the spontaneous firing of the lateral funiculus significantly. Fentanyl, 30 μg/kg i.v., depressed both the bradykinin‐induced response and spontaneous firing. These effects of fentanyl were antagonized completely by naloxone, 0.1 mg/kg i.v. Nitrous oxide, thiamylal, halothane and ether depressed the bradykinin‐induced response considerably, but it was not antagonized by naloxone, 0.1–2.0 mg/kg i.v. Enflurane had little effect on the bradykinin‐induced response. The effects of these anesthetics on spontaneous firing were divergent: nitrous oxide enhanced it while other drugs depressed it, to various degrees. All these data suggest that the neural and/or neurochemical mechanisms of anesthetic‐induced analgesia differ from mechanisms related to opioids.

Nitrous Oxide Activates the Supraspinal Pain Inhibition System

The neurophysiological mechanism of nitrous oxide‐induced analgesia was studied in decerebrate non‐anesthetized cats. Intra‐arterial injection of bradykinin was used as the test noxious stimulus and the neural response in the lateral funiculus of the spinal cord was measured by the multi‐unit recording technique. The effects of nitrous oxide on the neural activity of spinal cord were compared before and after the spinal cord transection. Nitrous oxide activated the spontaneous firing level, but depressed the bradykinin‐induced response. These effects were more significant before the cord transection than after it. These findings indicate that nitrous oxide exerts its analgesic action through both the direct intraspinal anti‐nociceptive action and an indirect action by activating the supraspinal descending inhibition system.

The divergent actions of volatile anaesthetics on background neuronal activity and reactive capability in the central nervous system in cats

The effects of halothane, isoflurane, and enflurane on background neuronal activity and reactive capability in the central nervous system were studied in cats. The background neuronal activity was assessed by midbrain reticular cell firing, which was measured by the method of multiunit activity, and the EEG in the cortex, amygdala, and hippocampus. The reactive capability was assessed by evoked responses in the visual neuronal pathway. All anaesthetics studied suppressed reticular cell firing in a dosedependent manner, and the suppression by halothane (43.8 ± 10.3% of control, mean ± SD) was less than isoflurane (66.5 ± 5.8%, P < 0.01) and enflurane (73.1 ± 8.8%, P < 0.05) at 1 MAC. Spontaneous EEG spikes developed at 4.8% isoflurane and 3.6% enflurane anaesthesia. Phasic activation of reticular cell firing was associated with EEG spikes during isoflurane and enflurane anaesthesia, and the activation during enflurane anaesthesia was greater than during isoflurane anaesthesia (P < 0.01). Photic stimulation provoked EEG spikes and repetitive stimulation induced seizure activity only at 3.6% enflurane anaesthesia. Halothane and isoflurane suppressed stimulation induced responses in the visual neuronal pathway. The amplitudes of N1 in visual cortical evoked responses induced by photic stimulation were suppressed to 70.1 ± 24.5% of control at 2.4% halothane and 39.3 ± 27.3% at 4.8% isoflurane. Enflurane, at 3.6%, augmented the evoked response induced by photic stimulation (398.4 ± 83.0% of control in the amplitude of N1). These results indicate that all the agents studied had suppressive actions on background neuronal activity in the order halothane < isoflurane = enflurane. The effects on reactive capability were divergent among agents, e.g., enflurane enhanced, halothane suppressed, and the actions of isoflurane were intermediate. We conclude that the anaesthetic effects on background activity and on reactive capability are divergent and that suppression of reactive capability is a factor in determining the ease of clinical application of the anaesthetics.RésuméL’étude porte sur les effets de l’halothane, l’isoflurane et de l’enflurane sur l’activité neuronale de fond et la capacité réactive du système nerveux central chez le chat. L’activité neuronale de fond est mesurée par la décharge des cellules réticulaires mésencéphaliques, ellemême par la méthode de l’activité multiunitaire et l’EEG cortical, amygdalien et hippocampique. La capacité réactive est évaluée les réponses évoquées sur la voie de conduction visuelle neuronale. Tous les anesthésiques suppriment la décharge de la cellule réticulaire proportionnellement à la concentration. La suppression par l’halothane (43,8 ± 10,3% du contrôle, moyenne ± E.T.) a été moindre que par l’isoflurane (66,5 ± 5,8%, P < 0,01) et l’enflurane (73,1 ± 8,8%, P < 0,01) à 1 MAC. Des pointes spontanées sont apparues avec l’anesthésie à l’isoflurane 4,8% et à l’enflurane 3,6%. L’activation phasique de la décharge de la cellule réticulaire est associée à des pointes EEG pendant l’anesthésie à l’isoflurane et à l’enflurane, et l’activation pendant l’enflurane est plus grande que pendant l’isoflurane (P < 0,01). La stimulation photique entraîne des pointes EEG et une stimulation répétée provoque de l’activité épileptique à seulement 3,6% d’enflurane. L’halothane et l’isoflurane suppriment les réponses évoquées induites par stimulation dans la voie de transmission neuronale visuelle. Les amplitudes de N1 pour les réponses évoquées induites au cortex visuel par stimulation photique sont supprimées à 70,1 ± 24,5% du contrôle avec halothane 2,4% et à 39,3 ± 27,3% avec l’isoflurane 4,8%. L’enflurane à 3,6% augmente la réponse évoquée induite par stimulation photique (398,4 ± 83,0 du contrôle dans l’amplitude de N1). Ces résultats indiquent que tous les agents étudiés ont une action suppressive sur l’activité neuronale de fond dans l’ordre halothane < isoflurane = halothane. Les effets sur la capacité réactive divergent parmi les agents, c’estàdire que l’enflurane l’augmente, l’halothane la supprime et l’isoflurane occupe une place intermédiare. Nous en concluons que les effets anesthésiques sur l’activité de fond et la capacité réactive divergent et que la suppression de la capacité réactive est un facteur déterminant sur la facilité de l’utilisation des anesthésiques en clinique.

Effects of different speeds of induction with sevoflurane on the EEG in man.

The effects of two kinds of induction speed of sevoflurane anesthesia on the EEG pattern were compared in the same individual using medical student volunteers: a first exposure of 4% was given, followed after full recovery, by incremental doses of 1, 2 and 4% successively, each being administered for 10 min. The arterial blood level of the anesthetic was measured using gaschrornatograph. The changes of EEG pattern during fast induction with 4% were not represented by the abbreviation of those observed during the slow induction with the incremental doses. The administration of 4% induced a sudden appearance of high voltage, rhythmic slow waves of 2–3 Hz at 1–3 min when the arterial blood anesthetic level increased maximally, which was then followed by a pattern of faster activities of 10—14 Hz mixed with 5–8 Hz slow waves. In contrast, the administration of incremental doses induced an increase in frequency and amplitude of EEG activities in the light plane, followed by their decreases in deeper planes. The final EEG patterns were identical for both these methods of induction. These findings confirmed our previous hypothesis that not only the arterial blood level of anesthetics but the rate of its increase are important factors determining the EEG pattern of anesthesia.

Antianalgesic Action of Thiamylal Sodium in Cats

The effects of thiamylal on the nociceptor‐driven neural activity in the spinal cord were studied in decerebrate, non‐anesthetized cats. Noxious stimulation was induced by the injection of bradykinin into the femoral artery and the neural response in the lateral funiculus was measured by the multi‐unit activity technique. The effects of thiamylal on the bradykinin‐induced response were compared before and after the spinal cord transection, above the recording site. Thiamylal, 5 mg/kg i.v., potentiated the response significantly before the cord transection and depressed it after the transection. These findings indicate that the antianalgesic action of thiamylal is induced at the spinal cord level: although this anesthetic agent does have a direct intraspinal depressant action, the multisynaptic neural network of the supraspinal pain inhibition system is more susceptible to the actions of anesthetics, and the depression of this descending system by thiamylal results in a release of spinal cord nociceptive neural mechanisms from the supraspinal control.

Clonidine premedication for sevoflurane anesthesia in upper abdominal surgery

The effects of clonidine as a preanesthetic medication were compared with diazepam on clinical courses of sevoflurane anesthesia in 22 patients undergoing upper abdominal surgery. The patients were divided into two groups of 11 patients each according to preanesthetic medication: atropine 0.5 mg i.m. plus clonidine 0.3 mg p.o., or atropine 0.5 mg i.m. plus diazepam 10 mg p.o. 60–90 min prior to induction of anesthesia. Anesthesia was induced with fentanyl and thiopental, and was maintained with sevoflurane, 0.5%–1.5%, nitrous oxide and oxygen, supplemented with fentanyl, 0.5 μg·kg−1·hr−1. While only one patient needed a vasodilator in the clonidine group for treatment of hypertension, seven patients needed it in the diazepam group. Pain score after extubation was higher in the diazepam group than in the clonidine group. The time when patients responded to verbal command after discontinuation of anesthetics was similar in both groups. Therefore, clonidine pretreatment was useful for sevoflurane anesthesia in upper abdominal surgery.

The Effects of Anesthetics on Spinal Cord Nociceptive Neural Activities

The effects of several anesthetics on spinal cord nociceptive neural mechanisms and their interactions with naloxone were studied in acute spinal cord transected cats. Intraarterial injection of bradykinin was used to stimulate chemical nociceptors. Spontaneous activity and the bradykinin-induced responses were recorded by the multiunit activity technique in the lateral funiculus. Thiamylal, nitrous oxide, halothane and diethylether suppressed the bradykinin-induced response considerably, but it was not antagonized by naloxone, 0.1–2.0 mg/kg iv. Enflurane had little effect on the bradykinin-induced response. The effects of these anesthetics on the spontaneous activity was divergent: nitrous oxide enhanced while the other anesthetics suppressed it to various degrees. Fentanyl, 30 μg/kg iv, suppressed both the bradykinin-induced response and the spontaneous firing. These effects were antagonized completely by naloxone, 0.1 mg/kg iv. All these findings indicate that anesthetics, except enflurane, suppress nociceptive neural mechanisms in the spinal cord and that their actions are not exerted through the opioid receptor-endorphin system.

The ventilation management during the reconstruction of the tracheo-bronchial tree in adults

The most important point of anesthetic management during the reconstruction of the tracheo-bronchial tree (TBT) is to secure the airway and to maintain adequate ventilation. We experienced 17 cases of reconstruction of the TBT. Various methods of ventilation were achieved; one-lung ventilation, right middle and lower lobes ventilation, and combinations of these. We used double-lumen tubes, single-lumen tubes with or without blocker, spiral tubes, and intravenous catheters. We selected an appropriate ventilation method suitable for the diverse operative modes and achieved satisfactory managements during operation.

Cyclic alteration in the anticonvulsant effect of nitrous oxide in rats.

The anticonvulsant action of nitrous oxide and its time course were studied in rats. Bicuculline, a GABA-receptor antagonist, was administered intravenously at a rate of 0.2 mg·kg−1·min−1 during exposure to air (n=60) or 75% nitrous oxide in oxygen (n=80). The convulsant dose of bicuculline was determined. The rats were divided into subgroups according to the duration of exposure to air or nitrous oxide, from 0 to 120 min at 15 min intervals. Although the convulsant dose of bicuculline was consistent in the air group (1.03±0.06 mg·kg−1, mean ± SEM), it showed two peaks at 30- and 90 min exposures to nitrous oxide. The threshold dose in the nitrous oxide group was significantly higher than in the air group at only 15- and 30 min exposures (1.50±0.16, 2.15±0.25 mg·kg−1, respectively,P<0.05). We conclude that nitrous oxide has an anticonvulsant action against bicuculline-induced seizure, and that a cyclic nature exists in its action.