RESUMEN
The direct and indirect effects of nitrous oxide (N2O) on the nociceptive responses of lumbar dorsal horn neurons, and the indirect effects on midbrain reticular formation (MRF) neurons and thalamic neurons were determined in goats anaesthetized with isoflurane. The technique used enabled the differential delivery of N2O to either the torso or the cerebral circulation, thus allowing assessment of the direct spinal and indirect brain effects of N2O. Systemic delivery of N2O appeared to have divergent effects, facilitating (4/11) or depressing (7/11) the responses of dorsal horn neurons. Such divergent effects were also observed when N2O was differentially delivered to the circulation in the torso (i.e. the spinal cord). Likewise, MRF and thalamic responses to noxious stimulation were variably affected by administration of N2O to the torso, with some cells facilitated (7/13 MRF neurons, 3/8 thalamic neurons) and others depressed (6/13 MRF neurons, 5/8 thalamic neurons). It appears that N2O has variable effects on the caprine CNS. The facilitatory action of N2O might partially explain why it is a relatively weak anaesthetic.
Asunto(s)
Anestésicos por Inhalación/farmacología , Sistema Nervioso Central/efectos de los fármacos , Cabras/fisiología , Neuronas/efectos de los fármacos , Óxido Nitroso/farmacología , Animales , Sistema Nervioso Central/citología , Sistema Nervioso Central/fisiología , Depresión Química , Electroencefalografía/veterinaria , Isoflurano/farmacología , Formación Reticular/citología , Formación Reticular/efectos de los fármacos , Formación Reticular/fisiología , Médula Espinal/citología , Médula Espinal/efectos de los fármacos , Médula Espinal/fisiología , Tálamo/citología , Tálamo/efectos de los fármacos , Tálamo/fisiologíaRESUMEN
UNLABELLED: Anesthetics such as isoflurane act in the spinal cord to suppress movement in response to noxious stimulation. Spinal anesthesia decreases hypnotic/sedative requirements, possibly by decreasing afferent transmission of stimuli. We hypothesized that isoflurane action in the spinal cord would similarly depress the ascending transmission of noxious input to the thalamus and cerebral cortex. In six isoflurane-anesthetized goats, we measured electroencephalographic (EEG) and thalamic single-unit responses to a clamp applied to the forelimb. Cranial bypass permitted differential isoflurane delivery to the torso and cranial circulations. When the cranial-torso isoflurane combination was 1.3% +/- 0.2%-1.0% +/- 0.4% the noxious stimulus did not evoke significant changes in the EEG or thalamic activity: 389 (153-544) to 581 (172-726) impulses/min, (median, 25th-75th percentile range, P: > 0.05). When the cranial-torso isoflurane combination was 1.3% +/- 0.2%-0.3% +/- 0.2%, noxious stimulation increased thalamic activity: 804 (366-1162) to 1124 (766-1865) impulses/min (P: < 0.05), and the EEG "desynchronized": total EEG power decreased from 25 +/- 20 microV(2) to 12 +/- 8 microV(2) (P: < 0.05). When the cranial-torso isoflurane was 1.7% +/- 0.1%-0.3% +/- 0.2%, the noxious stimulus did not significantly affect thalamic: 576 (187-738) to 1031 (340-1442) impulses/min (P: > 0.05), or EEG activity. The indirect torso effect of isoflurane on evoked EEG total power (12.6 +/- 2.7 microV(2)/vol%, mean +/- SE) was quantitatively similar to the direct cranial effect (17.7 +/- 3.0 microV(2)/vol%; P: > 0.05). These data suggest that isoflurane acts in the spinal cord to blunt the transmission of noxious inputs to the thalamus and cerebral cortex, and thus might indirectly contribute to anesthetic endpoints such as amnesia and unconsciousness. IMPLICATIONS: Isoflurane action in the spinal cord diminished the transmission of noxious input to the brain. Because memory and consciousness are likely dependent on the "arousal" state of the brain, this indirect action of isoflurane could contribute to anesthetic-induced amnesia and unconsciousness.
Asunto(s)
Anestésicos por Inhalación/farmacología , Electroencefalografía/efectos de los fármacos , Isoflurano/farmacología , Vías Nerviosas/efectos de los fármacos , Dolor/fisiopatología , Médula Espinal/efectos de los fármacos , Tálamo/fisiología , Animales , Depresión Química , Potenciales Evocados/efectos de los fármacos , Femenino , Miembro Anterior/inervación , Cabras , Masculino , Médula Espinal/fisiología , Transmisión Sináptica/efectos de los fármacos , Tálamo/efectos de los fármacosRESUMEN
BACKGROUND: Isoflurane depresses the electroencephalographic (EEG) activity and exerts part of its anesthetic effect in the spinal cord. The authors hypothesized that isoflurane would indirectly depress the EEG and subcortical response to noxious stimulation in part by a spinal cord action. METHODS: Depth electrodes were inserted into the midbrain reticular formation (MRF) and thalamus of six of seven isoflurane-anesthetized goats, and needle-electrodes were placed into the skull periosteum. In five of seven goats, an MRF microelectrode recorded single-unit activity. The jugular veins and carotid arteries were isolated to permit cranial bypass and differential isoflurane delivery. A noxious mechanical stimulus (1 min) was applied to a forelimb dewclaw at each of two cranial-torso isoflurane combinations: 1.1+/-0.3%-1.2+/-0.3% and 1.1+/-0.3-0.3+/-0.1% (mean +/- SD). RESULTS: When cranial-torso isoflurane was 1.1-1.2%, the noxious stimulus did not alter the EEG. When torso isoflurane was decreased to 0.3%, the noxious stimulus activated the MRF, thalamic, and bifrontal-hemispheric regions (decreased high-amplitude, low-frequency power). For all channels combined, total (-33+/-15%), delta(-51+/-22%), theta (-33+/-19%), and alpha (-26+/-16%) power decreased after the noxious stimulus (P<0.05); beta power was unchanged. The MRF unit responses to the noxious stimulus were significantly higher when the spinal cord isoflurane concentration was 0.3% (1,286+/-1,317 impulses/min) as compared with 1.2% (489+/-437 impulses/min, P<0.05). CONCLUSIONS: Isoflurane blunted the EEG and MRF-thalamic response to noxious stimulation in part via an action in the spinal cord.
Asunto(s)
Anestésicos por Inhalación/farmacología , Electroencefalografía/efectos de los fármacos , Isoflurano/farmacología , Dolor/fisiopatología , Formación Reticular/efectos de los fármacos , Médula Espinal/efectos de los fármacos , Médula Espinal/fisiología , Tálamo/efectos de los fármacos , Animales , Análisis de los Gases de la Sangre , Glucemia/metabolismo , Estimulación Eléctrica , Electrodos Implantados , Cabras , Hematócrito , Microelectrodos , Estimulación Física , Técnicas EstereotáxicasRESUMEN
BACKGROUND: Anesthetics, including isoflurane, depress the electroencephalogram (EEG). Little is known about the quantitative effects of isoflurane on EEG and subcortical electrical activity responses to noxious stimulation. The authors hypothesized that isoflurane would depress the results of EEG and subcortical response to noxious stimulation at concentrations less than those needed to suppress movement. Furthermore, determination of regional differences might aid in elucidation of sites of anesthetic action. METHODS: Ten goats were anesthetized with isoflurane, and minimum alveolar concentration (MAC) was determined using a noxious mechanical stimulus. Depth electrodes were inserted into the midbrain reticular formation and thalamus. Needle electrodes placed in the skull periosteum measured bifrontal and bihemispheric EEG. The noxious stimulus was applied at each of four anesthetic concentrations: 0.6, 0.9, 1.1, and 1.4 MAC. RESULTS: At an isoflurane concentration of 0.6 MAC, the noxious stimulus activated the midbrain reticular formation, thalamic, and bifrontal-hemispheric regions, as shown by decreased high-amplitude, low-frequency power. For all channels combined (mean +/- SD), total (-33+/-7%), delta (-47+/-12%), theta (-23+/-12%), and alpha (-21+/-6%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 0.9 MAC, total (-35+/-5%), delta (-42+/-7%), theta (-35+/-8%), and alpha (-23+/-11%) power decreased after the noxious stimulus (P < 0.001); beta power was unchanged. At 1.1 MAC only one site, and at 1.4 MAC, no site, had decreased power after the noxious stimulus. CONCLUSIONS: Isoflurane blunted EEG and midbrain reticular formation-thalamus activation response to noxious stimulation at concentrations (1.1 MAC or greater) necessary to prevent movement that occurred after noxious stimulation. It is unknown whether this is a direct effect or an indirect effect via action in the spinal cord.
Asunto(s)
Anestesia por Inhalación , Anestésicos por Inhalación/farmacología , Electroencefalografía/efectos de los fármacos , Isoflurano/farmacología , Formación Reticular/efectos de los fármacos , Tálamo/efectos de los fármacos , Anestésicos por Inhalación/farmacocinética , Animales , Corteza Cerebral/efectos de los fármacos , Sincronización Cortical/efectos de los fármacos , Femenino , Cabras , Isoflurano/farmacocinética , Movimiento/efectos de los fármacos , Dolor/fisiopatología , Estimulación Física , Alveolos Pulmonares/metabolismo , Formación Reticular/fisiología , Tálamo/fisiologíaRESUMEN
Operative charts were reviewed in 86 patients with Charcot-Marie-Tooth disease, a condition characterized by chronic muscular denervation. A total of 161 surgical procedures was performed. Major complications were few, and only one operative death occurred, unrelated to anaesthesia. Succinylcholine and malignant hyperthermia triggering agents were used in 41 (48%) and 77 (90%) patients, respectively, without untoward effects. Contrary to previous reports, this survey supports the safe use of succinylcholine and MH triggering agents in this disease.