Brazilian Journal of Anesthesiology
https://app.periodikos.com.br/journal/rba/article/doi/10.1590/S0034-70942002000100013
Brazilian Journal of Anesthesiology
Special Article

Mecanismo de ação dos anestésicos inalatórios

Action mechanism of inhalational anesthetics

Renato Ângelo Saraiva

http://dx.doi.org/10.1590/S0034-70942002000100013 Braz J Anesthesiol, vol.52, n1, p.114-123, 2002
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Resumo

JUSTIFICATIVA E OBJETIVOS: Estudos clínicos e experimentais têm sido desenvolvidos para identificar os locais onde os anestésicos (inalatórios) atuam e para determinar quais as alterações funcionais que esses fármacos produzem nas estruturas do sistema nervoso central determinantes do estado de anestesia que é observado clinicamente. O objetivo deste trabalho é descrever os resultados obtidos por vários autores em estudos clínicos e experimentais realizados recentemente na tentativa de esclarecer os mecanismos de ação dos anestésicos inalatórios no sistema nervoso central. CONTEÚDO: Para facilitar a compreensão dos complexos mecanismos de ação dos anestésicos inalatórios no sistema nervoso central, eles foram divididos em três níveis: o macroscópico, o microscópico e o molecular. Recentemente um grupo de autores descreveram estes mecanismos de ação em: orgânicos, celulares, e inibidores da entropia. Estes mecanismos tentariam explicar o estado de anestesia que teria como característica a capacidade de prover ao paciente duas ações principais: 1) imobilidade, inibição da resposta a estímulos nociceptivos; e 2) amnésia. Outros efeitos (desejáveis) também são obtidos pela administração de anestésicos: analgesia e hipnose. Entretanto, tais efeitos seja isoladamente ou juntos, não definem o estado de anestesia. Embasados nestes conceitos, este grupo adota e divulga a classificação dos anestésicos em: 1) anestésicos completos, os que produzem imobilidade e amnésia; e 2) incompletos ou não imobilizantes, os que não produzem imobilidade mas produzem amnésia. CONCLUSÕES: De acordo com os resultados de vários estudos realizados recentemente, provavelmente a amnésia e a inconsciência ocorrem pela ação do anestésico predominantemente no cérebro, enquanto a imobilidade, ou seja, a inibição da resposta ao estímulo nociceptivo por movimento, seria pela ação do anestésico preferencialmente e inicialmente na medula espinhal. Estas ações ocorrem por inibição da transformação de energia (entropia) que forma os potenciais de ação nas células (fibras) nervosas, especialmente nas sinapses.

Palavras-chave

ANESTÉSICOS, Inalatórios

Abstract

BACKGROUND AND OBJECTIVES: Clinical and experimental studies have been developed to identify inhalational anesthetics action sites to determine clinically observed functional changes produced on central nervous system structures responsible for the anesthetic status. This study aimed at reviewing results obtained by several authors in recent clinical and experimental studies in an attempt to explain action mechanisms of inhalational anesthetics on the central nervous system. CONTENTS: To help understanding the complex action mechanisms of inhalational anesthetics on the central nervous system, these were divided in three levels: macroscopic, microscopic, and molecular. A group of authors have recently divided those action mechanisms in: organic, cellular, and entropy inhibitors. These mechanisms would try to explain the anesthetic status able to provide patients with two major reactions: 1) immobility in response to noxious stimuli and 2) amnesia. Other desirable effects, such as analgesia and hypnosis are also obtained by inhalational anesthesia, however such effects per se or in combination, do not define the anesthetic status. Based on those concepts, this group classifies inhalational anesthetics as: 1) complete anesthetics, or providing immobility and amnesia; and 2) incomplete anesthetics, or not providing immobility, but providing amnesia. CONCLUSIONS: According to several recent studies, it is possible that amnesia and unconsciousness are a consequence of the anesthetic action predominantly on the brain, while immobility, that is, inhibition of motor response to noxious stimuli, would be a consequence of the preferential and initial anesthetic action on the spinal cord. These actions occur by energy transformation inhibition (entropy) generating action potentials in nervous cells (fibers), particularly the synapses.

Keywords

ANESTHETICS, Inhalational

References

Halsey MJ. Mechanism of General Anesthesia. Anesthetic Uptake and Action. 1974:45-76.

Eger II EI, Koblin DD, Harris RA. Hypothesis: inhaled anesthetics produce immobility and amnesia by different mechanism at different sites. Anesth Analg. 1997;84:915-918.

Dutton RC, Rampil IJ, Eger II EI. Inhaled nonimmobilizers do not alter the middle latency auditory evoked response of rats. Anesth Analg. 2000;90:213-217.

Trudell JR, Koblin DD, Eger II EI. A molecular description of how the nobel gases and nitrogen bind to a model site of anesthetic action. Anesth Analg. 1998;87:411-418.

Eger II EI. What is general anesthetic action?. Anesth Analg. 1993;77:408-409.

Kissin I, Gelman S. Components of anaesthesia. Br J Anaesth. 1988;61:237-242.

Richards CD, Russel WJ, Samage JC. The action of ether and metoxyflurane on synaptic transmission in isolated preparation of the mammalian cortex. J Physiol. 1975;248:121-142.

Nicoll RA. The effect of anaesthetic on synaptic excitation and inhibition in the olfactory bulb. J Physiol. 1972;223:803-814.

MacIver MB, Roth SH. Inhalational anaesthetic exhibit pathway specific and differential actions on hippocampal synaptic response in vitro. Br J Anaesth. 1988;60:680-684.

Antognini JF, Schwartz K. Exaggerated anesthetic requirements in the preferentially anesthetized brain. Anesthesiology. 1993;79:1244-1249.

Rampil IJ, Mason P, Singh H. Anesthetic potency (MAC) as independent of forebrain structures in the rat. Anesthesiology. 1993;78:707-712.

Maurer AJ, Sessler DI, Eger II EI. The nonimmobilizer 1,2 - Diclorohexafluorcyclobutane (2 - n) does not affect thermoregulation in rat. Anesth Analg. 2000;91:1013-1016.

Kandolh KL, Clorkoff BS, Sonner JM. Non anesthetics can suppress learning. Anesth Analg. 1996;82:321-326.

Halsey MJ, Roberts MG, McPhie G. Halothane and perfluoro pentane actions on hippocampal CA1 neurons. Anesthesiology. 1993;79:A402.

Antognini JF, Carstens E, Sudo M. Isoflurane depreses electroencephalografic and medial thalamic responses to noxious stimulation via indirect spinal action. Anesth Analg. 2000;91:1282-1288.

Rampil IJ. Anesthetic potency is not altered after hypothermic spinal cordtransection in rats. Anesthesiology. 1994;80:606-610.

Sebel PS, Lang E, Rampil IJ. A multicenter study of bispectral electroencephalogram analysis for monitoring anesthetic effect. Anesth Analg. 1997;84:891-899.

Malha ME. Electrophysiologic monitoring of the brain and spinal cord. ASA Refresher Courses in Anesthesiology. 1991;19:87-99.

Saraiva RA. Monitorização Eletroneurofisiológica da Anestesia. Anestesia: Atualização e Reciclagem. 2000:31-37.

Tanelian DL, Kosek P, Mody I. The roler of GABA A receptor/chloride channel complex in Anesthesia. Anesthesiology. 1993;78:757-776.

Richards CD, White AN. The action of volatile anaesthetics on synaptic transmission in the dentate gyrus. J Physiology. 1972;252:241-246.

Franks NP, Lieb WR. Stereospecific effects of inhational general anesthetic optical isomers on nerve íon channels Science. 1991;254:427-430.

Pahorille A, Cieplak P, Wilson MA. Interactions of anesthetics with the membrane water interface. Chem Phys. 1996;204:337-345.

Guyton AC. Tratado de Fisiologia Médica. 1993:34-59.

Franks NP, Lieb WR. Molecular and cellular mechanisms of general anaesthesia. Nature. 1994;367:607-614.

Kending JJ, Kodde A, Gibbs LM. Correlates of anesthetic properties in isolated spinal cord cyclobutanes. Eur J Pharmacol. 1994;264:427-436.

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