Alkire M T, Haier R J, Fallon J H
Department of Anesthesiology, University of California at Irvine, Irvine, California 92697, USA.
Conscious Cogn. 2000 Sep;9(3):370-86. doi: 10.1006/ccog.1999.0423.
A unifying theory of general anesthetic-induced unconsciousness must explain the common mechanism through which various anesthetic agents produce unconsciousness. Functional-brain-imaging data obtained from 11 volunteers during general anesthesia showed specific suppression of regional thalamic and midbrain reticular formation activity across two different commonly used volatile agents. These findings are discussed in relation to findings from sleep neurophysiology and the implications of this work for consciousness research. It is hypothesized that the essential common neurophysiologic mechanism underlying anesthetic-induced unconsciousness is, as with sleep-induced unconsciousness, a hyperpolarization block of thalamocortical neurons. A model of anesthetic-induced unconsciousness is introduced to explain how the plethora of effects anesthetics have on cellular functioning ultimately all converge on a single neuroanatomic/neurophysiologic system, thus providing for a unitary physiologic theory of narcosis related to consciousness.
一个关于全身麻醉导致意识丧失的统一理论必须解释各种麻醉剂产生意识丧失的共同机制。在全身麻醉期间从11名志愿者获得的功能性脑成像数据显示,在两种不同的常用挥发性麻醉剂作用下,丘脑和中脑网状结构区域的活动受到特异性抑制。结合睡眠神经生理学的研究结果对这些发现进行了讨论,并探讨了这项工作对意识研究的意义。据推测,与睡眠导致意识丧失一样,麻醉导致意识丧失的基本共同神经生理机制是丘脑皮质神经元的超极化阻滞。本文介绍了一个麻醉导致意识丧失的模型,以解释麻醉剂对细胞功能的众多影响最终如何都汇聚于单一的神经解剖学/神经生理系统,从而为与意识相关的麻醉提供一个统一的生理学理论。