Núñez G, Urzúa J
Centro de Investigaciones Médicas, Facultad de Medicina, Pontificia Universidad Católica de Chile.
Rev Med Chil. 1998 Aug;126(8):993-1000.
General anesthesia is defined by reversible unconsciousness, lack of response to noxious stimuli, and amnesia, induced by chemical agents. Mechanisms underlying the anesthetic effect are not known. The most prevalent belief was that anesthetic drugs acted on the lipid cell membranes, based on the correlation between oil solubility and anesthetic potency. Later, it has been proposed that anesthetic agents act on specific proteins of the cellular membrane of neurons. Voltage-gated ionic channels are inhibited by anesthetic agents, being some subtypes more sensitive. Clinical concentration of anesthetic agents inhibit or stimulate excitatory or inhibitory neurotransmitter receptors, respectively. Specific receptor agonists and antagonists modify this effect. Intercellular channels (gap junctions) are also affected by anesthetic agents through direct interaction with some of their protein subunits. Thus, anesthesia would result from combined effects on specific proteins acting on neural cell excitability as well as transmission and propagation of nerve impulses.
全身麻醉的定义是由化学药物诱导产生的可逆性意识丧失、对有害刺激无反应和遗忘。麻醉作用的潜在机制尚不清楚。最普遍的观点是，基于油溶性与麻醉效能之间的相关性，麻醉药物作用于脂质细胞膜。后来，有人提出麻醉剂作用于神经元细胞膜的特定蛋白质。电压门控离子通道受到麻醉剂的抑制，某些亚型更为敏感。麻醉剂的临床浓度分别抑制或刺激兴奋性或抑制性神经递质受体。特异性受体激动剂和拮抗剂可改变这种效应。细胞间通道（缝隙连接）也会通过与某些蛋白质亚基的直接相互作用而受到麻醉剂的影响。因此，麻醉是对作用于神经细胞兴奋性以及神经冲动传递和传播的特定蛋白质产生综合作用的结果。
