Mechanisms of Anesthetic Emergence: Evidence for Active Reanimation

Abstract

Historically, emergence from anesthesia was believed to progress only through the passive elimination of pharmacologic agents from the brain. However, recent studies indicate that anesthetic emergence may not simply be a process mirroring the induction of anesthesia. Several substances reduce the duration of anesthesia but not its induction time. Their action is not the result of a passive process, because they actively affect the kinetics of neurotransmitters or the endogenous sleep circuit to shorten anesthesia. The latest notable substance among this group of agents is methylphenidate, an inhibitor of dopamine and norepinephrine transporters. Studies on emergence from anesthesia aim not only to stimulate scientific interest but also to improve the clinical course following general anesthesia, when patients sometimes experience life-threatening complications such as myocardial infarction, bronchial asthma, and cerebral hemorrhage. This review discusses recent advances in this field, focusing mainly on the role of neurotransmitters and neuromodulators in anesthetic emergence.