The Role of Orexinergic Neuron on Intravenous Anesthesia

摘要

Effect of orexin (OX), an endogenous wake-promoting substance, on anesthesia was studied in vivo and in vitro. In vivo, we found OX decreased barbiturates and ketamine anesthesia time in rats. OXA receptor is responsible for the OX effect. Others reported OX decreased propofol, sevoflurane, and isoflurane anesthesia time. OX did not affect any induction time of these anesthetics. In vitro, we found barbiturates, ketamine, and benzodiazepines attenuated OX-induced noradrenaline release from the rat cerebral cortex. GABAergic neuron would not be involved in this interaction. Plasma OXA and norepinephrine levels were significantly increased after emergence from total intravenous anesthesia (propofol and fentanyl) and inhaled anesthesia (sevoflurane and fentanyl) in human.