Adachi Naoto
Medical Division, Mabuchi Clinic, Kyoto 600-8357.
Masui. 2006 May;55(5):542-51.
Many investigators have attempted to protect the brain against ischemia by reducing the cerebral metabolic rate using anesthetic agents. However, the magnitude of suppression of the cerebral metabolic rate does not correlate with neuroprotective effects of anesthetics, suggesting that other factors besides reduction in the cerebral metabolic rate contribute to the protection. Facilitation of protein synthesis, GABAergic activity, and anti-oxidant action are likely factors responsible for beneficial effects of barbiturates and propofol. Although the brain is protected during anesthesia, anesthetics cannot provide effects sufficiently enough to recover damage caused by severe ischemia. Further, no desired outcome has been reported by treatments after ischemic events.
许多研究人员试图通过使用麻醉剂降低脑代谢率来保护大脑免受缺血损伤。然而，脑代谢率的抑制程度与麻醉剂的神经保护作用并不相关，这表明除了脑代谢率降低之外，其他因素也有助于发挥保护作用。促进蛋白质合成、GABA能活性和抗氧化作用可能是巴比妥类药物和丙泊酚产生有益作用的因素。虽然在麻醉期间大脑受到保护，但麻醉剂无法提供足够的效果来恢复严重缺血造成的损伤。此外，缺血事件后的治疗尚未报告有理想的结果。
