Matchett Gerald A, Allard Martin W, Martin Robert D, Zhang John H
Department of Anesthesiology, School of Medicine, Loma Linda University, Loma Linda, CA 92350, USA.
Neurol Res. 2009 Mar;31(2):128-34. doi: 10.1179/174313209X393546.
Intra-operative cerebral ischemia can be catastrophic, and volatile anesthetic agents have been recognized for their potential neuroprotective properties since the 1960s. In this review, we examine the neuroprotective effects of five volatile anesthetic agents in current or recent clinical use: isoflurane, sevoflurane, desflurane, halothane and enflurane.
A review of publications in the National Library of Medicine and National Institutes of Health database from 1970 to 2007 was conducted.
Volatile anesthetic agents have been shown to be neuroprotective in multiple animal works of ischemic brain injury. Short-term neuroprotection (<1 week post-ischemia) in experimental cerebral ischemia has been reported in multiple works, although long-term neuroprotection (> or = 1 week post-ischemia) remains controversial. Comparison works have not demonstrated superiority of one specific volatile agent over another in experimental models of brain injury. Relatively few human works have examined the protective effects of volatile anesthetic agents and conclusive evidence of a neuroprotective effect has yet to emerge from human works.
Proposed mechanisms related to the neuroprotective effect of volatile anesthetic agents include activation of ATP-dependent potassium channels, up-regulation of nitric oxide synthase, reduction of excitotoxic stressors and cerebral metabolic rate, augmentation of peri-ischemic cerebral blood flow and up-regulation of antiapoptotic factors including MAP kinases.
术中脑缺血可能是灾难性的,自20世纪60年代以来,挥发性麻醉剂就因其潜在的神经保护特性而受到认可。在本综述中,我们研究了目前或近期临床使用的五种挥发性麻醉剂的神经保护作用:异氟烷、七氟烷、地氟烷、氟烷和恩氟烷。
对1970年至2007年美国国立医学图书馆和国立卫生研究院数据库中的出版物进行了综述。
挥发性麻醉剂已在多项缺血性脑损伤动物研究中显示出神经保护作用。多项研究报道了实验性脑缺血中的短期神经保护作用(缺血后<1周),尽管长期神经保护作用(缺血后≥1周)仍存在争议。比较研究尚未在脑损伤实验模型中证明一种特定挥发性麻醉剂优于另一种。相对较少的人体研究考察了挥发性麻醉剂的保护作用,人体研究尚未得出神经保护作用的确凿证据。
与挥发性麻醉剂神经保护作用相关的推测机制包括激活ATP依赖性钾通道、上调一氧化氮合酶、减少兴奋性毒性应激源和脑代谢率、增加缺血周围脑血流量以及上调包括丝裂原活化蛋白激酶在内的抗凋亡因子。