Jevtović-Todorović V, Kirby C O, Olney J W
Department of Anesthesiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
J Cereb Blood Flow Metab. 1997 Feb;17(2):168-74. doi: 10.1097/00004647-199702000-00006.
In acute brain injury syndromes, the potent N-methyl-D-aspartate (NMDA) antagonist, MK-801, can prevent neuronal degeneration, and the general anesthetics, isoflurane and propofol, may also provide neuroprotective benefits. An obstacle to the use of NMDA antagonists for neuroprotective purposes is that they can cause a neurotoxic vacuole reaction in cerebrocortical neurons. This study demonstrates the ability of isoflurane and propofol to prevent the neurotoxic vacuole reaction induced by MK-801. Low sedative doses of inhaled isoflurane (1%) or intravenous (i.v.) propofol (7.5 mg/kg/h) were as effective as higher general anesthetic doses. Thus, in the clinical management of acute brain injury conditions such as stroke and brain trauma, administration of one of these anesthetic agents together with an NMDA antagonist may be an excellent formula for obtaining optimal neuroprotection while eliminating serious side effects.
在急性脑损伤综合征中，强效的N-甲基-D-天冬氨酸（NMDA）拮抗剂MK-801可预防神经元变性，而全身麻醉药异氟烷和丙泊酚也可能具有神经保护作用。将NMDA拮抗剂用于神经保护目的的一个障碍是它们可在大脑皮质神经元中引起神经毒性空泡反应。本研究证明了异氟烷和丙泊酚预防MK-801诱导的神经毒性空泡反应的能力。低镇静剂量的吸入异氟烷（1%）或静脉注射丙泊酚（7.5毫克/千克/小时）与较高的全身麻醉剂量效果相同。因此，在中风和脑外伤等急性脑损伤疾病的临床管理中，将这些麻醉药之一与NMDA拮抗剂联合使用，可能是在消除严重副作用的同时获得最佳神经保护效果的理想方案。
