Effects of the N-methyl-D-aspartate receptor blocker MK-801 on neurologic function after experimental brain injury.
Effects of the N-methyl-D-aspartate receptor blocker MK-801 on neurologic function after experimental brain injury.
复制标题
N-甲基-D-天冬氨酸受体阻滞剂 MK-801 对实验性脑损伤后神经功能的影响。
DOI：
10.1089/neu.1989.6.247
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发表时间：
1989
影响因子：
4.2
通讯作者：
Simon,R
中科院分区：
文献类型：
--
作者：
Mcintosh,TK;Vink,R;Soares,H;Hayes,R;Simon,R
兴奋性氨基酸（EAA）神经传递的药理学抑制可减轻全脑和局灶性缺血和低血糖模型中的细胞死亡，并改善实验性创伤性脊髓损伤后的神经学结局。本研究探讨了非竞争性N-甲基-D-天冬氨酸（NMDA）受体阻滞剂MK-801对实验性液压脑损伤（FP）后大鼠心血管和神经功能的影响。动物在FP脑损伤前15 min或FP脑损伤后15 min接受MK-801（1 mg/kg）或生理盐水（等体积）静脉推注。MK-801预处理显著改善了损伤后心血管变量，减轻了损伤后神经功能障碍。MK-801的损伤后治疗也显著改善了心血管变量，但对损伤后神经功能评分影响不大。这些结果表明，EAA神经递质可能参与创伤性脑损伤的病理生理学后遗症和NMDA受体的非竞争性阻断脑损伤前可能会减少EAA诱导的损伤和限制神经功能障碍。
Pharmacologic inhibition of excitatory amino acid (EAA) neurotransmission attenuates cell death in models of global and focal ischemia and hypoglycemia and improves neurologic outcome after experimental traumatic spinal cord injury. The present study examined the effects of the noncompetitiveN-methyl-d-aspartate (NMDA) receptor blocker MK-801 on cardiovascular and neurologic function after experimental fluid-percussion (FP) brain injury in the rat. Animals received either an intravenous bolus of MK-801 (1 mg/kg) or saline (equal volume) 15 min prior to FP brain injury or 15 min following FP brain injury. MK-801 pretreatment significantly improved postinjury cardiovascular variables and attenuated postinjury neurologic dysfunction. Postinjury treatment with MK-801 also significantly improved cardiovascular variables, but had little effect on postinjury neurologic scores. These results suggest that EAA neurotransmitters may be involved in the pathophysiological sequelae of traumatic brain injury and that noncompetitive blockade of the NMDA receptor prior to brain injury may reduce EAA-induced damage and limit neurologic dysfunction.