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脑微透析测量的细胞外谷氨酸在严重创伤性脑损伤中的作用。

Role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury.

机构信息

Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

J Neurosurg. 2010 Sep;113(3):564-70. doi: 10.3171/2009.12.JNS09689.

Abstract

OBJECT

Authors of several studies have implied a key role of glutamate, an excitatory amino acid, in the pathophysiology of traumatic brain injury (TBI). However, the place of glutamate measurement in clinical practice and its impact on the management of TBI has yet to be elucidated. The authors' objective in the present study was to evaluate glutamate levels in TBI, analyzing the factors affecting them and determining their prognostic value.

METHODS

A prospective study of patients with severe TBI was conducted with an inclusion criterion of a Glasgow Coma Scale score < or = 8 within 48 hours of injury. Invasive monitoring included intracranial pressure measurements, brain tissue PO(2), jugular venous O(2) saturation, and cerebral microdialysis. Patients received standard care including mass evacuation when indicated and treatment of elevated intracranial pressure values. Demographic data, CT findings, and outcome at 6 months of follow-up were recorded.

RESULTS

One hundred sixty-five patients were included in the study. Initially high glutamate values were predictive of a poor outcome. The mortality rate was 30.3% among patients with glutamate levels > 20 micromol/L, compared with 18% among those with levels < or = 20 micromol/L. Two general patterns were recognized: Pattern 1, glutamate levels tended to normalize over the monitoring period (120 hours); and Pattern 2, glutamate levels tended to increase with time or remain abnormally elevated. Patients showing Pattern 1 had a lower mortality rate (17.1 vs 39.6%) and a better 6-month functional outcome among survivors (41.2 vs 20.7%).

CONCLUSIONS

Glutamate levels measured by microdialysis appear to have an important role in TBI. Data in this study suggest that glutamate levels are correlated with the mortality rate and 6-month functional outcome.

摘要

目的

几项研究的作者暗示谷氨酸(一种兴奋性氨基酸)在创伤性脑损伤(TBI)的病理生理学中起关键作用。然而,谷氨酸测量在临床实践中的地位及其对 TBI 管理的影响尚未阐明。作者在本研究中的目的是评估 TBI 中的谷氨酸水平,分析影响谷氨酸水平的因素,并确定其预后价值。

方法

对严重 TBI 患者进行前瞻性研究,纳入标准为伤后 48 小时内格拉斯哥昏迷量表评分<或=8。有创监测包括颅内压测量、脑组织 PO 2 、颈静脉 O 2 饱和度和脑微透析。患者接受标准治疗,包括有指征时进行脑减压和治疗颅内压升高。记录人口统计学数据、CT 发现和 6 个月随访时的结果。

结果

165 例患者纳入研究。最初高谷氨酸值预测预后不良。谷氨酸水平>20μmol/L 的患者死亡率为 30.3%,而谷氨酸水平<或=20μmol/L 的患者死亡率为 18%。发现两种常见模式:模式 1,谷氨酸水平在监测期间趋于正常(120 小时);模式 2,谷氨酸水平随时间增加或持续异常升高。表现为模式 1 的患者死亡率较低(17.1%对 39.6%),幸存者 6 个月功能结局较好(41.2%对 20.7%)。

结论

微透析测量的谷氨酸水平在 TBI 中似乎具有重要作用。本研究数据表明,谷氨酸水平与死亡率和 6 个月功能结局相关。

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本文引用的文献

1
Dendritic and mitochondrial changes during glutamate excitotoxicity.
Neuropharmacology. 2007 Dec;53(8):891-8. doi: 10.1016/j.neuropharm.2007.10.003. Epub 2007 Oct 14.
2
Excitatory amino acid inhibitors for traumatic brain injury.
Cochrane Database Syst Rev. 2004;2003(1):CD003986. doi: 10.1002/14651858.CD003986.pub2.
3
Intracerebral microdialysis in clinical practice: baseline values for chemical markers during wakefulness, anesthesia, and neurosurgery.
Neurosurgery. 2000 Sep;47(3):701-9; discussion 709-10. doi: 10.1097/00006123-200009000-00035.
4
Neuroprotective therapy.
Semin Neurol. 1998;18(4):485-92. doi: 10.1055/s-2008-1040901.
5
Novel pharmacologic strategies in the treatment of experimental traumatic brain injury: 1998.
J Neurotrauma. 1998 Oct;15(10):731-69. doi: 10.1089/neu.1998.15.731.
6
Factors affecting excitatory amino acid release following severe human head injury.
J Neurosurg. 1998 Oct;89(4):507-18. doi: 10.3171/jns.1998.89.4.0507.
8
Exciting your neurons to death: can we prevent cell loss after brain injury?
Pediatr Neurosurg. 1994;21(2):117-22; discussion 123. doi: 10.1159/000120825.
9
Clinical experience with excitatory amino acid antagonist drugs.
Stroke. 1995 Mar;26(3):503-13. doi: 10.1161/01.str.26.3.503.

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