Biochemical analysis of the cerebrospinal fluid: evidence for catastrophic energy failure and oxidative damage preceding brain death in severe head injury: a case report
Biochemical analysis of the cerebrospinal fluid: evidence for catastrophic energy failure and oxidative damage preceding brain death in severe head injury: a case report
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DOI：
10.1016/j.clinbiochem.2004.09.013
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发表时间：
2005-01-01
影响因子：
2.8
通讯作者：
Lazzarino, G
中科院分区：
文献类型：
--
作者：
Cristofori, L;Tavazzi, B;Lazzarino, G
目的：比较1例致死性重型颅脑损伤（TBI）伴继发性损伤的生化指标和临床指标。设计和方法：对1例TBI患者置管进行颅内压（ICP）监测和脑脊液（CSF）抗坏血酸、丙二醛、氧嘌呤和核苷分析。结果：颅内压低于20 mm Hg时，氧化性脑损伤先于脑脊液ATP分解代谢物增加，持续氧化应激引起不可逆的能量状态紊乱，随后出现难愈性颅内压升高。脑死亡前36小时记录大量氧嘌呤和核苷释放。结论：通过脑脊液生化分析和预先修改临床参数，讨论了严重TBI伴继发性损伤的分子事件。(C) 2004加拿大临床化学学会。版权所有。
Objectives: To compare biochemical and clinical parameters in a case of fatal severe traumatic brain injury (TBI) with secondary insult.Design and methods: A TBI patient was catheterized for intracranial pressure (ICP) monitoring and cerebrospinal fluid (CSF) analysis of ascorbate, malondialdehyde, oxypurines, and nucleosides.Results: Oxidative brain damage preceded ATP catabolite increment in the CSF even with ICP below 20 mm Hg. Sustained oxidative stress caused irreversible energy state derangement followed by a refractory ICP rise. Massive oxypurine and nucleoside release was recorded 36 h before brain death.Conclusions: Molecular events, detected by biochemical CSF analysis and preceding modification of clinical parameters in severe TBI with secondary insult, are discussed. (C) 2004 The Canadian Society of Clinical Chemists. All rights reserved.