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Serum S-100B protein and neuron-specific enolase after traumatic acute subdural hematoma in the rat

大鼠创伤性急性硬膜下血肿后血清S-100B蛋白和神经元特异性烯醇化酶的测定

基本信息

批准号：
18591612
负责人：
SATOSHI Sawauchi
金额：
$ 1.39万
依托单位：
Jikei University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2006
资助国家：
日本
起止时间：
2006 至 2007
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18591612/
关键词：
Traumatic Brain Iniury Acute Subdural Hematoma S-100 protein Neuron Snecifie Ennlase Brain Swelling

项目摘要

The high mortality of acute subdural hematoma (SDH) is largely explained by its frequent association with primary brain damage consisting of contusion and brain swelling. However, the nature and causes of brain swelling after traumatic brain injury are multifactorial and poorly understood. S-100B proteins and neuron specific enolase (NSE) are considered to be neurobiochemical markers for the brain damage. Serum concentration and kinetics of S-100B protein and NSE provide the assessment of the primary brain damage after acute SDH. In the present study, we examined serum concentration and kinetics of S-100B protein and NSE on the physiological consequence and brain edema formation in the experimental animal model of SDH alone, SDH associated with diffuse brain injury (DBI), and SDH + DBI + hypoxemia. Serum S-100B protein and NSE were significantly correlated with injury severity. The significant correlation was found between the initial S-100B and NSE. In the group of SDH + DBI + hypoxia, the serum value of S-100B protein and NSE was significantly higher compared with SDH alone and SDH + DBI. Secondary increase of serum markers was associated with the presence of secondary insult such as hypoxia or hypotension. Given our findings, it is possible that the poor outcome of acute SDH depends not only on the characteristics of the hematoma itself, but also on the presence of additional cerebral parenchymal injury and secondary insult. Thus, it is possible that the brain swelling associated with acute SDH is mainly caused by cytotoxic brain edema aggravated by an additional secondary insult. In the future, S100B and NSE measurements might reliably predict secondary brain injury and also be used to monitor the efficacy of treatments.

急性硬膜下血肿(SDH)的高死亡率在很大程度上是由于它经常与包括挫伤和脑肿胀在内的原发脑损伤有关。然而，创伤性脑损伤后脑肿胀的性质和原因是多因素的，且知之甚少。S-100B蛋白和神经元特异性烯醇化酶被认为是脑损伤的神经生化标志物。血清S-100B蛋白和神经元特异性烯醇化酶的浓度和动态变化可作为评估急性SDH后原发性脑损伤的指标。在本研究中，我们在单纯SDH、SDH合并弥漫性脑损伤和SDH+DBI+低氧血症的实验动物模型上，检测了S-100B蛋白和NSE的血清浓度和动态变化对脑水肿形成和生理后果的影响。血清S-100B蛋白和神经元特异性烯醇化酶水平与创伤严重程度显著相关。初始S-100B与NSE呈显著正相关。SDH+DBI+缺氧组血清S-100B蛋白和NSE水平显著高于SDH单独组和SDH+DBI组。血清标志物的继发性升高与继发性损害的存在有关，如缺氧或低血压。根据我们的发现，急性SDH的不良预后可能不仅取决于血肿本身的特点，还取决于是否存在额外的脑实质损伤和继发性损害。因此，与急性SDH相关的脑肿胀可能主要是由细胞毒性脑水肿引起的，并因额外的二次损伤而加重。在未来，S100B和NSE测量可能可靠地预测继发性脑损伤，并用于监测治疗的疗效。