ADVANCED NEUROMONITORING, AND BIOCHEMICAL MARKERS IN ADULT PATIENTS WITH ANEURY

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。蛛网膜下腔出血（SAH）是一种具有严重后果的毁灭性事件，病死率在32%至67%之间。大约10-15%的SAH患者在到达医院之前死亡。血管痉挛（脑动脉血管收缩）引起的再出血和迟发性缺血性神经功能缺损在出血后的发病率和死亡率中占有重要地位。以下是具体目标。目的1.1：证明术中连续CBF和BtPO2监测可以在躯体感觉诱发电位（SSEP）和脑电图监测出现明显变化之前检测到脑灌注不足和缺氧。目的2.1：与标准的间歇性经颅超声、CT血管造影和/或脑动脉造影相比，评估连续床边生理趋势监测CBF和BtPO2以检测SAH后血管痉挛的发作。目的3.1：测量代表已知SAH后发生的重要病理机制谱的蛋白质数量随时间的浓度变化。这些蛋白包括：caspase-3、u-calpain、m-calpain和caspase-03以及calpain特异性的ai -spectrin分解产物。目的3.2：检查SAH后氧化应激相关标志物浓度随时间的变化。这些标记包括：总低分子量抗氧化剂的细胞外浓度，单个主要抗氧化剂，F-2异前列腺素。目的3.3：研究以前未发现的在SAH病理生理中起相关作用的新蛋白。将建立一组存档样本以供将来分析。目的3.4：检查SAH后脑损伤的生物标志物与颅内压、脑灌注压、CBF、BtPO2、脑温度和已知会加重SAH后预后的系统性继发性事件的存在之间的相关性。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Subarachnoid hemorrhage (SAH) is a devastating event with grave consequences reflected by case fatality rates which range between 32 and 67%. Approximately 10-15% of patients who suffer SAH die before reaching the hospital. Rehemorrhage and delayed ischemic neurological deficit from vasospasm (vasoconstriction of the cerebral arterial vasculature) contribute significant morbidity and mortality in the post-hemorrhage period. Below are the Specific Aims. Aim 1.1: Demonstrate that intraoperative continuous CBF and BtPO2 monitoring detects cerebral hypoperfusion and hypoxia prior to the onset of demonstrable changes in Somatosensory Evoked Potentials (SSEP) and EEG monitoring. Aim 2.1: Evaluate continuous bedside physiological trend monitoring CBF and BtPO2 to detect onset of vasospasm after SAH as compared to standard intermittent transcranial ultrasonography, CT angiography and/or cerebral arteriography. Aim 3.1: Measure change in concentration over time of number of proteins representing a spectrum of important pathological mechanisms known to occur after SAH. Such proteins include: caspase-3, u-calpain, m-calpain and caspase-03 and calpain specific aII-spectrin breakdown products. Aim 3.2: Examine change in concentration over time of relevant markers of oxidative stress after SAH. Such markers include: extracellular concentrations of total low molecular weight antioxidants, individual major antioxidants, F-2 isoprostanes. Aim 3.3: Examine novel proteins previously not identified as playing a relevant role in pathophysiology of SAH. A set of archive samples will be established for future analysis. Aim 3.4: Examine correlation between biomarkers of brain damage after SAH and intracranial pressure, cerebral perfusion pressure, CBF, BtPO2, brain temperature and presence of systemic secondary events known to worsen outcome after SAH.