ADVANCED NEUROMONITORING, AND BIOCHEMICAL MARKERS IN ADULT PATIENTS WITH ANEURY

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，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破坏性事件，其病死率在32%至67%之间。 大约10- 15%的SAH患者在到达医院之前死亡。 再出血和迟发性缺血性神经功能缺损的血管痉挛（脑动脉血管系统的血管收缩）造成显着的发病率和死亡率在出血后时期。 下面是具体目标。 目的1.1证明术中连续CBF和BtPO 2监测可在体感诱发电位（SSEP）和EEG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评价连续床旁生理趋势监测CBF和BtPO 2与标准间歇性经颅超声、CT血管造影和/或脑动脉造影相比检测SAH后血管痉挛发作的效果。 目的3.1测量多种蛋白质的浓度随时间的变化，这些蛋白质代表已知在SAH后发生的一系列重要病理机制。 这些蛋白质包括：caspase-3，u-钙蛋白酶，m-钙蛋白酶和caspase-03和钙蛋白酶特异性？II-血影蛋白分解产物。 目的3.2检测SAH后氧化应激相关标志物浓度随时间的变化。 这些标志物包括：细胞外浓度的总低分子量抗氧化剂，个别的主要抗氧化剂，F-2异前列腺素。 目的3.3检测以前未被鉴定为在SAH的病理生理学中发挥相关作用的新蛋白质。 将建立一组存档样本，用于未来分析。 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、BtPO 2、脑温度和已知会使SAH后结局恶化的全身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 percent 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 ?II-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.