ADVANCED NEUROMONITORING, AND BIOCHEMICAL MARKERS IN ADULT PATIENTS WITH ANEURY

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 蛛网膜下腔出血(SAH)是一种破坏性事件，其严重后果反映在病死率为32%至67%之间。大约10%-15%的SAH患者在到达医院之前死亡。再出血和血管痉挛(脑动脉血管收缩)造成的迟发性缺血性神经功能障碍在出血后时期会导致显著的发病率和死亡率。以下是具体目标。 目的1.1说明术中连续监测CBF和BtPO2可在体感诱发电位(SSEP)和脑电监测出现明显变化之前发现脑低灌注和缺氧。 目的2.1与标准间歇性经颅超声、CT血管造影和/或脑动脉造影术比较，评价连续床边监测CBF和BtPO2以判断蛛网膜下腔出血后血管痉挛的发生。 目的3.1测量蛛网膜下腔出血后代表一系列重要病理机制的蛋白质的浓度随时间的变化。这些蛋白质包括：caspase-3、u-calain、m-calain和caspase-03以及calain特异性的？II-血影蛋白分解产物。 目的3.2检测蛛网膜下腔出血(SAH)后氧化应激相关标志物浓度随时间的变化。这些标记物包括：细胞外总低分子抗氧化剂浓度、个别主要抗氧化剂、F-2异前列腺素。 目的3.3研究在蛛网膜下腔出血(SAH)的病理生理学中尚未发现的新蛋白。将建立一套档案样本，以供将来分析。 目的3.4探讨蛛网膜下腔出血后脑损伤的生物标志物与颅内压、脑灌注压、脑血流量、血氧饱和度、脑温、全身继发事件的相关性。

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.