ADVANCED NEUROMONITORING, AND BIOCHEMICAL MARKERS IN ADULT PATIENTS WITH ANEURY

成年动脉瘤患者的高级神经监测和生化标记物

• 批准号: 7605460
• 负责人: stephen john lewis
• 金额: $ 0.21万
• 依托单位: UNIVERSITY OF FLORIDA
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-12-23 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7605460
• 关键词: Adult; Angiography; Antioxidants; Archives; Arteriographies; Biochemical Markers; Biological Markers; Brain; Brain Injuries; Calpain; Case Fatality Rates; Caspase; Cerebral perfusion pressure; Cerebrum; Computer Retrieval of Information on Scientific Projects Database; Core-Binding Factor; Electroencephalography; Event; Functional disorder; Funding; Future; Grant; Hemorrhage; Hospitals; Hypoxia; Individual; Institution; Intracranial Pressure; Intracranial Subarachnoid Hemorrhages; Isoprostanes; Measures; Molecular Weight; Monitor; Morbidity - disease rate; Neurologic; Outcome; Oxidative Stress; Patients; Physiological; Play; Proteins; Range; Research; Research Personnel; Resources; Role; Sampling; Somatosensory Evoked Potentials; Source; Spectrin; Standards of Weights and Measures; Subarachnoid Hemorrhage; Temperature; Time; Ultrasonography; United States National Institutes of Health; Vasospasm; caspase-3; cerebral hypoperfusion; extracellular; m-calpain; mortality; novel; numb protein; trend; vasoconstriction

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.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 蛛网膜下腔出血 (SAH) 是一种毁灭性事件，其病死率在 32% 至 67% 之间，后果严重。 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）引起的迟发性缺血性神经功能缺损导致出血后的发病率和死亡率显着升高。 以下是具体目标。 目标 1.1 证明术中连续 CBF 和 BtPO2 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。 目标 2.1 与标准间歇经颅超声检查、CT 血管造影和/或脑动脉造影相比，评估连续床旁生理趋势监测 CBF 和 BtPO2，以检测 SAH 后血管痉挛的发作。 目标 3.1 测量代表 SAH 后已知发生的一系列重要病理机制的蛋白质数量浓度随时间的变化。 此类蛋白质包括：caspase-3、u-钙蛋白酶、m-钙蛋白酶和caspase-03以及钙蛋白酶特异性αII-血影蛋白分解产物。 目标 3.2 检查 SAH 后氧化应激相关标志物浓度随时间的变化。 这些标志物包括：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异前列烷。 目标 3.3 检查以前未鉴定为在 SAH 病理生理学中发挥相关作用的新蛋白质。 将建立一组档案样本以供将来分析。 目标 3.4 检查 SAH 后脑损伤生物标志物与颅内压、脑灌注压、CBF、BtPO2、脑温度以及已知会恶化 SAH 后结局的全身继发事件之间的相关性。