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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 亚蛛网膜下腔出血（SAH）是一个毁灭性的事件，严重的后果反映出病例死亡率在32％至67％之间。 在到达医院之前，大约10-15％的患者死亡。 血管痉挛（大脑动脉血管的血管收缩）的重新出血和延迟的缺血性神经缺陷延迟，在洪流后时期造成了显着的发病率和死亡率。 以下是具体目标。 AIM 1.1证明，术中连续CBF和BTPO2监测在发作前显示体感觉诱发潜力（SSEP）和EEG监测之前，检测脑部灌注不足和缺氧。 AIM 2.1评估与标准的间歇性经颅超声检查，CT血管造影和/或脑动脉造影相比，与标准的SAH相比，评估CBF和BTPO2的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。 AIM 3.1测量浓度随着代表SAH后已知发生的一系列重要病理机制的蛋白质数量的变化。 这样的蛋白质包括：caspase-3，U-钙蛋白酶，M-钙蛋白酶和caspase-03以及钙蛋白酶特异性？II-谱蛋白分解产物。 AIM 3.2检查SAH后相关氧化应激的相关标记的浓度变化。 这样的标记包括：总低分子量抗氧化剂，个别主要抗氧化剂，F-2异丙烷的细胞外浓度。 AIM 3.3检查以前未被认为在SAH的病理生理学中起着相关作用的新型蛋白质。 将建立一组档案样本以供将来分析。 AIM 3.4检查SAH后脑损伤的生物标志物与颅内压，脑灌注压力，CBF，BTPO2，大脑温度以及SAH后已知会恶化的全身次级事件的存在之间的相关性。