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.
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