Cerebral Oxygen Metabolism after Aneurysmal Subarachnoid Hemorrhage
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It is concluded that the initial aneurysm rupture produces a primary reduction in CMRO2, and that subsequent vasospasm causes ischemia, indicative of cerebral ischemIA without infarction.Abstract:
Previous studies of cerebral oxygen metabolism and extraction in patients with subarachnoid hemorrhage (SAH) have yielded conflicting results. We used positron emission tomography (PET) to measure ...read more
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Cortical Blood Flow and Cerebral Perfusion Pressure in a New Noncraniotomy Model of Subarachnoid Hemorrhage in the Rat
TL;DR: It is demonstrated that although reduced CPP causes the initial decrease in cortical blood flow after SAH, secondary reductions occurring after CPP has reached its nadir are caused by other factors such as acute vasoconstriction.
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Quantitative BOLD: Mapping of human cerebral deoxygenated blood volume and oxygen extraction fraction: Default state
Xiang He,Dmitriy A. Yablonskiy +1 more
TL;DR: The objective of this study was to develop a BOLD MR‐based method that allows quantitative evaluation of tissue hemodynamic parameters, such as the blood volume, deoxyhemoglobin concentration, and oxygen extraction fraction (OEF).
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Blood flow and oxygen delivery to human brain during functional activity: Theoretical modeling and experimental data
Mark A. Mintun,Brian Nils Lundstrom,Abraham Z. Snyder,Andrei G. Vlassenko,Gordon L. Shulman,Marcus E. Raichle +5 more
TL;DR: Findings strongly indicate that the increase in CBF associated with physiological activation is regulated by factors other than local requirements in oxygen.
Journal ArticleDOI
Hypoperfusion without Ischemia Surrounding Acute Intracerebral Hemorrhage
Allyson R. Zazulia,Michael N. Diringer,Tom O. Videen,Robert E. Adams,Kent D. Yundt,Venkatesh Aiyagari,Robert L. Grubb,William J. Powers +7 more
TL;DR: CMRO2 was reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF rather than the increased OEF that occurs in ischemia.
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Delayed cerebral vasospasm and nitric oxide: review, new hypothesis, and proposed treatment.
TL;DR: A two-stage hypothesis of pathogenesis of delayed cerebral vasospasm is presented developed in the Vascular Laboratory of Surgical Neurology Branch of the National Institute of Neurological Disorders and Stroke using a primate model of SAH and suggests that the key treatment should be focused on preventing oxyHb neurotoxicity, inhibiting BOX production, and exogenous NO delivery.
References
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Surgical Risk as Related to Time of Intervention in the Repair of Intracranial Aneurysms
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Relation of Cerebral Vasospasm to Subarachnoid Hemorrhage Visualized by Computerized Tomographic Scanning
TL;DR: The results indicate that blood localized in the subarachnoid space in sufficient amount at specific sites is the only important etiological factor in vasospasm and it should be possible to identify patients in jeopardy from vasospasms and institute early preventive measures.