Titlebook: Cerebral Blood Flow; Mechanisms of Ischem Michael R. Pinsky Book 2002 Springer Science+Business Media New York 2002 PET.Trauma.acute stroke

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History of Cerebral Blood Flow Assessment mass, this principle simply states that the quantity of a substance taken up by an organ per unit of time is equal to the blood flow through that organ multiplied by the difference between its arterial and venous concentrations.

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Neural Regulation of the Cerebral Circulation control of the systemic circulation [see ref 1 for a historical review]. However, evidence accumulated over the past 100 years indicates that cerebral blood vessels are in a dynamic state. Thus, the cerebral vasculature is endowed with complex regulatory systems that allow the brain to finely regul

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Role of Endothelium in Regulation of the Brain Microcirculationl conditions is by the release endothelium-derived relaxing factor(s) (EDRFs). These factors include nitric oxide, endothelium-derived hyperpolarizing factor(s) and prostacyclin [., .]. Although there are a few exceptions [see . and . for detailed reviews, .], the vast majority of available evidence

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Triggering Events in Ischemic Brain Damagedients across cell membranes. When sufficiently severe, and sufficiently prolonged, ischemia leads to brain damage. This is of two major types. In one, typically caused by brief periods of global or focal ischemia, damage occurs as selective neuronal necrosis, affecting neuronal populations which ar

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Ischemic Mechanisms in Traumatic Brain Injuryclinical condition, the precise role of ischemia in the evolution of secondary damage after traumatic brain injury has remained difficuk to define. Similarly, studies of the effects of the appHcation of therapies targeting secondary ischemic damage in traumatic brain injury are limited. In this chap

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Coupling and Compartmentation of Cerebral Blood Flow and Metabolism organization? To answer these general questions, we must understand at least four relationships which reasonable considerations suggest underlie the link between brain function and brain energy metaboHsm. These relationships link:

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The Genetic Control of Ischemic Neuronal Cell Deathrosis after cerebral ischemia remains controversial. Strictly speaking, apoptosis includes certain key morphologic features: condensation and cleavage of nuclear chromatin, and the formation of budding cytoplasmic appendages known as apoptotic bodies. In addition, intracellular membranes and the pla

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Cerebral Resuscitation from Temporary Complete Global Brain Ischemiaommon cause of sudden coma and death [.,.]. Sudden CA kills about 400,000 persons each year in the U.S. In addition, in the over 100,000 accidental deaths each year, coma occurs as a result of trauma, intoxication, asphyxiation, severe shock, or other insults. This talk focused on CPCR research resu

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