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Hyperthermia and Brain Ischemia
1997This chapter reviews recent experimental studies concerning the detrimental consequences of hyperthermia on ischemic outcome. The chapter also discusses potential mechanisms underlying the detrimential consequences of mild hyperthermia. Fever is frequently observed following cardiopulmonary resuscitation and is considered prognostic of poor outcome in ...
Raul Busto, W. Dalton Dietrich
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Inflammation of the Brain after Ischemia
1996Cytokines which promote emigration of leukocytes from the vascular lumen into the injured brain tissue are produced at the site of incipient cerebral infarction. The blood-borne invaders then accelerate the decomposition of brain cells by their toxic by-products, phagocytic action, and by the immune reaction.
Kyuya Kogure +4 more
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Catecholamines in Experimental Brain Ischemia
Archives of Neurology, 1975Local cerebral ischemia was produced in rats by internal carotid artery injection of 35 mu carbon microspheres, and brain norepinephrine (NE), dopamine, and cyclic adenosine 3, 5-monophosphate (cAMP) were measured in embolized and intact hemispheres at intervals up to four hours. Sham-operated animals were controls.
Kyuya Kogure +4 more
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Neurogenesis following brain ischemia
Developmental Brain Research, 2002Following 5 or 10 min of global ischemia in the adult gerbil there is a tenfold increase in the birth of new cells in the subgranular zone of dentate gyrus of the hippocampus as assessed using BrdU incorporation. This begins at 7 days, peaks at 11 days, and decreases thereafter. Over the next month approximately 25% of the newborn cells disappear.
Ramon Bernabeu +2 more
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Vascular Protection in Brain Ischemia
Cerebrovascular Diseases, 2006Vascular damage occurring after cerebral ischemia may lead to a worse outcome in patients with ischemic stroke, as it facilitates edema formation and hemorrhagic transformation. There are several phases in the development of vascular injury (acute, subacute and chronic) and different mediators act in each one.
Mar Castellanos +4 more
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1995
Stroke is the second or third major cause of death in the “industrialized countries.” About 30% of patients die within a year after the first insult, and 20% remain dependent on care. So far there is no effective therapy available but one is desperately needed.
Karl Rudolphi, Peter Schubert
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Stroke is the second or third major cause of death in the “industrialized countries.” About 30% of patients die within a year after the first insult, and 20% remain dependent on care. So far there is no effective therapy available but one is desperately needed.
Karl Rudolphi, Peter Schubert
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Global Brain Ischemia and Reperfusion
Annals of Emergency Medicine, 1996Brain damage accompanying cardiac arrest and resuscitation is frequent and devastating. Neurons in the hippocampus CA1 and CA4 zones and cortical layers III and V are selectively vulnerable to death after injury by ischemia and reperfusion. Ultrastructural evidence indicates that most of the structural damage is associated with reperfusion, during ...
Donald J. DeGracia +6 more
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Cerebral ischemia and brain histamine
Brain Research Reviews, 2005Cerebral ischemia induces excess release of glutamate and an increase in the intracellular Ca(2+) concentration in neurons, which provokes enzymatic process leading to irreversible neuronal injury. Histamine plays a role as a neurotransmitter in the mammalian brain, and histamine release from nerve endings is enhanced in ischemia by facilitation of ...
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1977
Complete cessation of cerebral blood flow causes an almost immediate suppression of higher central nervous function (41), followed by a breakdown of cell metabolism within a few minutes (36, 37). The biochemical and functional sequel of ischemic suppression has been studied extensively in various laboratories, and the results obtained are quite similar
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Complete cessation of cerebral blood flow causes an almost immediate suppression of higher central nervous function (41), followed by a breakdown of cell metabolism within a few minutes (36, 37). The biochemical and functional sequel of ischemic suppression has been studied extensively in various laboratories, and the results obtained are quite similar
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Experimental ischemia of the brain
1977Cerebral ischemia as seen by the vascular surgeon generally is the consequence of regional stenosis or occlusion of the main supply vessels of the brain. The pathophysiology of regional ischemia is a very complex one: areas of no-flow or low-flow are surrounded by regions of reactive hyperemia, causing different degrees of ischemic cell damage. Changes
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