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brain ischemia/fever

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Hyperthermia and hypermetabolism in focal cerebral ischemia.

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The reliable and reproducible creation of an animal model of focal cerebral ischemia is not easily accomplished. Using a transortibal approach, we showed that occlusion of the posterior cerebral artery (PCA), middle cerebral artery (MCA), and the contralateral anterior cerebral artery (ACA) created
Brief and non-lethal cerebral ischemia produces most severe neuronal damage when such ischemia is induced repeatedly at 1-h intervals. We examined whether spontaneous postischemic hyperthermia is an aggravating factor for the cumulative damage following repeated ischemia in the gerbil. We maintained

Effect of mild hyperthermia on recovery of metabolic function after global cerebral ischemia in cats.

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We investigated the effect of mild whole-body hyperthermia before and after 16 minutes of global cerebral ischemia on metabolic recovery during recirculation in cats using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Hyperthermia (temperature 40.6 +/- 0.2 degrees C) was induced

Predictive Factors of Fever After Aneurysmal Subarachnoid Hemorrhage and Its Impact on Delayed Cerebral Ischemia and Clinical Outcomes.

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OBJECTIVE Fever is relatively common and worsens neurologic injury after aneurysmal subarachnoid hemorrhage (SAH). The aim of this study was to display the time course of body temperature, identify predictive factors of fever after SAH, and evaluate its impact on delayed cerebral ischemia (DCI) and

Heat shock protein 72 overexpression protects against hyperthermia, circulatory shock, and cerebral ischemia during heatstroke.

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This study extends our earlier studies in rats by applying our heatstroke model to a new species. Additionally, transgenic mice are used to examine the role of heat shock protein (HSP) 72 in experimental heatstroke. Transgenic mice that were heterozygous for a porcine HSP70i gene ([+]HSP72),

Effects of hyperthermia on infarct volume in focal embolic model of cerebral ischemia in rats.

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Hyperthermia worsens outcome of stroke in patients and also in animal models. In the present study, we tested the effects of hyperthermia in a focal embolic model of cerebral ischemia in rats. Focal ischemic injury was induced by embolizing a preformed clot into the middle cerebral artery.
Calbindin D-28K (CB), a Ca2+-binding protein, maintains Ca2+ homeostasis and protects neurons against various insults. Hyperthermia can exacerbate brain damage produced by ischemic insults. However, little is reported about the role of CB in the brain under hyperthermic condition during ischemic
Hyperthermia can exacerbate the brain damage produced by ischemia. In the present study, we investigated the effects of hyperthermia before and during ischemia-reperfusion on neuronal damage and glial changes in the gerbil hippocampus following transient cerebral ischemia using cresyl violet

Delayed postischemic hyperthermia in awake rats worsens the histopathological outcome of transient focal cerebral ischemia.

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OBJECTIVE Over the past several years, it has been demonstrated that mild intraischemic or immediate postischemic hyperthermia worsens ischemic outcome in models of global and focal ischemia. Periods of hyperthermia are commonly seen in patients after stroke and cardiac arrest. The hypothesis tested

Hyperthermia enhances spectrin breakdown in transient focal cerebral ischemia.

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Calpain-mediated spectrin degradation is triggered by cerebral ischemia and, when persistent, is thought to signal irreversible neuronal injury. Hyperthermia superimposed upon cerebral ischemia may exacerbate the injury process. In this study, we compared the extent of spectrin degradation in the
The metabolic effects of graded whole body hypothermia on complete global cerebral ischemia and recirculation was investigated in the cat. Hypothermia was induced to one of three levels prior to ischemia; T = 26.8 degrees +/- 0.5 degrees C (n = 4), T = 32.1 degrees +/- 0.2 degrees C (n = 5), and T =
Transport of a polyamine (PA), spermidine (SPMD) into rat brain at various early postischemic periods was studied. Rats underwent 20 min of four-vessel occlusion (4VO) followed by 5, 10, 30 and 60 min of recirculation (RC) periods with natural brain temperature. 3H-aminoisobutyricacid (AIB) and

Hyperthermia nullifies the ameliorating effect of dizocilpine maleate (MK-801) in focal cerebral ischemia.

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The present study was inspired by two previous findings from the laboratory. The first was that dizocilpine maleate (MK-801) fails to reduce infarct size when the middle cerebral artery (MCA) is permanently occluded by an intraluminal filament technique in rats. In seeking the reasons for this we

Caspase inhibitors reduce neuronal injury after focal but not global cerebral ischemia in rats.

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OBJECTIVE Studies show that blocking the activation of caspases by the caspase inhibitors z-VAD.FMK and z-DEVD.FMK can reduce ischemic neuronal injury after cerebral ischemia. Because the severity of ischemia was mild in some studies, we tested the efficacy of these caspase inhibitors on moderately

Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans.

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BACKGROUND The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans. METHODS Nineteen patients with chronic hepatitis C virus infection, not responding to
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