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hyperoxia/accident vascular cerebral
L'enllaç es desa al porta-retalls
Pàgina 1 des de 173 resultats
Interrelations between blood-brain barrier permeability and matrix metalloproteinases are differently affected by tissue plasminogen activator and hyperoxia in a rat model of embolic stroke.
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BACKGROUND
In ischemic stroke, blood-brain barrier (BBB) regulations, typically involving matrix metalloproteinases (MMPs) and inhibitors (TIMPs) as mediators, became interesting since tissue plasminogen activator (tPA)-related BBB breakdown with risk of secondary hemorrhage was considered to
T2*-weighted magnetic resonance imaging with hyperoxia in acute ischemic stroke.
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OBJECTIVE
We describe the first clinical application of transient hyperoxia ("oxygen challenge") during T2*-weighted magnetic resonance imaging (MRI), to detect differences in vascular deoxyhemoglobin between tissue compartments following stroke.
METHODS
Subjects with acute ischemic stroke were
Advances in Normobaric Hyperoxia Brain Protection in Experimental Stroke.
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As we all know that stroke is still a leading cause of death and acquired disability. Etiological treatment and brain protection are equally important. This review aimed to summarize the advance of normobaric-hyperoxia (NBHO) on brain protection in the setting of experimental stroke and brain
Endothelial dysfunction abrogates the efficacy of normobaric hyperoxia in stroke.
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Hyperoxia has been uniformly efficacious in experimental focal cerebral ischemia. However, pilot clinical trials have showed mixed results slowing its translation in patient care. To explain the discordance between experimental and clinical outcomes, we tested the impact of endothelial dysfunction,
Normobaric hyperoxia and delayed tPA treatment in a rat embolic stroke model.
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In a rat embolic stroke (eMCAO) model, the effects of 100% normobaric hyperoxia (NBO) with delayed recombinant tissue plasminogen activator (tPA) administration on ischemic lesion size and safety were assessed by diffusion- and perfusion (PWI)-weighted magnetic resonance imaging. NBO or room air
Reduction of zinc accumulation in mitochondria contributes to decreased cerebral ischemic injury by normobaric hyperoxia treatment in an experimental stroke model.
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Cerebral ischemia interrupts oxygen supply to the affected tissues. Our previous studies have reported that normobaric hyperoxia (NBO) can maintain interstitial partial pressure of oxygen (pO2) in the penumbra of ischemic stroke rats at the physiological level, thus affording significant
Cerebrovascular reactivity in acute hyperoxia in patients with acute ischaemic stroke.
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This study aimed to assess the effect of acute hyperoxia on cerebral and systemic heamodynamics and the plasma concentration of prostacyclin and thromboxane in patients with stroke.
Mean blood flow velocity (MBFV), pulsatility and resistance indices of the middle cerebral artery using transcranial
Normobaric hyperoxia reduces MRI diffusion abnormalities and infarct size in experimental stroke.
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BACKGROUND
Hyperbaric oxygen therapy is considered an important stroke treatment strategy.
BACKGROUND
To determine whether normobaric oxygen is neuroprotective, and, if so, what the therapeutic time window is.
METHODS
Experiment 1-Serial diffusion- and perfusion-weighted MRI (DWI and PWI) was
Normobaric hyperoxia therapy for traumatic brain injury and stroke: a review.
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Traumatic brain injury (TBI) and acute ischaemic stroke are major causes of mortality and morbidity and there is an urgent demand for new neuroprotective strategies following the translational failure of neuroprotective drug trials. Oxygen therapy--especially normobaric, may offer a simple and
Hyperoxia potentiated sonothrombolysis as a method of acute ischemic stroke therapy.
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The main goal in the treatment of acute ischemic stroke is prompt arterial recanalization. Thrombolysis with recombinant tissue plasminogen activator (rtPA) is efficient in humans, but shows significant problems including slow and incomplete recanalization and frequent bleeding complications.
Normobaric hyperoxia-based neuroprotective therapies in ischemic stroke.
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Stroke is a leading cause of death and disability due to disturbance of blood supply to the brain. As brain is highly sensitive to hypoxia, insufficient oxygen supply is a critical event contributing to ischemic brain injury. Normobaric hyperoxia (NBO) that aims to enhance oxygen delivery to hypoxic
Neuroprotection caused by hyperoxia preconditioning in animal stroke models.
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Ischemic tolerance induced by hyperoxia (HO) can protect against brain injury and neurodegenerative diseases. Although multiple studies demonstrate neuroprotection by HO, the exact mechanism(s) of HO neuroprotection has not been elucidated. Here, I first review related mechanisms of brain ischemia
Normobaric hyperoxia protects the blood brain barrier through inhibiting Nox2 containing NADPH oxidase in ischemic stroke.
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Normobaric hyperoxia (NBO) has been shown to be neuro- and vaso-protective during ischemic stroke. However, the underlying mechanisms remain to be fully elucidated. Activation of NADPH oxidase critically contributes to ischemic brain damage via increase in ROS production. We herein tested the
Does normobaric hyperoxia increase oxidative stress in acute ischemic stroke? A critical review of the literature.
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Stroke, one of the most debilitating cerebrovascular and nuerological diseases, is a serious life-threatening condition and a leading cause of long-term adult disability and brain damage, either directly or by secondary complications. Most effective treatments for stroke are time dependent such as
Effects of Normobaric Hyperoxia in Severe Acute Stroke: a Randomized Controlled Clinical Trial Study.
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Oxygen therapy might increase damaged tissue oxygenation, turn on the aerobic pathway, and save neurons from death and could improve clinical outcome of the patients with stroke and head trauma. Hyperbaric oxygen therapy is accompanied by some unfavorable effects. Results of normobaric oxygen
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