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Pagina 1 a partire dal 105 risultati
Normobaric hyperoxia retards the evolution of ischemic brain tissue toward infarction in a rat model of transient focal cerebral ischemia.
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OBJECTIVE
Oxygen therapy has been long considered a logical therapy for ischemic stroke. Our previous studies showed that normobaric hyperoxia (normobaric hyperoxia (NBO), 95% O2 with 5% CO2) treatment during ischemia reduced ischemic neuronal death and cerebromicrovascular injury in animal stroke
Delayed protective effects of hyperoxia against cardiac arrhythmias and infarction in anesthetized rats.
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BACKGROUND
Previous studies have shown that pretreatment with normobaric hyperoxia has cardioprotective effect in isolated rat heart. The present study was designed to test the hypothesis that pretreatment normobaric hyperoxia could induce delayed cardioprotection effect in an in vivo regional heart
Hyperoxia in patients with cardiogenic shock after myocardial infarction supported with venoarterial extracorporeal membrane oxygenation
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Background: Venoarterial extracorporeal membrane oxygenation (V-A ECMO) improves perfusion and oxygenation in patients with cardiogenic shock. However, it can also result in supranormal oxygen exposure. Recent evidence suggests hyperoxia
Exposure of rats to hyperoxia enhances relaxation of isolated aortic rings and reduces infarct size of isolated hearts.
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Exposure of rats to hyperoxia before organ harvesting protected their isolated hearts against global ischaemia-reperfusion injury in a previous study. The present study investigates whether hyperoxia influences vasomotor function and regional ischaemia of the heart. Isolated rings of the thoracic
Pretreatment with hyperoxia reduces in vivo infarct size and cell death by apoptosis with an early and delayed phase of protection.
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OBJECTIVE
Exposure to normobaric hyperoxia protects the heart against ischemia-reperfusion injury ex vivo. In the present study, we investigated the effect of the early and late phase of hyperoxia on in vivo myocardial infarction and apoptosis.
METHODS
Rats were exposed to room air preoxygenation
Normobaric hyperoxia delays perfusion/diffusion mismatch evolution, reduces infarct volume, and differentially affects neuronal cell death pathways after suture middle cerebral artery occlusion in rats.
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Normobaric hyperoxia (NBO) has been shown to extend the reperfusion window after focal cerebral ischemia. Employing diffusion (DWI)- and perfusion (PWI)-weighted magnetic resonance imaging (MRI), the effect of NBO (100% started at 30 mins after middle cerebral artery occlusion (MCAO)) on the
Normobaric hyperoxia improves cerebral blood flow and oxygenation, and inhibits peri-infarct depolarizations in experimental focal ischaemia.
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Normobaric hyperoxia is under investigation as a treatment for acute ischaemic stroke. In experimental models, normobaric hyperoxia reduces cerebral ischaemic injury and improves functional outcome. The mechanisms of neuroprotection are still debated because, (i) inhalation of 100% O2 does not
Laser microdissection and capture of pure cardiomyocytes and fibroblasts from infarcted heart regions: perceived hyperoxia induces p21 in peri-infarct myocytes.
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Myocardial infarction caused by ischemia-reperfusion in the coronary vasculature is a focal event characterized by an infarct-core, bordering peri-infarct zone and remote noninfarct zone. Recently, we have reported the first technique, based on laser microdissection pressure catapulting (LMPC),
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
[Hazards of hyperoxia in patients with myocardial infarction and heart failure].
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Effects of hyperoxia on myocardial injury following cardioversion-A randomized clinical trial.
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Oxygen has long been assumed beneficial for all ill and injured patients. However, hyperoxia may be harmful and aggravate myocardial injury such as that caused by myocardial infarction. We aimed to investigate if hyperoxia increases myocardial injury following direct current cardioversion compared
Hyperoxia and transforming growth factor β1 signaling in the post-ischemic mouse heart.
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OBJECTIVE
Following ischemic injury, myocardial healing and remodeling occur with characteristic myofibroblast trans-differentiation and scar formation. The current study tests the hypothesis that hyperoxia and nitric oxide (NO) regulate TGF-β1 signaling in the post-ischemic
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
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,
Hyperoxia and antioxidants during major non-cardiac surgery and risk of cardiovascular events: Protocol for a 2x2 factorial randomised clinical trial.
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