hypothermia/accident vascular cerebral

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Combining Normobaric Oxygen with Ethanol or Hypothermia Prevents Brain Damage from Thromboembolic Stroke via PKC-Akt-NOX Modulation.

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In a thromboembolic stroke model after reperfusion by recombinant tissue plasminogen activator (rt-PA), we aimed to determine whether therapeutic hypothermia (TH) and ethanol (EtOH) in combination with low concentration (60 %) of normobaric oxygen (NBO) enhanced neuroprotection, as compared to using

Phenothiazines Enhance Mild Hypothermia-induced Neuroprotection via PI3K/Akt Regulation in Experimental Stroke.

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Physical hypothermia has long been considered a promising neuroprotective treatment of ischemic stroke, but the treatment's various complications along with the impractical duration and depth of therapy significantly narrow its clinical scope. In the present study, the model of reversible right

Longitudinal MRI evaluation of neuroprotective effects of pharmacologically induced hypothermia in experimental ischemic stroke.

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Pharmacologically induced hypothermia (PIH) shows promising neuroprotective effects after stroke insult. However, the dynamic evolution of stroke infarct during the hypothermic therapy has not been understood very well. In the present study, MRI was utilized to longitudinally characterize the

Reduction of diffusion-weighted MRI lesion volume after early moderate hypothermia in ischemic stroke.

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BACKGROUND Large areas of restricted diffusion in the middle cerebral artery (MCA) territory are highly predictive of severe and potentially space-occupying MCA stroke. A reduction of diffusion-weighted MRI (DWI) lesions occurs in 20% to 40% of acute stroke patients with early

Ultrarapid, convection-enhanced intravascular hypothermia: a feasibility study in nonhuman primate stroke.

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OBJECTIVE Hypothermia has been shown to be neuroprotective in a variety of clinical settings. Unfortunately, poor delivery techniques and insufficient data in appropriate preclinical models have hampered its development in human stroke. To address these limitations, we have devised a 10F

Hypothermia bed system for stroke patients. Technical note.

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A new hypothermia bed system was used to induce mild hypothermia (33-35 degrees C) in six patients with stroke due to subarachnoid hemorrhage, hypertensive intracerebral hemorrhage, or embolic internal carotid artery occlusion. The system bed contained all necessary equipment including a respirator,

Hypothermia blocks ischemic changes in ubiquitin distribution and levels following stroke.

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Dysfunction of the ubiquitin-proteasome system has recently been linked to stroke. Ischemia may cause increased protein misfolding and inhibit the proteasome, shifting the balance from free ubiquitin to conjugated ubiquitin. In this study, we examine the effect of hypothermia on the distribution of

Hypothermia treatment ameliorated cyclin-dependent kinase 5-mediated inflammation in ischemic stroke and improved outcomes in ischemic stroke patients.

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The inflammatory response is a key mechanism of neuronal damage and loss during acute ischemic stroke. Hypothermia has shown promise as a treatment for ischemic stroke. In this study, we investigated the molecular signaling pathways in ischemic stroke after hypothermia

Hypothermia after acute ischemic stroke.

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Induced hypothermia after ischemic stroke is a promising neuroprotective therapy and is the most potent in pre-clinical models. Technological limitations and homeostatic mechanisms that maintain core body temperature, however, have limited the clinical application of hypothermia. Advances in

Induced hypothermia for acute stroke.

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Induced hypothermia is one of the most promising neuroprotective therapies. Technological limitations and homeostatic mechanisms that maintain core body temperature have impeded the clinical use of hypothermia. Recent advances in intravascular cooling catheters and successful trials of hypothermia

The emerging role of induced hypothermia in the management of acute stroke.

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Current treatment of acute stroke remains unsatisfactory. This review presents experimental and clinical data which suggest that mild induced hypothermia could be a potent and practicable neuroprotective treatment of acute ischaemic stroke and intracerebral haemorrhage. Hypothermia, if proven to be

Hypothermia in Acute Stroke.

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Moderate hypothermia (MH) is neuroprotective in animal models of focal ischemia when it is induced during, or within few hours after, onset of ischemia. In patients with acute stroke, several observational studies suggested normothermia or mild hypothermia as independent prognostic factors for

Delayed hypothermia in malignant ischaemic stroke.

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Moderate hypothermia may reduce mortality in malignant brain infarction. However, due to the extremely limited number of patients treated, it is still unknown whether it may be beneficial if undertaken several days after acute stroke, when the probability of a malignant oedema is higher. We report

Energy expenditure in ischemic stroke patients treated with moderate hypothermia.

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OBJECTIVE To determine total energy expenditure (TEE) in patients with acute ischemic stroke in the territory of the middle cerebral artery (MCA), treated with moderate hypothermia (33 degrees C). METHODS Prospective study in a neurological ICU. METHODS Ten consecutive patients with severe MCA

Local hypothermia and optimal temperature for stroke therapy in rats.

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BACKGROUND Local hypothermia induced by intravascular infusion of cold saline solution effectively reduces brain damage in stroke. We further determined the optimal temperature of local hypothermia in our study. METHODS Seventy-eight adult male Sprague Dawley rats (260 - 300 g) were randomly divided

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