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subarachnoid hemorrhage/hypoxia
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Pagina 1 a partire dal 236 risultati
Downregulating hypoxia-inducible factor-1α expression with perfluorooctyl-bromide nanoparticles reduces early brain injury following experimental subarachnoid hemorrhage in rats.
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The aim of the present study was to investigate the effects of perfluorooctyl-bromide (PFOB) nanoparticles on hypoxia-inducible factor 1 alpha (HIF-1α) and its downstream target genes in early brain injury (EBI) after subarachnoid hemorrhage (SAH). Healthy male Sprague Dawley rats (n=100) were
Early CT signs of hypoxia in patients with subarachnoid hemorrhage presenting with cardiac arrest: early CT signs in SAH patients presenting with CA.
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BACKGROUND
For cardiac arrest (CA) victims, brain computed tomography (CT) may serve as a prognosticator. Loss of gray-white matter discrimination (GWMD) and sulcal edema/effacement are reliable CT signs of hypoxia, and a time window may exist for development of these signs. Most data are derived
Impact of restrictive fluid protocol on hypoxemia after aneurysmal subarachnoid hemorrhage.
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In patients with aneurysmal subarachnoid hemorrhage (aSAH), acute cardiac dysfunction and triple-H-therapy, can lead to hypoxemia. Our aim was to assess impact of a protocoled fluid restrictive approach on hypoxemia in these patients.
We included prospectively ICU patients with aSAH admitted within
Anemia is associated with metabolic distress and brain tissue hypoxia after subarachnoid hemorrhage.
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BACKGROUND
Anemia is frequently encountered in critically ill patients and adversely affects cerebral oxygen delivery and brain tissue oxygen (PbtO2). The objective of this study is to assess whether there is an association between anemia and metabolic distress or brain tissue hypoxia in patients
Preoperative hypoxemia in conscious patients after subarachnoid hemorrhage.
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We retrospectively examined partial arterial pressure of oxygen (Pao2) afer subarachnoid hemorrhage (SAH), adjusted for patient-related risk factors for hypoxemia in 51 adult patients with no disturbance of consciousness undergoing surgery for clipping of intracranial aneurysms. A control group of
Reduced cerebral blood flow but intact reactivity to hypercarbia and hypoxia following subarachnoid hemorrhage in rabbits.
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Subarachnoid hemorrhage (SAH) was produced in rabbits by four subarachnoid injections of blood (n = 7) or saline (n = 6); a control group (n = 6) had no injections. Basilar artery vasospasm was assessed by serial angiograms. Resting CBF (microspheres) and CBF reactivity to hypercapnia (65 and 85 mm
[The relationship between hypoxia-inducible factor-1α expression and apoptosis in early brain injury after subarachnoid hemorrhage].
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OBJECTIVE
To investigate the association of hypoxia-inducible factor-1α (HIF-1α) expression and apoptosis in the cerebral cortex following subarachnoid hemorrhage (SAH).
METHODS
Subarachnoid hemorrhage was induced by modified monofilament puncture method in rats. Thirty-five adult male
Effects of deferoxamine-activated hypoxia-inducible factor-1 on the brainstem after subarachnoid hemorrhage in rats.
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OBJECTIVE
Hypoxia-inducible factor (HIF)-1 is a transcription factor that regulates the expression of various neuroprotective genes. The goal of this study was to clarify the relationship between HIF-1 expression and subarachnoid hemorrhage (SAH) and to characterize the effects of deferoxamine
Hypoxemia associated with nimodipine in a patient with an aneurysmal subarachnoid hemorrhage.
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OBJECTIVE
A case of probable nimodipine-induced hypoxemia in a patient undergoing treatment for aneurysmal subarachnoid hemorrhage (SAH) is reported.
CONCLUSIONS
A 62-year-old man hospitalized for SAH developed symptoms of respiratory distress on several occasions within days of initiation of
Cerebral perfusion pressure thresholds for brain tissue hypoxia and metabolic crisis after poor-grade subarachnoid hemorrhage.
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OBJECTIVE
To identify a minimally acceptable cerebral perfusion pressure threshold above which the risks of brain tissue hypoxia (BTH) and oxidative metabolic crisis are reduced for patients with subarachnoid hemorrhage (SAH).
METHODS
We studied 30 poor-grade SAH patients who underwent brain
Neuronal apoptosis in the dentate gyrus in humans with subarachnoid hemorrhage and cerebral hypoxia.
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Apoptosis of dentate granule cells is a typical feature of several animal models of disease. In 20 autopsy cases of subarachnoid hemorrhage (SAH) and global cerebral hypoxia caused by protracted shock or respiratory failure, we evaluated by light microscopy and in situ tailing whether this pattern
Potential contribution of hypoxia-inducible factor-1α, aquaporin-4, and matrix metalloproteinase-9 to blood-brain barrier disruption and brain edema after experimental subarachnoid hemorrhage.
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The current research aimed to investigate the role of hypoxia-inducible factor-1α (HIF-1α), aquaporin-4 (AQP-4), and matrix metalloproteinase-9 (MMP-9) in blood-brain barrier (BBB) dysfunction and cerebral edema formation in a rat subarachnoid hemorrhage (SAH) model. The SAH model was induced by
[Relationship between hypoxemia and urinary catecholamine excretion in subarachnoid hemorrhage and hypertensive intracerebral hemorrhage].
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Reversal of tissue hypoxia by a single intraventricular dose of sodium nitroprusside in a patient with severe medically refractory cerebral vasospasm after subarachnoid haemorrhage.
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Cardiac arrhythmias associated with subarachnoid hemorrhage: prospective study.
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This is a prospective study of cardiac arrhythmias in patients with acute subarachnoid hemorrhage (SAH) secondary to ruptured aneurysm. Twenty per cent of the patients had serious, life-threatening arrhythmias. However, 100% of the patients had some kind of cardiac arrhythmia. The arrhythmias
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