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infarction/turvotus
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 4396 tuloksia
Predictors of malignant cerebral edema in cerebral artery infarction: A meta-analysis.
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Malignant cerebral edema (MCE) is a life-threatening complication of acute cerebral stroke. To date, the focus has been on symptomatic treatment, rather than on prevention. Therefore, to identify high-risk patients and explore potential therapeutic approaches, we investigated the possible predictors
Predictors of malignant brain edema in middle cerebral artery infarction observed on CT angiography.
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Patients with middle cerebral artery (MCA) infarction accompanied by MCA occlusion with or without internal carotid artery (ICA) occlusion have a poor prognosis, as a result of brain cell damage caused by both the infarction and by space-occupying and life-threatening edema formation. Multiple
The severity of ischemia determines and predicts malignant brain edema in patients with large middle cerebral artery infarction.
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BACKGROUND
In order to determine the impact of the severity of ischemia on malignant edema formation, we investigated various degrees of perfusional deficit by (11)C-flumazenil PET in patients with large middle cerebral artery (MCA) infarction.
METHODS
17 patients with large MCA stroke were
The roles of MMP-9/TIMP-1 in cerebral edema following experimental acute cerebral infarction in rats.
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Matrix metalloproteinases 9 (MMP-9) and its endogenous inhibitor, tissue inhibitor of metalloproteinases 1 (TIMP-1), regulate homeostasis and turnover of the extra cellular matrix (ECM). They play important roles in acute cerebral infarction (ACI). The contributions of MMP-9 and TIMP-1 to the early
[Splenic infarct, lactate acidosis, and pulmonary edema as manifestations of a pheochromocytoma].
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The case of a 45-year-old woman with pheochromocytoma, who presented with severe abdominal pain and headache, diabetes mellitus, lactic acidosis and pulmonary edema, is described and discussed. Spleen infarction, not so far described as an ischemic complication of pheochromocytoma, was seen in
[A case of cerebral infarction treated with tissue-plasminogen activator exhibiting prolonged cerebral edema for more than 1 month].
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A 62-year-old man with hypertension and diabetes mellitus controlled by medication suddenly noticed slight hemiparesis and was admitted to our hospital. Tissue-plasminogen activator (t-PA) was administered as his NIHSS was 6 and there were no contraindications. His symptoms completely resolved after
Malignant cerebral edema after large anterior circulation infarction: a review.
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UNASSIGNED
Malignant infarction implies a large middle cerebral artery (MCA) stroke that leads to rapid clinical deterioration and edema formation, and can be associated with hemorrhagic transformation, herniation, and poor functional outcomes, including death. Malignant edema is brain edema
Acute hypertensive pulmonary edema after Cesarean section in a patient with an antepartum myocardial infarction -A case report-.
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We report a case of 29-year-old, morbidly obese, diabetic primigravida who had undergone previously primary percutaneous coronary intervention with stent placement for an inferior wall myocardial infarction at 10 weeks of gestation. She remained asymptomatic with medication during the remainder of
A CMR study of the effects of tissue edema and necrosis on left ventricular dyssynchrony in acute myocardial infarction: implications for cardiac resynchronization therapy.
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BACKGROUND
In acute myocardial infarction (AMI), both tissue necrosis and edema are present and both might be implicated in the development of intraventricular dyssynchrony. However, their relative contribution to transient dyssynchrony is not known. Cardiovascular magnetic resonance (CMR) can
Accumulated mannitol and aggravated cerebral edema in a rat model of middle cerebral artery infarction.
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OBJECTIVE
Repeated administration of mannitol in the setting of large hemispheric infarction is a controversial and poorly defined therapeutic intervention. This study was performed to examine the effects of multiple-dose mannitol on a brain edema after large hemispheric infarction.
METHODS
A middle
The effects of mannitol on cerebral edema after large hemispheric cerebral infarct.
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OBJECTIVE
To evaluate the effect of a single large dose of mannitol on midline tissue shifts after a large cerebral infarction.
BACKGROUND
Theoretically, mannitol use in the largest cerebral infarctions may preferentially shrink noninfarcted cerebral tissue, thereby aggravating midline tissue shifts
Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice.
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BACKGROUND
Following myocardial infarction (MI), peri-infarct myocardial edema formation further impairs cardiac function. Extracellular RNA (eRNA) released from injured cells strongly increases vascular permeability. This study aimed to assess the role of eRNA in MI-induced cardiac edema formation,
Dextrorphan reduces infarct volume, vascular injury, and brain edema after ischemic brain injury.
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Focal cerebral ischemia confined to the cerebral cortex in the right middle cerebral artery (MCA) territory was induced by temporary ligation of the MCA and both common carotid arteries (CCAs). Reperfusion was initiated by releasing all three arterial occlusions after 90 min of ischemia. Infarct
Intravenous immunoglobulin reduces infarct volume but not edema formation in acute stroke.
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OBJECTIVE
Intravenous immunoglobulin (IVIG) is used for treatment of immunodeficiencies and autoimmune disorders. Recently, IVIG has also been shown to reduce infarct size in acute stroke. Since edema treatment can provide secondary neuroprotective effects, we conducted the present study to evaluate
Reduction of copper, zinc-superoxide dismutase in knockout mice does not affect edema or infarction volumes and the early release of mitochondrial cytochrome c after permanent focal cerebral ischemia.
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Copper,zinc-superoxide dismutase (SOD1) was shown to be highly protective against ischemia/reperfusion injury in the brain. We have recently reported that SOD1 prevents the release of mitochondrial cytochrome c and subsequent apoptosis after ischemia/reperfusion in mice. To investigate its dose
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