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cerebral infarction/opuch
Odkaz sa uloží do schránky
Strana 1 od 2142 výsledky
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
Protective effect of green tea polyphenol EGCG against neuronal damage and brain edema after unilateral cerebral ischemia in gerbils.
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Previous studies have demonstrated that a green tea polyphenol, (-)-epigallocatechine gallate (EGCG), has a potent free radical scavenging and antioxidant effect. Glutamate leads to excitotoxicity and oxidative stress, which are important pathophysiologic responses to cerebral ischemia resulting 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
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
Cerebral ischemia and white matter edema in experimental hydrocephalus: a combined in vivo MRI and MRS study.
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T2 and diffusion weighted MRI, as well as 31P and 1H MRS were performed in kaolin-induced hydrocephalic rats. Extracellular white matter edema was detected in the early stages of progressive hydrocephalus. Phosphocreatine (PCr)/inorganic phosphate (Pi) ratios in hydrocephalic animals were decreased
[Macrophotographic measurement of brain surface area for evaluating brain edema after focal cerebral ischemia in mice].
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OBJECTIVE
To establish a new macrophotographic measurement of brain surface area to evaluate brain edema after focal cerebral ischemia in mice.
METHODS
Permanent focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice. The brains were removed 10,30 min,1,3,6,12 and 24
Recirculation after cerebral ischemia. Simultaneous measurement of cerebral bloodflow, brain edema, cerebrovascular permeability and cortical EEG in the rat.
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The 4-vessel occlusion rat model of cerebral ischemia was modified to permit the simultaneous measurement of cerebral blood flow (hydrogen clearance), brain edema (specific gravity), cerebrovascular permeability (14C-AIB) and electrocardiogram. Surgery was performed in one stage in the anesthetised,
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
[Mediator substances of brain edema in cerebral ischemia].
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Brain edema in focal or global cerebral ischemia is associated with formation and release of pathophysiologically active mediator compounds. Therapeutical methods which interfere with mediator compounds under these circumstances might improve specificity of treatment of ischemic brain edema and
Release of bradykinin and expression of kinin B2 receptors in the brain: role for cell death and brain edema formation after focal cerebral ischemia in mice.
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Pharmacological studies using bradykinin B2 receptor antagonists suggest that bradykinin, an early mediator of inflammation and the main metabolite of the kallikrein-kinin system, is involved in secondary brain damage after cerebral ischemia. However, the time-course of bradykinin production and
Effects of fluosol-DA on brain edema, energy metabolites, and tissue oxygen content in acute cerebral ischemia.
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Perfluorochemicals were developed as a blood substitute and were reported to have an advantage in oxygen transport compared with blood. The present study was undertaken to investigate the therapeutic effects of a perfluorochemical, FDA, on brain edema and metabolites in acute cerebral ischemia.
[The role of edema in cerebral ischemia. From physiopathology to therapeutics].
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Brain ischemia induces an original form of edema associating a "cytotoxic" component and a "vasogenic" component which is more inconstant. The authors set out a synthesis of fundamental research concerning the different factors of ischemic brain edema. Although anti-edematous drugs (steroids,
Significance of proton relaxation time measurement in brain edema, cerebral infarction and brain tumors.
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We examined the proton relaxation times in vitro in various neurological diseases using experimental and clinical materials, and consequently obtained significant results for making a fundamental analysis of magnetic resonance imaging (MRI) as followings. 1) In the brain edema and cerebral
Pentobarbital protection from cerebral infarction without suppression of edema.
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We studied the mechanism of barbiturate protection from focal cerebral infarction in cats by examining in detail edema formation 72 hours after acute, permanent occlusion of the left middle cerebral artery (LMCA). Neurological function, gas exchange, vital signs, and intracranial pressure (ICP) were
Nonhyperemic blood flow restoration and brain edema in experimental focal cerebral ischemia.
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The effect of suppression of postischemic reactive hyperemia on the blood-brain barrier (BBB) and ischemic brain edema after temporary focal cerebral ischemia was studied in cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow (rCBF) was measured by a thermal diffusion
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