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brain ischemia/ödem
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Seite 1 von 1908 Ergebnisse
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
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,
[The role of BDNF in brain ischemia pulmonary edema].
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Brain ischemia pulmonary edema(BIPE)is a critical type of the neurogenic pulmonary edema (NPE), with acute development and progression and high mortality. The study on mechanism of BIPE has important scientific significance and substantial practice values. NPE, as a complicated physiopathology
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,
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
[Protective effect of jiedu tongluo injection on cerebral edema in rats with lesion of cerebral ischemia/reperfusion].
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OBJECTIVE
To investigate the protective effects of Jiedu Tongluo injection on cerebral edema induced by focal lesion of cerebral ischemia/reperfusion, the hydrous content of brain and the expressions of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1),
Effects of electroacupuncture preconditioning on jugular vein glucose level and cerebral edema in rats undergoing cerebral ischemia reperfusion that induced injury.
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OBJECTIVE
To determine the effects of electroacupuncture (EA) preconditioning on the blood glucose level in jugular vein and water content in brain tissues in rats undergoing cerebral ischemia reperfusion that induced injury.
METHODS
90 healthy male Wister rats were randomly assigned to 3 groups:
The influence of phenylephrine-induced hypertension during focal cerebral ischemia on the formation of brain edema.
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The authors investigated the effects of phenylephrine-induced hypertension on the development of cerebral edema and neuronal dysfunction during focal cerebral ischemia. Mean arterial pressure was increased by 25-30 mm Hg immediately after middle cerebral artery occlusion (MCAO) in anesthetized rats.
[Changes in RCBF and edema after transient cerebral ischemia--ischemic threshold of postischemic hypoperfusion].
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Brain damage after transient cerebral ischemia may be related to changes in postischemic cerebral blood flow and brain edema. In this study, the relationship between postischemic cerebral blood flow and edema was evaluated in the gerbil. Bilateral carotid occlusion (for 1, 1.5, 5, 15, or 30 min) was
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