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peroxidase/edema
Врската е зачувана во таблата со исечоци
Страница 1 од 551 резултати
Effects of catalase, peroxidase, superoxide dismutase and 10 scavengers of oxygen radicals in carrageenin edema and in adjuvant arthritis of rats.
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Catalase, peroxidase and superoxide dismutase were found to inhibit significantly carrageenin edema and the primary phase of adjuvant arthritis in rats after i.v. injection. Heat-inactivated enzymes were as effective as the native enzymes. None of 10 scavengers of oxygen radicals inhibited the
Mechanisms of edema formation in experimental autoimmune encephalomyelitis. The contribution of inflammatory cells.
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Most of the central nervous system (CNS) endothelium regulates the passage of solutes and functions as a blood-brain barrier (BBB). During experimental autoimmune encephalomyelitis (EAE), an inflammatory demyelinating disease of the CNS, loss of BBB function occurs. The authors have previously shown
[The effects of taurine on oxidative processes in brain edema].
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OBJECTIVE
To investigate the free radical oxidation of lipids, oxidative modification of protein activity of glutathione peroxidase and glutathione reductase as well as the end product of nitric oxide - nitrite in the brain mitochondrial fraction of animals with experimentally induced cerebral edema
Selenium prevents mercuric chloride induced acute osmoregulatory failure without glutathione peroxidase involvement in the black bullhead (Ictalurus melas).
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The relationship between coelomic injections of mercuric chloride doses and osmoregulatory responses was measured. Response parameters were weight increases and blood osmolarity decreases 72 hr after dose administration. Massive edema and large decreases in blood osmolarity could be completely
Increased expression of extracellular glutathione peroxidase in mice with dextran sodium sulfate-induced experimental colitis.
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Extracellular glutathione peroxidase (E-GPx) is a selenoenzyme that reduces hydrogen peroxide and organic peroxides. All plasma glutathione peroxidase (GPx) activity in humans is attributable to E-GPx. The gastrointestinal (GI) tract also synthesizes and secretes E-GPx into the extracellular milieu.
Activities of lung NADPH-cytochrome C-reductase and of cytochrome P-450 peroxidase during the protection of rat from hyperoxic injury by polyriboinosinic acid-polyribocytidilic acid.
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Rats exposed to normobaric oxygen received a single i.p. injection of 2.5 mg/kg of poly I: poly C at various times (-120 to +36 h) before and after the beginning of oxygen exposure. Hyperoxic lung damage and modifications in cytochrome P-450 system components were evaluated. Our results confirmed
Electrolyte-induced demyelination in rats. 1. Role of the blood-brain barrier and edema.
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The blood-brain barrier (BBB) was studied in rats with electrolyte-induced demyelination (EID), an experimental model for central pontine myelinolysis. Intravenously injected peroxidase was extravasated at 3 h post hypertonic saline injection (PHS) into regions frequently involved in EID. Increased
[Pathohistological study on active endolymphatic hydrops in guinea pig--with stress stimulations].
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Recently Meniere's disease is believed to show a pathological features of endolymphatic hydrops, but the etiology of this disease has not yet been ascertained. Many investigators tried to create animal models with endolymphatic hydrops by obliterating endolymphatic sac and duct. However, these
[Role of perivascular phagocyte (FGP) of cerebral small blood vessel in cerebral edema].
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Small cerebral blood vessels are provided with slender phagocytic cells which were designated as FGP (fluorescent granular perithelial) cells from their localization and property. They were derived from pial cells and became potent in the uptake capacity for exogenous substance about at one week
[Peroxidation of arachidonic acid and brain edema].
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Recent studies suggest that peroxidation of arachidonic acid (AA) accumulating during ischemic insult, may be related to the occurrence of post-ischemic brain damage. Since the influence of the increased brain content of AA remains unclear, the present study was undertaken to explore whether the
The permeability of the blood-brain barrier to protein in the post-hypoxic cerebral edema of the rat.
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The permeability of the blood-brain barrier to protein was studied in the post-hypoxic cerebral edema of rats, using horseradish peroxidase (HRP) as a tracer protein. Under halothane anesthesia, HRP was injected intravenously. Then the animals were exposed to hypoxic-ischemia by inhalation of 5%
Effect of body temperature on brain edema and encephalopathy in the rat after hepatic devascularization.
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Brain edema is a fatal complication of fulminant hepatic failure and its pathogenesis remains unclear. To determine its presence in a model of ischemic hepatic failure, rats were subjected to a portacaval anastomosis followed by hepatic artery ligation. Brain water was measured using the sensitive
Photochemically induced cerebral infarction. II. Edema and blood-brain barrier disruption.
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Alterations in the blood-brain barrier to proteins, and regional water and electrolyte content were documented in a rat model of photochemically induced small-vessel thrombosis leading to infarction. Horseradish peroxidase (HRP) or Evans blue was given immediately following a 2-min photochemical
Some mechanisms of brain edema studied in a kainic acid model.
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Kainic acid (KA) is a potent neuroexcitatory drug widely used in the experimental study of seizure activity. Subcutaneous injection of KA into rats (10 mg/kg in saline 10 mg/ml; pH 7.0) induced longlasting status epilepticus followed by damage of CNS tissue in the entorhinal/pyriform cortex and in
Morphological estimation of brain extracellular fluid dynamics in cold-induced edema from the aspect of cerebrospinal fluid-extracellular fluid communication.
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Following the induction of cold injury in the parietal cortex of rats, the brain extracellular fluid dynamics under conditions of cryogenic edema were investigated morphologically from the aspect of extracellular fluid (ECF)-cerebrospinal fluid (CSF) communication using horseradish peroxidase (HRP)
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