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cytochrome oxidase/edema
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Paj 1 soti nan 30 rezilta yo
Cytochrome oxidase and hexokinase activities in an infusion edema model with preserved blood flow.
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Despite numerous investigations, the mechanisms underlying the neurological deficits observed in association with interstitial edema remain unclear. A recent study has demonstrated that the cerebral blood flow (CBF) in edematous white matter is unchanged if the blood flow values are corrected for
Changes in activity of cytochrome oxidase in the cochleae of guinea pigs with experimental endolymphatic hydrops.
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Cochlear dysfunction may indicate inadequate generation of intracellular metabolic energy which is necessary for the regulation of the transport of ions and fluid as well as production of electro-energy in the cochlea. Changes in cochlear function in the early stages of endolymphatic hydrops
Superoxide dismutase and cytochrome oxidase in collapsed lungs: possible role in reexpansion edema.
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This study examined the effects of lung collapse, a condition that causes relative hypoxia in lung tissues, on superoxide dismutase (SOD), cytochrome oxidase (cyt ox), and pyruvate kinase (py ki) activities in rabbits. Cyanide-insensitive respiration measurements were done in collapsed and
[Study on the mechanism of pulmonary edema after seawater drowning in rabbit].
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To study the mechanism of pulmonary edema after seawater drowning (PE-SWD), the indexes of blood-gas and acid-base in rabbits artery blood were measured by the blood-gas analyser. The activity of Na(+)-K(+)-ATPase, cytochrome oxidase(CYTO) and alkaline phospharase(ALP) in the lungs were measured and
Metabolic derangements in interstitial brain edema with preserved blood flow: selective vulnerability of the hippocampal CA3 region in rat hydrocephalus.
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Hydrocephalus induces interstitial brain edema, which causes neurological deficits, even if the intracranial pressure is maintained within the normal range, and the cerebral blood flow (CBF) does not decline to an ischemic level. The precise mechanisms underlying such edema-induced neuronal
Regulation of cytochrome oxidase redox state during umbilical cord occlusion in preterm fetal sheep.
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The preterm fetus is capable of surviving prolonged periods of severe hypoxia without neural injury for much longer than at term. To evaluate the hypothesis that regulated suppression of brain metabolism contributes to this remarkable tolerance, we assessed changes in the redox state of cytochrome
Changes of Ca2+-ATPase and cytochrome oxidase activity of myocardial cell under early and late ischemia:--comparison with ultrastructural changes.
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Using the histo- and cytochemical technique we assessed the Ca2+-transporting function of mitochondria (Mit) and sarcoplasmic reticulum (SR), and the ATP producing function of Mit in the ischemic myocardial cell of a dog's heart. In comparing ultrastructural ischemic changes, cytochrome oxidase (CO)
Inhibition of cytochrome oxidase and blue-light damage in rat retina.
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The activity of cytochrome oxidase, outer nuclear layer thickness, and edema were quantitatively evaluated in the blue-light exposed rat retina. Dark-adapted or cyclic-light reared rats were exposed to blue light with a retinal dose of 380 kJ/m2. Immediately, 1, 2, and 3 day(s) after exposure, the
Effects of cyclosporine pretreatment on tissue oxygen levels and cytochrome oxidase in skeletal muscle ischemia and reperfusion.
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We hypothesized that pretreatment with single-dose cyclosporine (CsA) prevents alterations and improves tissue oxygen and mitochondrial cytochrome oxidase redox (CytOx) state in skeletal muscle ischemia and reperfusion-reoxygenation (I/R). Latissimus dorsi muscle was prepared and mobilized in New
Cytochrome oxidase activity in rat retina after exposure to 404 nm blue light.
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Cytochrome oxidase (CYO), a key enzyme in the respiratory chain, was observed as an indicator of retinal metabolism after an in vivo blue light exposure. Thirty Sprague-Dawley rats were exposed to optic radiation of 404 nm with a retinal dose of 110kJ/m2. Immediately after exposure, the CYO activity
Cytochrome oxidase activity of Fuchs' endothelial dystrophy.
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The normal human corneal endothelial monolayer maintains stromal water equilibrium and thus, transparency, by means of a pump-leak mechanism. Water leaks into the stroma through non-tight lateral cell junctional complexes and is drawn out by an energy dependent cell membrane ion pump. We
Mirtazapine-induced steatosis .
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Mirtazapine is a commonly used drug indicated for the treatment of severe depression. It works as a presynaptic α2-adrenoreceptor antagonist that increases central noradrenergic and serotonergic neurotransmission, and it is metabolized by the p450 cytochrome oxidase system. There is
Inhibition of enzymes by short-wave optical radiation and its effect on the retina.
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INTRODUCTION AND HYPOTHESES: Exposure to short-wave optical radiation is a potential hazard for vision. In the present study, blue-light damage is studied in rat retina. It was hypothesized that the absorption of blue light by cytochrome oxidase in rat retina inhibits this enzyme, and may reduce the
Maturation of the mitochondrial redox response to profound asphyxia in fetal sheep.
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Fetal susceptibility to hypoxic brain injury increases over the last third of gestation. This study examined the hypothesis that this is associated with impaired mitochondrial adaptation, as measured by more rapid oxidation of cytochrome oxidase (CytOx) during profound asphyxia.
METHODS
Chronically
Anaerobic glycolysis preceding white-matter destruction in experimental neonatal hydrocephalus.
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The metabolic changes in neonatal hydrocephalus that lead to permanent brain injury are not clearly defined, nor is the extent to which these changes can be prevented by a cerebrospinal fluid shunt. To clarify these processes, cerebral glucose utilization was examined using [14C]2-deoxyglucose
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