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ascorbate/edema

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Ascorbate inhibits edema in brain slices.

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Ascorbate is an essential antioxidant in the CNS, localized predominantly in neuronal cytosol. Slices of mammalian brain rapidly lose ascorbate, however, when incubated in ascorbate-free media; brain slices also take up water and swell. Here we investigated water gain in coronal slices of rat

[Intravenous treatment of intracranial hypertension and cerebral edema with stabilized solutions of glycerol-sodium ascorbate].

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The blood-aqueous humor barrier in adult rhesus monkeys was opened by intracarotid infusion of a 25% mannitol solution. Each monkey had one to four infusions into the same artery, with at least one week between subsequent procedures. The monkeys were observed clinically for 3 to 212 days. Within an

Use of ascorbate in the preparation and maintenance of brain slices.

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Ascorbate and glutathione (GSH) are normally concentrated in brain cells at millimolar levels. However, both of these low-molecular-weight antioxidants are washed out of mammalian brain tissue during slice preparation and subsequent incubation. Ascorbate, which is not synthesized in the brain, can

A comparison of ascorbate and glucose transport in the heart.

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Multiple indicator-dilution experiments were done to compare the transcapillary exchange of tracer amounts of L-[14C]ascorbate and D-[3H]glucose (against an intravascular reference 131I-albumin) in Ringer-perfused (5 mM glucose) isolated rabbit hearts. The indicator-dilution curves for the two were

Ascorbic acid repletion: A possible therapy for diabetic macular edema?

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Macular edema poses a significant risk for visual loss in persons with diabetic retinopathy. It occurs when plasma constituents and fluid leak out of damaged retinal microvasculature in the area of the macula, causing loss of central vision. Apoptotic loss of pericytes surrounding capillaries is

Brain edema induced by in vitro ischemia: causal factors and neuroprotection.

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Decreased cerebral blood flow, hence decreased oxygen and glucose, leads to ischemic brain injury via complex pathophysiological events, including excitotoxicity, mitochondrial dysfunction, increased intracellular Ca2+, and reactive oxygen species (ROS) generation. Each of these could also

The glial antioxidant network and neuronal ascorbate: protective yet permissive for H(2)O(2) signaling.

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Increasing evidence implicates reactive oxygen species, particularly hydrogen peroxide (H(2)O(2)), as intracellular and intercellular messengers in the brain. This raises the question of how the antioxidant network in the brain can be sufficiently permissive to allow messages to be conveyed yet, at

Pulmonary edema fluid antioxidants are depressed in acute lung injury.

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OBJECTIVE To test the hypothesis that low concentrations of distal airspace water-soluble antioxidants are associated with acute lung injury. METHODS Prospective, cohort study. METHODS Medical intensive care unit of two tertiary care hospitals. METHODS Subjects were 29 patients with acute lung
Endogenous nitric oxide (NO, endothelium-derived relaxing factor) was stimulatory for histamine- and suppressive for serotonin-induced paw edema of mice. This action was mediated by guanosine 3',5'-cyclic monophosphate production. Local injection of superoxide dismutase (SOD), catalase,

A pilot clinical study of continuous intravenous ascorbate in terminal cancer patients.

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Case studies suggest that vitamin C, given intravenously at doses of 10-100 grams/day can improve patient well being and in some cases, reduce tumor size. While ascorbate is generally considered safe, clinical data on high intravenous doses is limited. Twenty-four late stage terminal cancer patients

Protective effect of vitreous against hemoglobin neurotoxicity.

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Hemorrhage into the brain parenchyma or subarachnoid space is associated with edema and vascular injury that is likely mediated at least in part by the toxicity of hemoglobin. In contrast, extravascular blood appears to be less neurotoxic when localized to the retina or adjacent vitreous, the gel

Oxidative stress and abnormal cholesterol metabolism in patients with adult respiratory distress syndrome.

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Oxidative stress has been implicated in the adult respiratory distress syndrome (ARDS). In this study, we determined the levels of selected antioxidants in the plasma of 25 patients with ongoing ARDS and 16 healthy control subjects. We also examined these plasmas and pulmonary edema fluid of ARDS

Ascorbic acid prevents VEGF-induced increases in endothelial barrier permeability.

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Vascular endothelial growth factor (VEGF) increases endothelial barrier permeability, an effect that may contribute to macular edema in diabetic retinopathy. Since vitamin C, or ascorbic acid, can tighten the endothelial permeability barrier, we examined whether it could prevent the increase in
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