ascorbic-acid and Carbon-Monoxide-Poisoning

ascorbic-acid has been researched along with Carbon-Monoxide-Poisoning* in 7 studies

Other Studies

7 other study(ies) available for ascorbic-acid and Carbon-Monoxide-Poisoning

ArticleYear
Preclinical evaluation of injectable reduced hydroxocobalamin as an antidote to acute carbon monoxide poisoning.
    The journal of trauma and acute care surgery, 2015, Volume: 79, Issue:4 Suppl 2

    Current management of acute inhalational carbon monoxide (CO) toxicity includes hyperbaric or normobaric O2 therapy. However, efficacy has not been established. The purpose of this study was to establish therapeutic proof of concept for a novel injectable antidote consisting of the combination of hydroxocobalamin and ascorbic acid into a reduced form (B12r) as demonstrated by clinically significant increase (>500 ppm) in CO2 production, reduced carboxyhemoglobin (COHgb) half-life (COHgb t1/2), and increased cerebral O2 delivery and attenuation of CO-induced microglial damage in a preclinical rodent model of CO toxicity.. B12r-mediated conversion of CO to CO2 and COHgb t1/2 in human blood were measured by gas analysis and Raman resonance spectroscopy. Rats were exposed to either air or CO and then injected with saline or B12r. Cognitive assessment was tested in a Morris water maze. Brain oxygenation was measured with Licox. Brain histology was assessed by fluorescent antibody markers and cell counts.. B12r resulted in significant CO2 production (1,170 ppm), compared with controls. COHgb t1/2 was reduced from 33 minutes (normal saline) to 17.5 (p < 0.001). In rat models, severe CO-induced brain hypoxia (PbtO2, 18 mm Hg) was followed by significant reduction in τ25 to 12 minutes for B12r rats versus 40 minutes for normal saline-treated rats (p < 0.0001). There was major attenuation of CO-induced microglial damage, although cognitive performance differences were minimal.. Our preclinical data suggest that the novel synergism of hydroxocobalamin with ascorbic acid has the potential to extract CO through conversion to CO2, independently of high-flow or high-pressure O2. This resulted in a clinically significant off-gassing of CO2 at levels five to eight times greater than those of controls, a clinically significant reduction in COHgb half-life, and evidence of increased brain oxygenation and amelioration of myoglial damage in rat models. Reduced hydroxocobalamin has major potential as an injectable antidote for CO toxicity.

    Topics: Animals; Antidotes; Ascorbic Acid; Carbon Monoxide Poisoning; Humans; Hydroxocobalamin; Immunohistochemistry; In Vitro Techniques; Male; Maze Learning; Microscopy, Confocal; Oxygen Inhalation Therapy; Rats; Rats, Long-Evans; Rats, Sprague-Dawley; Spectrum Analysis, Raman

2015
Involvement of extracellular ascorbate and iron in hydroxyl radical generation in rat striatum in carbon monoxide poisoning.
    Toxicology, 2009, Oct-01, Volume: 264, Issue:1-2

    Carbon monoxide (CO) poisoning stimulated generation in rat striatum of toxic hydroxyl radicals (*OH), which might participate in the CO-induced neuronal injury. Since an increase in extracellular ascorbate (AA) stimulated *OH generation in the presence of endogenous metals, including iron, in rat striatum in vivo, we examined the role of extracellular AA in *OH generation due to CO poisoning in the present study. The CO-induced *OH generation in the striatum was strongly suppressed by intrastriatal administration of active, but not inactivated, AA oxidase, which degrades extracellular AA. In addition, CO poisoning caused a significant increase in extracellular AA in rat striatum, suggesting a role of extracellular AA in the CO-induced *OH generation. However, the time-course of changes in extracellular AA could not be completely superimposed on that of the CO-induced *OH generation. On the other hand, the CO-induced *OH generation was completely suppressed by an iron chelator, deferoxamine. These findings suggest that *OH generation in rat striatum due to CO poisoning may involve both extracellular AA and chelatable iron.

    Topics: Ammonia; Animals; Antioxidants; Ascorbate Oxidase; Ascorbic Acid; Brain Chemistry; Carbon Monoxide Poisoning; Catechols; Hydroxybenzoates; Hydroxyl Radical; Iron; Iron Chelating Agents; Male; Microdialysis; Neostriatum; Rats; Rats, Sprague-Dawley; Stereotaxic Techniques

2009
[Resuscitation treatment of patients with carbon monoxide poisoning].
    Minerva anestesiologica, 1973, Volume: 39, Issue:6

    Topics: Ascorbic Acid; Carbon Monoxide Poisoning; Dihydroxyphenylalanine; Exchange Transfusion, Whole Blood; Humans; Hyperbaric Oxygenation; Resuscitation

1973
[On a very grave case of acute carbon monoxide poisoning favorably resolved with high doses of ascorbic acid with L-dopa].
    Minerva anestesiologica, 1971, Volume: 37, Issue:11

    Topics: Adult; Ascorbic Acid; Carbon Monoxide Poisoning; Dihydroxyphenylalanine; Humans; Male

1971
[The effect of prolonged, combined exposure to carbon monoxide, nitric oxide and ammonia on the supply and demand of the human organism in relation to vitamins A, B1, B2, B6, PP and C].
    Gigiena truda i professional'nye zabolevaniia, 1969, Volume: 13, Issue:7

    Topics: Ammonia; Ascorbic Acid; Carbon Monoxide Poisoning; Humans; Niacinamide; Nitric Oxide; Occupational Medicine; Pyridoxine; Riboflavin; Thiamine; Time Factors; Vitamin A; Vitamins

1969
[The character of the combined action of sulfurous gas and carbon monoxide in their simultaneous presence in the atmosphere].
    Gigiena i sanitariia, 1968, Volume: 33, Issue:4

    Topics: Adrenal Glands; Air Pollution; Animals; Ascorbic Acid; Carbon Monoxide Poisoning; Chronaxy; Environmental Exposure; Rats; Sulfur Dioxide

1968
[Capacity of some tissues of the animal body to regenerate dehydroascorbic acid in chronic carbon monoxide poisoning].
    Zdravookhranenie Belorussii, 1962, Volume: 8

    Topics: Air Pollutants; Animals; Ascorbic Acid; Carbon Monoxide; Carbon Monoxide Poisoning; Dehydroascorbic Acid; Vitamins

1962