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Ascorbate reduces gastric bleeding after hemorrhagic shock and retransfusion in rats.
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The rat gastric mucosa, superfused with 0.1 N HCl, was investigated following 15 min of hemorrhagic shock and 30 min of retransfusion after pretreatment with ascorbate (1 mg/100 g b.w. or 5 mg/100 g b.w.). The size of the ischemic areas and the amount of mucosal bleeding using 51Cr labeling of red
Ascorbate preserves gastric mucosal metabolism and microcirculation after hemorrhagic shock and retransfusion in rats.
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The gastric mucosal microcirculation and purine nucleotide metabolism were studied in rats after hemorrhagic shock and retransfusion. The mucosal surface density of perfused vessels (SDPV) and the mucosal levels of ATP, ADP, AMP, IMP, hypoxanthine and uric acid were measured following 15 min of
Efficacy of rapid bowel preparation with new 1 L polyethylene glycol ascorbate solution in severe acute lower GI bleeding.
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Blocking of endothelial-leukocyte interaction (rolling) does not improve reflow in the rat gastric mucosa after hemorrhagic shock and retransfusion.
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The polymorphonuclear neutrophilic granulocyte (PMN) has been implicated as one possible cause of the no-reflow phenomenon seen upon reperfusion after ischemia, by, for instance, the release of toxic substances and/or microvascular flow obstruction. In the present study we studied the effects of
Effect of hyperoxia on resuscitation of experimental combined traumatic brain injury and hemorrhagic shock in mice.
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BACKGROUND
Hypotension and hypoxemia worsen traumatic brain injury outcomes. Hyperoxic resuscitation is controversial. The authors proposed that hyperoxia would improve hemodynamics and neuronal survival by augmenting oxygen delivery despite increased oxidative stress and neuroinflammation in
Oxidative stress induced by destruxin from Metarhizium anisopliae (Metch.) involves changes in glutathione and ascorbate metabolism and instigates ultrastructural changes in the salivary glands of Spodoptera litura (Fab.) larvae.
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The cyclodepsipeptidic mycotoxin, destruxin, produced by Metarhizium anisopliae is known for its larvicidal properties. The crude destruxin-treated Spodoptera litura larvae revealed a decrease in thiol content and an increment in oxidation of glutathione to glutathione disulfide and ascorbate to
Ascorbate removes key precursors to oxidative damage by cell-free haemoglobin in vitro and in vivo.
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Haemoglobin initiates free radical chemistry. In particular, the interactions of peroxides with the ferric (met) species of haemoglobin generate two strong oxidants: ferryl iron and a protein-bound free radical. We have studied the endogenous defences to this reactive chemistry in a rabbit model
Increased extracellular ascorbate release reflects glutamate re-uptake during the early stage of reperfusion after forebrain ischemia in rats.
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Ascorbate is highly concentrated in neuropils, and its extracellular release is closely related to that of the excitatory neurotransmitters. Thus, the extracellular release of ascorbate and glutamate was measured during the early stage of forebrain ischemia-reperfusion in the rat hippocampus using a
Comparison of the anti-scorbutic activity of L-ascorbic acid and Ester C in the non-ascorbate synthesizing Osteogenic Disorder Shionogi (ODS) rat.
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The Osteogenic Disorder Shionogi (ODS) rat, Clea Inc., Tokyo, Japan lacks the ability to synthesize L-ascorbic acid (AA). As with man, monkey and the guinea pig, this rat lacks L-gulonolactone oxidase necessary for the synthesis of AA from glucose. This study shows this animal to be an alternative
Roles of histamine receptors and oxyradicals in aggravation of acid-induced gastric haemorrhagic ulcers in endotoxaemic rats.
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We clarified the roles of histamine H(1)-, H(2)-, H(3)-receptors and oxyradicals in the exacerbation of acid-induced gastric haemorrhage and stomach ulcer in endotoxaemic rats by measuring changes in gastric mucosal glutathione concentrations, lipid peroxide generation and histamine levels as well
A high-throughput screening assay of ascorbate in brain samples.
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Ascorbate is a vital reductant/free radical scavenger in the CNS, whose content defines - to a large extent - the redox status and the antioxidant reserves. Quick, reliable and specific methods for its measurement in brain samples are highly desirable. We have developed a new high-throughput
Ascorbate regulation of collagen biosynthesis in Ehlers-Danlos syndrome, type VI.
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We studied two unrelated individuals with Ehlers-Danlos syndrome type VI, which is characterized by congenital hypotonia, lax joints, severe kyphoscoliosis, friable skin, and hemorrhagic hypotrophic scars. The diagnosis was confirmed by decreased hydroxylysine residues in dermal collagen and
High plasma ascorbic acid levels in premature neonates with intraventricular hemorrhage.
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The accumulation of ascorbic acid in the brain by active transport establishes a high brain-plasma gradient of the vitamin. An insult to the CNS may result in an efflux of ascorbate into the circulation with a consequent rise of plasma levels. We measured plasma ascorbic acid levels in premature
Relationship between hemorrhagic ocular diseases and vitamin C deficiency: clinical and experimental data.
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The hematic level of ascorbic acid was significantly lower with respect to that of healthy subjects in 55 patients with hemorrhagic ocular diseases. Experiments on albino guinea pigs showed that an induced hypovitaminosis C (2 weeks of scorbutigenic diet followed by a maintenance dose of 0,5 mg of
[Glucose, ascorbic acid and hydrogen peroxide as ingredients of endoscopic hemostasis in bleeding ulcer].
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Glucose and ascorbate used for endoscopic hemostasis metabolic preventive to prevent recurrent ulcer bleeding. Unacceptable joint use in endohemostasis ascorbate and hydrogen peroxide.
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