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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
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
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
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
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
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
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
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
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
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
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
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
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 and ascorbate used for endoscopic hemostasis metabolic preventive to prevent recurrent ulcer bleeding. Unacceptable joint use in endohemostasis ascorbate and hydrogen peroxide.