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xanthine/hemorrhage
Link salvestatakse lõikelauale
Leht 1 alates 132 tulemused
Determination of serum adenosine deaminase and xanthine oxidase levels in patients with crimean-congo hemorrhagic fever.
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OBJECTIVE
Crimean-Congo hemorrhagic fever is an acute viral hemorrhagic fever with a high mortality rate. Despite increasing knowledge about hemorrhagic fever viruses, little is known about the pathogenesis of Crimean-Congo hemorrhagic fever. In this study, we measured serum adenosine deaminase and
Effect of a xanthine oxidase inhibitor on adenine nucleotide degradation in hemorrhagic shock.
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Biochemical effects of treatment with a xanthine oxidase inhibitor (allopurinol) were investigated in an experimental hemorrhagic shock procedure. Allopurinol pretreatment abolished the increase in plasma uric acid which occurs in untreated dogs during hemorrhagic hypotension and resulted in a much
Xanthine oxidase inhibition prevents mesenteric blood flow deficits after resuscitated hemorrhagic shock by preserving endothelial function.
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To determine the contribution of xanthine oxidase-mediated endothelial dysfunction to the blood flow deficits seen in the mesenteric circulation after resuscitated hemorrhagic shock, rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment
Xanthine oxidase-derived oxygen radicals increase lung cytokine expression in mice subjected to hemorrhagic shock.
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Acute inflammatory lung injury often complicates hemorrhagic shock, a systemic ischemia-reperfusion syndrome. Because oxygen radicals are generated during ischemia-reperfusion, and oxygen radicals can activate nuclear regulatory factors that affect transcription of proinflammatory cytokines, we
Role of xanthine oxidase inhibition in survival from hemorrhagic shock.
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The irreversible loss of adenine nucleotides and the formation of free radicals have both been suggested as causes of irreversibility following prolonged hemorrhagic shock. This study was performed to assess the effect of xanthine oxidase inhibition (allopurinol 50 mg/kg/day), free radical
Xanthine oxidase inhibition after resuscitated hemorrhagic shock restores mesenteric blood flow without vasodilation.
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To determine the contribution of xanthine oxidase-mediated reperfusion injury to the blood flow deficits seen in the intestinal microcirculation after resuscitated hemorrhagic shock, rats were prepared for intravital microscopic study then bled to 50% of baseline blood pressure for 60 min. Treatment
Hemorrhagic shock-induced bacterial translocation is reduced by xanthine oxidase inhibition or inactivation.
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Experiments were performed to determine whether bacterial translocation (BT) after hemorrhagic shock is due to a reperfusion injury mediated by xanthine oxidase-derived oxidants. Rats were subjected to 30 minutes of shock (30 mm Hg) followed by reinfusion of shed blood. Twenty-four hours after
Inhibition of xanthine oxidase does not influence immunosuppression after hemorrhagic shock.
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BACKGROUND
Resuscitated hemorrhagic shock causes global ischemia reperfusion with generation of toxic oxygen metabolites. We hypothesized that the immunosuppression that follows hemorrhagic shock may be linked to this process.
METHODS
Forty-five male Sprague-Dawley rats (weight, 250-300 g) were bled
Xanthine oxidase activity in the circulation of rats following hemorrhagic shock.
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Reactive oxygen metabolites generated from xanthine oxidase play an important role in the pathogenesis of ischemia-induced tissue injury. In a hemorrhagic shock model of ischemia-reperfusion, the intracellular enzyme xanthine oxidase was released into the vasculature. This intravascular source of
Production of uric acid in cerebrospinal fluid after subarachnoid hemorrhage in dogs: investigation of the possible role of xanthine oxidase in chronic vasospasm.
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Based on accumulating evidence of the role of xanthine oxidase (XO) in generating oxygen free radicals and causing tissue damage during ischemia, we examined the possible role of XO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). After inducing SAH in dogs by two
Interactions between CBP, NF-kappaB, and CREB in the lungs after hemorrhage and endotoxemia.
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The transcriptional regulatory factor nuclear factor (NF)-kappaB has a central role in modulating expression of proinflammatory mediators that are important in acute lung injury. In vitro studies have shown that competition between NF-kappaB and cAMP response element binding protein (CREB) for
Effect of a novel xanthine derivative on experimental ulcers in rats.
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The effects of the novel xanthine derivative 3-ethyl-1-(6-hydroxy-6-methylheptyl)-7-propylxanthine (A90 6119, CAS 134072-58-5) on various experimentally induced ulcers was investigated in rats. A90 6119 produced a dose-dependent inhibition of gastric ulcers induced by water immersion stress and
Influence of pentoxifylline and albifylline on liver microcirculation and leukocyte adhesion after hemorrhagic shock in the rat.
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The aim of this study was to evaluate the effects of two xanthine derivates, pentoxifylline (PTX) and its more metabolically stable analogue, albifylline (HWA 138), on hepatic sinusoidal perfusion and leukocyte endothelial interactions in the liver after hemorrhagic shock. Sprague-Dawley rats (n = 8
Increased plasma concentrations of activin a predict intraventricular hemorrhage in preterm newborns.
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BACKGROUND
Intraventricular hemorrhage (IVH) is a major cause of neurologic disabilities in preterm newborns. We evaluated the use of plasma activin A concentrations to predict the development of perinatal IVH.
METHODS
We measured nucleated erythrocyte (NRBC) counts, plasma activin A, hypoxanthine
Administration of glutamine after hemorrhagic shock restores cellular energy, reduces cell apoptosis and damage, and increases survival.
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BACKGROUND
Hemorrhagic shock causes a rapid depletion of adenosine triphosphate (ATP) and an increase of the terminal metabolite xanthine. Free radicals generated from xanthine oxidase play a major role in cell injury. Programmed cell death, apoptosis, is a major pathway causing reperfusion injury.
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