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oxidase/verenvuoto
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Sivu 1 alkaen 547 tuloksia
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
Extracellular matrix modulator lysyl oxidase colocalizes with amyloid-beta pathology in Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis--Dutch type.
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Accumulation of amyloid-beta (Aβ) in brain vessel walls and parenchyma, known as cerebral amyloid angiopathy (CAA) and senile plaques (SPs), respectively, plays a key role in Alzheimer's disease (AD) and hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D) pathogenesis.
[Effects of Nao-Yi-An granule on activity of cytochrome c oxidase in hippocampus of experimental intracerebral hemorrhagic rats].
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OBJECTIVE
To explore the neuronal protective effects of a traditional Chinese medicine complex Nao-Yi-An granule(NYA) on experimental intracerebral hemorrhage(ICH) in rats.
METHODS
Eighty collagenase-induced ICH rats were used. At 12 h, 24 h, 2 d, 4 d, 7 d, cytochrome c oxidase(CO) activity was
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
[Effect of temperature of fluid infusion on diamine oxidase, MB isoenzyme of creatine kinase, creatine-kinase and lactate dehydrogenase in hemorrhagic shock rabbits].
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OBJECTIVE
To investigate the effects of different temperatures of fluid infusion on diamine oxidase(DAO), MB isoenzyme of creatine kinase (CK-MB), creatine kinase (CK) and lactate dehydrogenase (LDH) in rabbit with hemorrhagic shock so as to provide a clue to improve the nursing care in patients
Dependence of liver injury after hemorrhage/resuscitation in mice on NADPH oxidase-derived superoxide.
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Hemorrhagic shock and resuscitation cause hepatocellular damage by mechanisms involving oxidative stress. However, the sources of free radicals mediating hepatocellular injury remain controversial. Thus, this study tested the hypothesis that NADPH oxidase plays a role in producing hepatocellular
Gene damages of mitochondrial DNA encoding cytochrome oxidase of intestinal epithelial cells in hemorrhagic shock rats.
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OBJECTIVE
To investigate the detrimental effects of hemorrhagic shock on the structure and function of mitochondria DNA (mtDNA) encoding cytochrome oxidase genes in intestinal epithelial cells.
METHODS
Wistar rats were used and divided into two groups: hemorrhagic shock group and control group.
Inhibitors of NADPH oxidase reduce the organ injury in hemorrhagic shock.
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Reactive oxygen species contribute to the multiple organ dysfunction syndrome in hemorrhagic shock. Here, we investigate the effects of two chemically distinct inhibitors of NADPH oxidase on the circulatory failure and the organ dysfunction and injury associated with hemorrhagic shock in the
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
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