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allopurinol/hypoxia
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Influence of hypoxanthine, allopurinol and adenine on resistance of rats and hamsters to hypobaric hypoxia.
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The survival time of rats and hamsters in lethal hypoxia was measured after a sublethal exposure and a normoxia break, at the beginning of which purines were administered intraperitoneally in the following dosages: 25 mg/kg hypoxanthine, 50 mg/kg allopurinol, 25 mg/kg adenine. In rats,
Effect of allopurinol on hypoxia-induced modification of the NMDA receptor in newborn piglets.
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The present study tests the hypothesis that pretreatment with allopurinol, a xanthine oxidase inhibitor, will prevent modification of the NMDA receptor during cerebral hypoxia in newborn piglets. Eighteen newborn piglets were studied. Six normoxic control animals were compared to six untreated
Allopurinol protects enterocytes from hypoxia-induced apoptosis in vivo.
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BACKGROUND
Reactive oxygen species can cause apoptosis and may be involved in hypoxic injury to the small bowel. Xanthine oxidase (XO) has been implicated in reactive oxygen species production. We hypothesized that administration of allopurinol would protect rat enterocytes from hypoxia-induced
Does allopurinol prevent myocardial injury as a result of hypoxia-re-oxygenation in rats?
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We made use of the xanthine oxidase inhibitor allopurinol and examined changes related to myocardial injury of the rat heart during hypoxia-re-oxygenation. The rat heart was perfused using the Langendorff method. With low-oxygen perfusion for 60 min in a solution saturated with mixed gases of 95% N2
Study of rat hepatocytes in primary culture submitted to hypoxia and reoxygenation: action of the cytoprotectors prostaglandin E1, superoxide dismutase, allopurinol and verapamil.
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Exposure of hepatocytes to pathological conditions in a microenvironment of hypoxia and reoxygenation is very frequent in hepatic diseases. Several substances present perspectives for cytoprotective action on hepatocyte submitted to reoxygenation after hypoxia and simple hypoxia.
We research
Failure of allopurinol to protect against cerebral injury when given after the start of hypoxia.
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One cause of ischemic brain injury is free radical formation during recirculation. Allopurinol inhibits xanthine oxidase, an important source of free oxygen radicals. It is known that allopurinol pre-treatment has a protective action during cerebral ischemia. In the present study we exposed slices
Behavioral and neurodevelopmental outcome of children after maternal allopurinol administration during suspected fetal hypoxia: 5-year follow up of the ALLO-trial.
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OBJECTIVE
To evaluate the long-term neurodevelopmental and behavioral outcome of antenatal allopurinol treatment during suspected fetal hypoxia.
METHODS
We studied children born from women who participated in a randomized double-blind placebo controlled multicenter study (ALLO-trial). Labouring
Nucleotide concentrations in hepatocytes during anoxia and reoxygenation in presence of allopurinol and oxypurinol.
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In hepatocytes of starved rats nucleotide, nucleoside and nucleobase concentrations were measured during and following anoxia. A complete restoration of ATP is observed during reoxygenation after anoxic periods less than 60 minutes. GTP cannot be completely restored after 30 minutes of anoxia.
Effect of allopurinol on uric acid levels and brain cell membrane Na+,K(+)-ATPase activity during hypoxia in newborn piglets.
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Oxygen-free radicals generated by xanthine oxidase during hypoxia-ischemia may result in cellular injury through harmful effects on membrane phospholipids. The present study investigated the effect of administration of allopurinol, an inhibitor of xanthine oxidase, on free-radical generation and
Dose-dependent effects of allopurinol on human foreskin fibroblast cells and human umbilical vein endothelial cells under hypoxia.
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Allopurinol, an inhibitor of xanthine oxidase, has been used in clinical trials of patients with cardiovascular and chronic kidney disease. These are two pathologies with extensive links to hypoxia and activation of the transcription factor hypoxia inducible factor (HIF) family. Here we analysed the
Early midzonal cell death during low-flow hypoxia in the isolated, perfused rat liver: protection by allopurinol.
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Trypan blue uptake and lactate dehydrogenase release were measured as indices of irreversible cell damage in isolated, perfused rat livers during low-flow hypoxia. In livers from fasted rats perfused in the anterograde direction, trypan blue uptake took place beginning at about 45 min of hypoxia.
Superoxide dismutase and allopurinol prevent the pressor effects of angiotensin II and histamine in the guinea-pig isolated perfused lung exposed to hypoxia.
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1. In the guinea-pig isolated perfused lung exposed to hypoxia by infusing N2-gassed Krebs solution, angiotensin II and histamine produced a reduced vasoconstrictor response when compared with the responses obtained in nonhypoxic lung. 2. These reduced vasoconstrictor responses were prevented by
Gastric mucosal electrical potential difference, pH, blood flow, and morphology during hypoxia and selective gastric ischaemia with and without allopurinol pretreatment in anaesthetized dogs.
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Ischaemia has been implicated in the pathogenesis of gastric mucosal disorders. The aim of this investigation was to study the gastric mucosal electrical potential difference (PD), pH, blood flow and morphology during hypoxia, gastric ischaemia, and gastric ischaemia following inhibition of free
Allopurinol modulates reactive oxygen species generation and Ca2+ overload in ischemia-reperfused heart and hypoxia-reoxygenated cardiomyocytes.
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Myocardial oxidative stress and Ca2+ overload induced by ischemia-reperfusion may be involved in the development and progression of myocardial dysfunction in heart failure. Xanthine oxidase, which is capable of producing reactive oxygen species, is considered as a culprit regarding
Effects of allopurinol on cardiac function and oxidant stress in chronic intermittent hypoxia.
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BACKGROUND
Obstructive sleep apnea is associated with left ventricular (LV) dysfunction, oxidant stress, and chronic intermittent hypoxia (CIH). Allopurinol (ALLO) is a xanthine oxidase inhibitor that also scavenges free radicals.
OBJECTIVE
Using an animal model of CIH we hypothesized that ALLO
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