purine/hypoxia

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Endothelial cells cope with hypoxia-induced depletion of ATP via activation of cellular purine turnover and phosphotransfer networks.

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Intravascular ATP and adenosine have emerged as important regulators of endothelial barrier function, vascular remodeling and neovascularization at various pathological states, including hypoxia, inflammation and oxidative stress. By using human umbilical vein endothelial cells (HUVEC) and bovine

Changes by short-term hypoxia in the membrane properties of pyramidal cells and the levels of purine and pyrimidine nucleotides in slices of rat neocortex; effects of agonists and antagonists of ATP-dependent potassium channels.

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In a first series of experiments, intracellular recordings were made from pyramidal cells in layers II-III of the rat primary somatosensory cortex. Superfusion of the brain slice preparations with hypoxic medium (replacement of 95%O2-5%CO2 with 95%N2-5%CO2) for up to 30 min led to a time-dependent

Release of adenosine and other purines from hippocampal slices stimulated electrically or by hypoxia/hypoglycemia. Effect of chlormethiazole.

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The ATP stores of rat hippocampal slices were labelled with [3H]-adenine. The efflux of endogenous and [3H]-purines was stimulated electrically or by combined hypoxia/hypoglycemia. The efflux of endogenous adenosine, inosine and hypoxanthine was also increased. Chlormethiazole (30-300 microM)

Identification of agents that reduce renal hypoxia-reoxygenation injury using cell-based screening: purine nucleosides are alternative energy sources in LLC-PK1 cells during hypoxia.

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Acute tubular necrosis is a clinical problem that lacks specific therapy and is characterized by high mortality rate. The ischemic renal injury affects the proximal tubule cells causing dysfunction and cell death after severe hypoperfusion. We utilized a cell-based screening approach in a

Purine and pyrimidine metabolism and electrocortical brain activity during hypoxemia in near-term lambs.

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Insufficient cerebral O(2) supply leads to brain cell damage and loss of brain cell function. The relationship between the severity of hypoxemic brain cell damage and the loss of electrocortical brain activity (ECBA), as measure of brain cell function, is not yet fully elucidated in near-term

Interstitial purine metabolites and lactate during regional myocardial hypoxia.

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OBJECTIVE Adenosine is a well known vasodilator believed to contribute to metabolic adjustments of the coronary circulation. The purpose of this study was to assess changes in interstitial fluid adenosine, adenosine metabolites, and lactate during prolonged regional, non-ischaemic myocardial

Influence of perinatal hypoxia on purine contents in erythrocytes of newborn infants.

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Alterations in the levels of hypoxanthine and some other purine derivatives occurring in the erythrocytes from umbilical cord blood of newborn infants with perinatal hypoxia were examined. Newborn babies were divided into two groups which included infants with favourable (Group 1) and complicated

The effect of hypoxia on the activity of purine nucleoside phosphorylase in rats.

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The activity of purine nucleoside phosphorylase (PNP) in rat erythrocytes fractionated by centrifugation in microhematocrit capillaries was studied. After seven-day hypoxia (54 kPa) the PNP activity was increased by 67 +/- 4% (S.E.M.) in the lightest fraction of erythrocytes; on the fifth day after

Comparison of cord purine metabolites to maternal and neonatal variables of hypoxia.

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Umbilical arterial concentrations of purine metabolites were evaluated prospectively as markers of hypoxia. The results suggest that hypoxanthine accumulates in association with fetal acidosis and reduced levels of buffer base (P less than .01). Acute hypoxemia defined by umbilical arterial oxygen

[Effect of chronic intrauterine hypoxia on purine compound metabolism in the erythrocytes of newborn infants in the early neonatal period].

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The content of purine compounds in red blood cells was measured and compared in 21 neonates with a history of chronic intrauterine hypoxia, depending on the condition at birth and the early period of adaptation. The content of purine compounds in whole blood was measured at the moment of birth and

Purine metabolites and lactate as parameters of hypoxia in the newborn infant.

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In order to evaluate possible biochemical parameters of tissue hypoxia, arterial samples from 29 sick neonates were taken at 6-h intervals for lactate and blood gas analyses, as well as assays of purine metabolites in plasma. The state of the infant at each sampling was arbitrarily classified as

HIF-1 alpha is an essential effector for purine nucleoside-mediated neuroprotection against hypoxia in PC12 cells and primary cerebellar granule neurons.

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Hypoxia-inducible factor-1 alpha (HIF-1alpha) and purine nucleosides adenosine and inosine are critical mediators of physiological responses to acute and chronic hypoxia. The specific aim of this paper was to evaluate the potential role of HIF-1alpha in purine-mediated neuroprotection. We show that

Purine nucleosides support the neurite outgrowth of primary rat cerebellar granule cells after hypoxia.

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Mammalian neurons require a constant supply of oxygen to maintain adequate cellular functions and survival. Following sustained hypoxia during ischemic events in brain, the energy status of neurons and glia is compromised, which may subsequently lead to cell death by apoptosis and necrosis.

[Purine base metabolism in the mother-placenta-fetus system in experimental hypoxia].

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In acute deficiency of oxygen inhibition of purine bases turnover as well as degradation of their high molecular precursors occurred in the system mother-placenta-fetus. Acute hypoxia was accompanied by distinct increase in content of adenine, xanthine + + guanine and uric acid in blood of pregnant

Purine nucleoside-mediated protection of chemical hypoxia-induced neuronal injuries involves p42/44 MAPK activation.

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Hypoxia in brain may lead to cell death by apoptosis and necrosis. Concomitant is the formation of purine nucleosides, e.g. adenosine, a powerful endogenous neuroprotectant. Despite vigorous studies, many aspects of the mechanisms involved in purine-based protection are still unclear. In this study,

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