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Strana 1 od 102 výsledky
The measurement of hypoxanthine, xanthine, inosine and uridine in umbilical cord blood and fetal scalp blood samples as a measure of fetal hypoxia.
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Hypoxanthine, xanthine, inosine, urate and uridine, were measured in 149 samples of umbilical cord plasma using high pressure liquid chromatography. In spite of a good correlation with the simpler oxygen consumption method for measuring hypoxanthine, there was no clear discrimination between hypoxic
Avian vitreous humor concentrations of inosine, hypoxanthine, xanthine, uric acid, uracil and uridine as influenced by age and sex: their relevance as indicators of ante-mortem hypoxia.
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An investigation was made to determine the effects of age and sex on postmortem concentrations (mumol/l) of inosine, hypoxanthine, xanthine, uric acid, uracil and uridine in the vitreous humor of chickens (Gallus domesticus). Five male and 5 female chickens were sampled each week from 0-10 weeks of
Dynamic Restructuring of the Myocardial Mitochondria in Response to Uridine Modulation of the Activity of Mitochondrial ATP-Dependent Potassium Channel under Conditions of Acute Hypoxic Hypoxia.
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We studied the effects of in vivo modulation of activity of mitochondrial ATP-dependent potassium channel (mitoKATP) by uridine on the morphofunctional state of mitochondria in rat cardiomyocytes under conditions of acute hypoxia. Preinjection of uridine to animals reduced the number of
Cerebrospinal fluid concentrations of hypoxanthine, xanthine, uridine and inosine: high concentrations of the ATP metabolite, hypoxanthine, after hypoxia.
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CSF obtained for clinical purposes from newborn, children and adults has been analysed by high pressure liquid chromatography for hypoxanthine, xanthine, inosine, uridine and urate. Large rises in hypoxanthine and to a lesser extent xanthine occur for about 24 h after hypoxia. High concentrations
Uridine as a protector against hypoxia-induced lung injury.
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The effect of the activation of the mitochondrial ATP-dependent potassium channel (mitoKATP) on the ultrastructure of rat lung in acute hypoxic hypoxia (7% of oxygen in nitrogen, exposure 30 min) was studied. It was shown that uridine, a precursor of the mitoKATP activator UDP,
Direct effects of graded hypoxia on intact and denuded rabbit cranial arteries.
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In isolated rabbit common carotid, internal carotid, and basilar arteries denuded of endothelium, mounted for measurement of contractile activity, and contracted with 10 microM serotonin (common and internal carotid) or 100 microM uridine 5'-triphosphate (UTP; basilar), 20 min of severe (PO2 = 15
Opposite alterations in cerebrospinal fluid uridine after severe cerebral ischemia or intrathecal blood injection.
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1. Rats which survived hypoglycemia by insulin, hypoxia by 10% O2, or ischemia by carotid ligation and hypotension to 40 mm Hg, evidenced no changes in cerebrospinal fluid (CSF) uridine. Animals which died soon after the above interventions or as a result of KCl-induced cardiac arrest had elevated
Response of human mature adipocytes to hypoxia-reoxygenation.
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OBJECTIVE
Adipocytes are metabolically active cells and have endocrine functions, such as cytokine secretion. Notably, adipocytes are found underneath skin and are thought to be involved in the body's response to ischemia-reperfusion (I-R). I-R injury is an important factor in the pathogenesis of
Serial expression of hypoxia inducible factor-1α and neuronal apoptosis in hippocampus of rats with chronic ischemic brain.
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OBJECTIVE
The purpose of this study is to investigate serial changes of hypoxia-inducible factor 1α (HIF-1α), as a key regulator of hypoxic ischemia, and apoptosis of hippocampus induced by bilateral carotid arteries occlusion (BCAO) in rats.
METHODS
Adult male Wistar rats were subjected to the
[Elimination of disorders of the elasticity and contractile function of nonischemic portions of the heart in myocardial infarct by using glucose and uridine].
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A study of an isolated auricle showed that one day after the infarction the extensibility of the atrial myocardium was reduced, the Starling curve was depressed to result in about a two-fold decrease of the peak systolic tension, and atrial myocardial resistance to hypoxia and excessive calcium was
Effect of electrical convulsions on uridine labeling and activity pattern in nerve cells in mice.
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Male white mice were exposed to electroshock and then injected intravenously with 5-[3H]uridine immediately after the shock. After 5, 30, or 60 min or 6, 12, or 24 h, the mice were killed, microautoradiographs were prepared, and grains were counted in the cortex, hippocampus, and basal ganglia. The
Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct.
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We have previously found that uridine 5'-triphosphate (UTP) significantly reduced cardiomyocyte death induced by hypoxia via activating P2Y(2) receptors. To explore the effect of UTP following myocardial infarction (MI) in vivo we studied four groups: sham with or without LAD ligation, injected with
Tissue-specific changes in RNA synthesis in vivo during anoxia in crucian carp.
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The overall energy budget for protein synthesis (i.e., transcription plus translation) is thought to consist of fixed and variable components, with RNA synthesis accounting for the former and protein synthesis the latter. During anoxia, the downregulation of protein synthesis (i.e., the variable
Uridine-5'-triphosphate (UTP) maintains cardiac mitochondrial function following chemical and hypoxic stress.
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Previously we found that uridine-5'-triphosphate (UTP) significantly decreased cultured cardiomyocyte death, induced by hypoxia via activating P2Y(2) receptors, reduced infarct size and maintained higher ATP levels in an in vivo model. Mitochondrial contribution to the progression of cardiomyocyte
Uridine prodrug improves memory in Tg2576 and TAPP mice and reduces pathological factors associated with Alzheimer's disease in related models.
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Uridine prodrug PN401 has been shown to have neuroprotective effects in models of Parkinson's disease and Huntington's disease. These age-related neurodegenerative diseases including Alzheimer's disease (AD) are associated with mitochondrial dysfunction, oxidative stress, and inflammation.
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