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hypoxanthine/инфаркт
Линкът е запазен в клипборда
Страница 1 от 59 резултата
A comparative study of the concentrations of hypoxanthine, xanthine, uric acid and allantoin in the peripheral blood of normals and patients with acute myocardial infarction and other ischaemic diseases.
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The aim of this study was the elucidation of the role of the xanthine oxidoreductase in the purine metabolism in ischaemic diseases of man. The serum concentrations of hypoxanthine, xanthine, uric acid and allantoin were determined in peripheral blood samples from patients with angina pectoris,
[Hypoxanthine content of peripheral venous blood in infarct and ischemia of the myocardium].
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Uric acid infarctions in the kidneys of newborn infants. A study on the changing incidence and on oxypurine ratios.
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Among 1115 newborns who died during 1957--1976, 136 (12.2%) showed macroscopic renal uric acid infarctions. The incidence depended on the age of the infants and their fluid supply during the first days of life. After introduction of parenteral alkali-glucose infusion in the treatment of perinatal
[Metabolic pool of purine and pyrimidine compounds in the venous blood of patients with myocardial infarction and stenocardia].
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Venous blood acid-soluble fraction was investigated by means of high-efficiency liquid chromatography in patients with myocardial infarction and angina pectoris. Myocardial ischemia is shown to result in marked changes of purine and pyrimidine metabolism. A rise in intermediate and end products of
Post-mortem hypoxanthine levels in the vitreous humour. An introductory report.
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Post-mortem hypoxanthine levels in vitreous humour were determined in 86 consecutive legal autopsy cases. In cases of sudden death caused by trauma or by myocardial infarction, levels ranging from 0 to 540 mumol/l were found. The mean value was about ten times higher than normal in vivo plasma
Allopurinol therapy of ischemic heart disease with infarct extension.
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OBJECTIVE
Free radicals produced by the hypoxanthine-xanthine oxidase reaction in ischemia/reperfusion experiments have been proposed as contributing to myocardial cell necrosis in acute myocardial infarction. In this study, the hypothesis was tested that a commonly observed late phase of necrosis,
Myocardial salvage with trolox and ascorbic acid for an acute evolving infarction.
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Both Trolox (a water-soluble analogue of alpha-tocopherol) and ascorbic acid were more effective than superoxide dismutase or catalase in protecting myocyte cell cultures from free radical attack (induced by hypoxanthine and xanthine oxidase). In a canine model of two hours of left anterior
Failure of the xanthine oxidase inhibitor allopurinol to limit infarct size after ischemia and reperfusion in dogs.
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During the acute phase of myocardial ischemia, adenine nucleotides are degraded to nucleosides and bases, especially inosine and hypoxanthine. Simultaneously, xanthine dehydrogenase is converted to xanthine oxidase, an enzyme that converts hypoxanthine to xanthine, and xanthine to uric acid,
Arrhythmias and infarction in the ischemic pig heart are not mediated by xanthine oxidase-derived free oxygen radicals.
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Xanthine oxidase activities of pig myocardium and blood during and following myocardial ischemia were measured using HPLC, and electrochemical detection of hypoxanthine, xanthine and uric acid. Myocardial ischemia was produced by occluding the anterior descending coronary artery two-thirds of the
Xanthine oxidase inhibition does not limit canine infarct size.
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BACKGROUND
Evidence supporting the role of xanthine oxidase in myocardial reperfusion injury is based on studies with pharmacological interventions used to inhibit enzyme function. Controversy exists, however, regarding the true role of xanthine oxidase in reperfusion injury. This study was
Effect of ischemia and infarction on regional content of adenine nucleotides and derivatives in canine left ventricle.
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Samples of myocardium from four areas of ischemic and infarcted canine ventricle were examined over a 20-day period for content of the three adenine nucleotides as well as inosine, hypoxanthine, adenosine, and inosine monophosphate. The adenosine triphosphate (ATP) content of central and peripheral
Infarct size reduction with the nucleoside transport inhibitor R-75231 in swine.
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Adenosine (Ado) has been reported to be cardioprotective in several models of myocardial ischemia. The nucleoside transport inhibitor R-75231 (R-75) has been reported to enhance local Ado concentrations and postischemic recovery of function, but little is known regarding its effects on myocardial
Adenosine deaminase inhibition augments interstitial adenosine but does not attenuate myocardial infarction.
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OBJECTIVE
The objectives were to determine the effects of the adenosine deaminase inhibitor pentostatin (deoxycoformycin) on interstitial fluid (ISF) adenosine before, during, and after myocardial ischaemia and to ascertain whether augmented endogenous ISF adenosine reduces myocardial
Purine metabolites in the CSF in presenile and senile dementia of Alzheimer type, and in multi infarct dementia.
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Concentrations of hypoxanthine, xanthine, uric acid and creatinine were measured in CSF of patients suffering form presenile and senile dementia of Alzheimer type (PDAT, SDAT) and multi infarct dementia (MID) and in a reference group of young neurotic patients. There was no difference in
Effects of ischemia, preconditioning, and adenosine deaminase inhibition on interstitial adenosine levels and infarct size.
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In order to examine the relationship between local adenosine concentrations before, during, and after ischemia and the extent of ischemic myocardial damage, measurements of interstitial fluid (ISF) nucleosides were made using microdialysis probes implanted in the ischemic region of isoflurane
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