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purine/infarction
Veza se sprema u međuspremnik
Stranica 1 iz 121 rezultatima
[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
Myocardial infarction and purine transport inhibition in anaesthetised ferrets.
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The potential cytoprotective effect of the purine transport inhibitor S-(p-nitrobenzyl)-6-thioinosine (NBTI) in a model of myocardial ischaemia and reperfusion was investigated in the anaesthetised ferret. The left anterior descending coronary artery (LAD) was occluded for 90 min, producing
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
Chronic xanthine oxidase inhibition following myocardial infarction in rabbits: effects of early versus delayed treatment.
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Xanthine oxidase (XO) expression is increased in the failing heart, and animal studies in rodents and dogs showed that XO inhibition with allopurinol can improve left ventricular (LV) function and myocardial oxygen efficiency in the failing heart. The purpose of this study was to determine whether
A novel purine analogue bearing nitrate ester prevents platelet activation by ROCK activity inhibition.
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Natural purines like ATP, ADP and adenosine have crucial roles in platelet physiology. This knowledge has been significant in drug development and today ADP receptor antagonists are widely used for prevention of thrombotic events following myocardial infarction and ischaemic stroke. Recent studies
Effects of isradipine on hemodynamic parameters and ventricular tachycardia in healed myocardial infarction.
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The calcium-entry blocker isradipine was tested in a closed-chest pig model for chronic myocardial infarction. Ischemia was evoked in anesthetized pigs (25-35 kg) by inflating a catheter balloon in the left anterior descending coronary artery for at least 45 min. Hemodynamic monitoring and signal
Uric acid kinetic studies in the immediate post-myocardial-infarction period.
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The etiology of hyperuricemia following myocardial infarction was investigated by uric acid kinetic studies carried out on seven male patients following myocardial infarction and on two control subjects. The patients selected had uncomplicated myocardial infarction and were maintained on a
Effects of levosimendan on cardiac gene expression profile and post-infarct cardiac remodelling in diabetic Goto-Kakizaki rats.
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The calcium sensitizer levosimendan has shown beneficial effects on cardiac remodelling in spontaneously diabetic Goto-Kakizaki (GK) rats 12 weeks after experimental myocardial infarction (MI). However, the short-term effects and the cellular mechanisms remain partially unresolved. The aim was to
Stroke in purine nucleoside phosphorylase deficiency.
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The first documented case of cerebrovascular disease occurring in a 13-year-old girl with purine nucleoside phosphorylase deficiency is reported. This patient, the oldest known survivor with purine nucleoside phosphorylase deficiency, had previously experienced multiple sequential neurologic
[Determination of purine and pyrimidine derivatives in acid-soluble fractions of organs and tissues using high-performance reverse-phase ion-pair chromatography].
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Simultaneous separation of the main ribonucleotides, nucleosides and bases was carried out using tetrabutyl ammonium phosphate (TBA) hetaerons with a reversed-phase (C18) packing material. Chromatographic properties of purine and pyrimidine metabolites in radially compressed NovaPak C18 system was
LC/MS-based polar metabolite profiling reveals gender differences in serum from patients with myocardial infarction.
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Myocardial infarction (MI), a leading cause of death worldwide, results from prolonged myocardial ischemia with necrosis of myocytes due to a blood supply obstruction to an area of the heart. Many studies have reported gender-related differences in the clinical features of MI, but the reasons for
Cardiac outflow of amino acids and purines during myocardial ischemia and reperfusion.
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A novel application of microdialysis was studied, in which myocardial outflow of amino acids and purines was monitored by intravasal microdialysis in the myocardial venous outflow during ischemia and reperfusion. Microdialysis catheters were introduced into the great cardiac vein, pulmonary artery,
Metabolic pathways involved in Xin-Ke-Shu protecting against myocardial infarction in rats using ultra high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry.
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Xin-Ke-Shu (XKS) is a patent drug used for coronary heart diseases in China. This study evaluated the protective effect of XKS against isoproterenol (ISO)-induced myocardial infarction (MI). For its underlying mechanism in rats with MI, a metabonomic approach was developed using ultra
Recognition and activation of ryanodine receptors by purines.
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Ryanodine receptor (RyR) is a tetrameric, high molecular weight protein that functions as a calcium release channel. It plays a key role in phenomena such as signal transduction, excitation-contraction and excitation-secretion coupling. Hyperthermia maligna, central core disease and myocardial
Extracellular purine metabolism in blood vessels (Part II): Activity of ecto-enzymes in blood vessels of patients with abdominal aortic aneurysm.
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Both platelet aggregation and high blood pressure are associated with development of atherosclerosis. Among other factors that modulate platelet aggregation and blood pressure, extracellular purines (e-purines) influence these processes via purinoceptors P1 and P2 for which they are natural ligands.
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