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Página 1 a partir de 51 resultados
Comparison of the effects of adenosine, inosine, and their combination as an adjunct to reperfusion in the treatment of acute myocardial infarction.
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Adenosine and inosine are both key intracellular energy substrates for nucleotide synthesis by salvage pathways, especially during ischemic stress conditions. Additionally they both possess cell protective and cell repair properties. The objective of this study is to detect potential advantages of
Effect of inosine on ventricular regional perfusion and infarct size after coronary occlusion.
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In 16 dogs inosine was infused at 0.5 mmol/min i.v. for 5 min beginning 15 min after coronary occlusion. Tracer microspheres were used to estimate flow in subepicardium and subendocardium of nonischemic, central ischemic, and borderline ischemic muscle. Estimates of flow before occlusion, 5 min
[Stimulation of reparative processes in myocardial infarction: comparative evaluation of the effects of piracetam and inosine].
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A study of 102 patients with primary macrofocal myocardial infarction, admitted to hospital within the first 6 hours after the onset of the disease, and experimental evidence obtained in 110 Wistar rats are reported. In a control group of myocardial infarction patients, collagen synthesis was
[Effect of inosine on the course of experimental myocardial infarct].
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On a model of experimental myocardial infarction produced through ligation of the anterior descending branch of the coronary artery it is shown that inosine is capable of raising the activity of a number of respiratory enzymes, chiefly in the extra-infarction sectors of the myocardium, as well as in
[Indications for the use of inosine in myocardial infarct (a clinical and experimental study)].
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The effect of the nucleoside Inosie-F (inosin) on the intracardiac hemodynamics and the contraction and relaxation of a diseased myocardium was studied in the clinic and in experiments. An examination was made of 102 patients with macrofocal myocardial infarction (22 received inosin by intravenous
Inosine alters gene expression and axonal projections in neurons contralateral to a cortical infarct and improves skilled use of the impaired limb.
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Recovery after stroke and other types of brain injury is restricted in part by the limited ability of undamaged neurons to form compensatory connections. Inosine, a naturally occurring purine nucleoside, stimulates neurons to extend axons in culture and, in vivo, enhances the ability of undamaged
[Theoretical bases and preliminary practical results of the treatment of acute myocardial infarct with inosine].
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[Effect of inosine on the course of myocardial infarct].
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Effect of adenosine and inosine on experimental myocardial infarction in rats.
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[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
Metabolomic analysis of serum and myocardium in compensated heart failure after myocardial infarction.
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[Clearance and transformation of inosine in the body].
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In 5 patients with myocardial infarction the ways of the inosine transformation and its clearance rate following injection of this drug in an amount of 200 to 400 mg were studied. After inosine introduction into the organism it is shown to immediately break down to hypoxanthine which makes
Sustained protection by iloprost of the porcine heart in the acute and chronic phases of myocardial infarction.
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The effects of iloprost (ZK 36 374) on myocardial ischemia and infarction were studied in three groups of four anesthetized and heparinized pigs. Coronary microembolization was evoked by the injection of microspheres (50 microM) into the left coronary artery. A dose of 12 million beads/kg was
[Ways of drug action on the restorative processes in the myocardium in experimental myocardial infarct].
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On a model of experimental myocardial infarction there is demonstrated the stimulating effect of inosine (most distinctly) and also of stimulants of the nucleic acids synthesis and of retabolil on the formation of the post-infarction scar, the processes of compensatory hyperfunction and hypertrophy,
Suppression of the degradation of adenine nucleotides during ischemia may not be a sufficient mechanism for infarct size limitation by preconditioning.
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Preconditioning is known to decelerate degradation of the tissue adenine nucleotides during ischemia and to delay ischemic myocardial necrosis. However, it is not known whether these two phenomena are related. To obtain an insight into this question, the present study examined whether adenosine and
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