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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Modern clinicians encounter considerable difficulties in the diagnosis and treatment of ischemic heart disease which is first of all due to insufficient knowledge of the main mechanisms of the development of coronary insufficiency, myocardial dystrophy, myocardial necrosis, and cardiosclerosis. From the point of view of molecular cardiology, myocardial hypoxia cannot be considered as the foundation for ischemic disease. Metabolic insufficiency of the heart both of coronary and non-coronary origin should also be taken into account. Apart from ischemic (coronary) disease, ischemia of the myocardium alongside with metabolic disorders occurs in most diverse conditions and diseases. Therefore, in future this diagnosis will be reconsidered towards a more accurate determination of the causes of these disorders. Examples from clinical practice are presented for the discussion os such causes and mechanisms. A classification of the causes of metabolic heart deficiency and its outcomes is proposed.
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PMID:[Pathogenesis and classification of ischemic heart disease]. 68

The synthetic acetylcholine analogue ethyl-3-(2,2-dimethyl-2-ethyl-hydrazinium) propionic iodide (EDIHYP) exerts a powerful antiarrhythmic action in cardiac ischemic, reperfusion, and adrenergic lesions, as well as in infarction and postinfarction cardiosclerosis, as evidenced by animal experiments. The study was undertaken to examine the electrophysiological mechanism of EDIHYP s action on isolated rat heart cardiomyocytes. It was shown that the agent substantially reduced the resting potential, as well as action potential amplitude and duration in total ischemia and resultant reperfusion. The antiarrhythmic changes provided a multiple decrease in the duration of ventricular tachycardia and cardiac fibrillation in reperfusion. Thus, the fact that EDIHYP has a direct action on the bioelectrical activity of cardiomyocytes may play an important role in its antiarrhythmic effect in the whole body.
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PMID:[Bioelectrical mechanism of the anti-arrhythmia effect of a synthetic acetylcholine analog EDIHYP]. 177 21

Adaptation of animals to short-term stress exposure (ASE) protected the heart against arrhythmias in acute ischemia and reperfusion and eliminated the decrease in threshold of fibrillation and arrhythmias is acute myocardial infarction and postinfarction cardiosclerosis. Cardioprotective effect of ASE was provided not only by the activation of GABAergic, opioidergic and cholinergic stress-limiting system but also by a mechanism formed at the level of heart itself. Isolated hearts of animals adapted to short-term stress exposure possessed a strikingly enhanced resistance to toxic doses of catecholamines, Ca2+, and to reperfusion damage following total ischemia. Contracture-inducing and arrhythmogenic effects of these factors and the release of CK into the perfusate were manifold reduced in ASE. Mitochondria and elements of SR Ca-pump isolated from the hearts of adapted animals were much more resistant to autolysis. This phenomenon of adaptive stabilization of structures (PhASS) was accompanied by the accumulation of HSP 71 and a simultaneous increase in the heart thermal stability. In the coronary artery ligation the PhASS lacked the anti-ischemic effect, but it provided a decrease of the necrotic zone by more than 40%, the ischemic zone being unchanged, due to its cytoprotective effect.
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PMID:Adaptive protection of the heart and stabilization of myocardial structures. 187 72

It was shown in experiments on Wistar male rats that ethyl, 3/2, ethyl, 2/2, dimethylhydrazine propionate iodate (EDIHYP), a synthetic acetylcholine analogue, eliminates in situ the fall of the ventricular fibrillation threshold and the extrasystole observed on the background of vagal bradycardia in experimental myocardial infarction and postinfarction cardiosclerosis. The elimination of disturbed heart electric stability was not accompanied by cholinergic, negative chronotropic effect of the drug. In isolated heart, high concentrations of EDIHYP (10(-4) M) had negative chronotropic effect but lacked antiarrhythmic effect in local ischemia and reperfusion. The bradycardia induced by EDIHYP was absent and the antiarrhythmic effect was strikingly pronounced on the background of muscarinic receptors blockade with atropine. Thus EDIHYP realizes its antiarrhythmic effect not via muscarinic receptors but by some other way which requires studying by methods of molecular pharmacology.
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PMID:[Correction of disorders of electric stability of the heart and arrhythmia by using a synthetic analog of acetylcholine]. 205 62

It was shown that adaptation to intermittent hypoxia in altitude chamber prevented the poststress fall of the electrical threshold of heart fibrillation. In acute ischemia, the number of fibrillation episodes and the death rate of preadapted animals were 2-3 fold lower than in controls. The adaptation to hypoxia resulted in a significant increase in concentration of opioid peptide beta-endorphin in adrenal glands while stress-induced changes in beta-endorphin in brain structures of adapted animals were much less pronounced. In animals with postinfarction cardiosclerosis, the course of hypoxic actions resulted in restoration of the decreased heart fibrillation threshold, reduced the heart ectopic activity which had developed on the background of vagal bradycardia, and eliminated depression of the heart contractile function. Simultaneously, the adaptation induced a decrease of the postinfarction scar by one-third and an increase of vascularization of the myocardial zone adjacent to the scar.
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PMID:Prevention and elimination of heart arrhythmias by adaptation to intermittent high altitude hypoxia. 296 94

Marked systemic resistance to damaging effects of stress develops as a result of repeated short-term stress exposures. This kind of adaptation is ensured by the activation of stress-limiting systems, namely, the opioidergic, GABA-ergic, serotoninergic, as well as antioxidant and prostaglandin ones. Proceeding from the stress-limiting system concept, adaptation to repeated stress exposure, as well as metabolites, synthetic analogues and activators of stress-limiting systems were successfully used to prevent and eliminate cardiac arrhythmias and fibrillations associated with acute ischemia, myocardial infarction and postinfarction cardiosclerosis. Prospects of further studies of stress-limiting systems' metabolites and activators as antiarrhythmic agents are considered.
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PMID:[Stress-limiting systems and the problem of the prevention of arrhythmia]. 365 20

An experience with the surgical and conservative treatment of 196 patients with acute thromboses and embolism of the extremity arteries in patients with arteriosclerotic and postinfarction cardiosclerosis has shown the conservative treatment of arterial embolism to have little effect. Results of the surgical treatment were regularly better in patients admitted to the hospital at earlier terms after acute occlusion of the vessel, with mild ischemia and the absence of a considerable atherosclerotic lesion of the extremity interrupting the major blood flow. For prophylactics of a repeated embolism of considerable significance were found to be correcting operations on the heart and the continuous anticoagulating therapy.
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PMID:[Treatment of acute thromboses and embolisms of the arteries of the extremities in cardiosclerosis patients]. 383 55

A total of 64 patients with coronary heart disease were examined using contrast coronaro-ventriculography, veloergometry and estimation of the lactic acid level in the coronary sinus blood. Fifty-seven patients were referred to obsidan therapy by the "blind" method. Two groups of patients with asynergies of ischemic and cicatricial genesis were singled out. The sensitivity of the ST segment depression and sigma R increment as objective signs of ischemia significantly reduced in the presence of postinfarction cardiosclerosis. Obsidan monotherapy caused a rise of load power and volume of work performed in the patients with asynergies of ischemic origin: an antianginal effect of the drug in such cases was comparable to that in the patients without disturbed myocardial regional cantractility.
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PMID:[Diagnostic and treatment characteristics of ischemic heart disease patients with asynergies]. 408 46

Hearts of 38 men dying suddenly of acute coronary insufficiency and autopsied within 3 hours after death were examined. Foci of acute ischemic injuries in different parts of the myocardium were studied by histochemical methods for which the activity of succinate dehydrogenase and phosphorylase were determined. Early ischemic lesions in the myocardium were found in 22 fatalities, of them 5 had acute myocardial infarction, in 9 foci of ischemia were combined with the presence of postinfarction scars and fine focal cardiosclerosis, in 8 cases foci of early ischemia were the only changes in the myocardium. The majority of the decreased had stenosing atherosclerosis of the coronary arteries. Localization of ischemia foci in the myocardium did not always correspond to the severity of stenosing or the presence of thrombosis of the artery supplying the corresponding parts of the heart muscle. No foci of ischemia in the myocardium were found in 16 decreased who also had quite marked coronary atherosclerosis.
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PMID:[Early ischemic injuries of the myocardium in sudden cardiac death]. 742 69

There was shown an antiarrhythmic effect of adaptation to intermittent hypobaric hypoxia in ischemia, reperfusion, experimental infarction and postinfarction cardiosclerosis (F.Z. Meerson, 1988). These results was obtained in whole animal experiments. In our study it was demonstrated that the antiarrhythmic effect of adaptation to hypoxia persisted in hearts after isolation, in absence of the effect of neural and humoral factors on the organ. Adaptation of animals to intermittent hypoxia was produced by "stepwise" elevations in an altitude chamber: first day--1000 m; second day--2000 m; third day--3000 m and rest of the days--to 4000 m above sea level. The course of doses adaptation to hypoxia lasted for 40 days; each daily exposure lasted 5 hours. The analysis of arrythmogenic and contractural effects of hypercalcium perfusion and "calcium paradox" phenomenon shows a significant decrease of these effects in hearts of adapted animal. The bioelectrical activity investigation of papillary muscles cardiomyocytes, obtained from hearts of adapted animals, was shown, in hypercalcium perfusion condition, a complex of antiarrhythmogenic changes which was expressed in limitation of rest and action potentials decreasing and in maintenance of the action potential duration. In papillary muscles, obtained from adapted animals, the contracture and the depression of contractility was also smaller. In experiments on resting papillary muscles we found that adaptation to intermittent hypoxia significantly decreased contractural and depolarizing effects of low-sodium perfusion. Thus adaptation to intermittent hypobaric hypoxia resulted, at cardiomyocytes level, in a complex of antiarrhythmic changes which may indicate a protective effect of this kind of adaptation in cardiac arrhythmias.
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PMID:The antiarrhythmic effect of adaptation to intermittent hypoxia. 1020 94


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