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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Impaired metabolism interferes with the active extrusion of intracellular sodium and results in intracellular edema. In the brain and regionally in the kidney, elevation of extracellular osmolality is accompanied by a reduction of ischemic cell swelling and improvement of reflow of blood after arterial occlusion. Studies were therefore performed to examine the effect of elevation of extracellular osmolality on ischemic myocardial physiology and by morphologic examination on the extent of acute injury and subsequent necrosis. Under conditions of controlled hemodynamics, administration of hyperosmotic mannitol resulted in improvement of function of the canine heart with regional ischemia, a lessening of the extent of ischemic injury assessed by electrocardiographic ST segment mapping, and improved total and collateral blood flow. Metabolic studies under conditions of controlled hemodynamics revealed that hyperosmotic mannitol reduced the myocardial oxygen requirement of the ischemic heart. Mannitol dilated large collateral conductance vessels in addition to improving blood flow through the region of myocardial ischemia. Under conditions of ischemia induced by a prolonged reduction in coronary perfusion, hyperosmotic mannitol attenuated the progressive rise in vascular resistance. Direct morphologic examination of areas of myocardium subjected to total interruption of blood flow followed by reflow of blood revealed swelling of both myocardial and capillary endothelial cells early during the reflow period. The extent of swelling was substantially reduced with elevation of the extracellular osmolality with mannitol. Simarilty, osmolality elevation strikingly reduced the extent of eventual myocardial necrosis following prolonged periods of reflow of blood.
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PMID:Effects of hyperosmotic mannitol in reducing ischemic cell swelling and minimizing myocardial necrosis. 125 68

Disorders of contractile function constitute one of the earliest events to follow acute coronary occlusion, and occur in the central ischemic region within approximately 10 seconds. Measurements of regional myocardial dimensions and function in the central, border, and normal zones around an area of ischemia allow assessment of such changes, and when these disorders are persistent after permanent coronary occlusion they may offer an indirect means for assessing the severity and extent of myocardial ischemia and infarction. Recent experimental studies that used pairs of miniature ultrasonic crystals implanted within the subendocardium of open-chested and chronically instrumented, unanesthetized dogs indicate that functional function may be studied simultaneously in these regions; a holosystolic bulge rapidly develops in the central zone of ischemia while hypokinesis is apparent in marginal zones bordering the central region. It has been shown that function in the marginal zone reflects the balance between oxygen supply and demand and may be favorably or unfavorably influenced by acute therapeutic interventions. This finding suggests that the extent of an ischemic region may be altered by such therapy.Our studies further indicate that regional changes in dynamic wall thickness closely parallel the characteristics of shortening of nearby subendocardial segments, indicating that measurement of wall thickness alone may be useful for characterizing regional function. Studies in chronically instrumented animals also have established that the miniature crystals are useful for measuring regional dimensions and function over prolonged periods of time; for example, reduction in end-diastolic dimensions that reflex tissue loss over a 3- to 4-week period after coronary occlusion is substantially greater in the central ischemic regions than in the marginal zones. It is proposed that persistent changes in myocardial function and progressive alterations changes in dimensions over time offer indirect measures of the extent and severity of ischemic damage and infarction. With the development of improved echocardiographic or other clinically applible methods, such measurements may be a useful tool for assessing the effects of therapy on myocardial infarct size.
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PMID:Analysis of regional myocardial function, dimensions, and wall thickness in the characterization of myocardial ischemia and infarction. 125 75

The metabolic and hemodynamic effects of methylprednisolone sodium succinate (40 mg/kg body weight) after acute myocardial ischemia were determined in 24 heparinized mongrel dogs. Myocardial ischemia was produced by ligation of the left anterior descending coronary artery. Catheters in the coronary sinus and the vein draining the left anterior descending coronary arterial area were used to collect blood samples from nonischemic and ischemic myocardium. Lactate, pyruvate, glucose, free fatty acids and oxygen were measured in arterial and venous blood from ischemic and nonischemic areas before and 3, 30 and 60 minutes after myocardial ischemia in animals with (Group II) and without (Group I) steroid treatment. In both Groups I and II glucose, lactate, free fatty acids, oxygen and coronary blood flow in nonischemic areas were not significantly changed, whereas glucose uptake in ischemic areas was significantly increased with myocardial ischemia and remained elevated. In Group I lactate uptake in ischemic areas became negative after coronary arterial ligation and remained so; in Group II, it increased after 30 (70%) and 60 (111%) minutes. Free fatty acid uptake in ischemic areas was reduced after myocardial ischemia in Group I, but in Group II it increased after 30 (224%) and 60 minutes (173%), and there was a concomitant increase in oxygen uptake. Pyruvate uptake in nonischemic areas decreased after 60 minutes in Group I, whereas it was reduced after 30 (68%) and 60 minutes (513%) in Group II. The changes were similar in ischemic myocardium. There were no significant changes in hemodynamic indexes. Coronary blood flow in ischemic areas decreased in Group I after myocardial ischemia and further after 30 and 60 minutes, but in Group II it increased after 30 (82%) and 60 minutes (53%). The data indicate that administration of methylprednisolone results in improved collateral blood flow into the infarcted area and a significantly improved metabolic response of ischemic myocardium. The glucocorticoid may also have a direct benefical effect on carbohydrate metabolism and cause the increased pyruvate neccesary to maintain the generation of energy-producing substrates. The results also suggest that methylprednisolone increases cell survival time and results in greater salvage of ischemic myocardium.
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PMID:Beneficial metabolic effects of methylprednisolone sodium succinate in acute myocardial ischemia. 125 93

Estimation of exercise tolerance in patients with heart disease and significant symptoms can usually not be expressed in terms of maximal oxygen uptake or power at a fixed heart rate calculated from a 'steady state' exercise test. The exercise tolerance can be expressed only by the maximal power developed, when limited by symptoms. For this purpose the level of tolerance is better assessed by a test with small increments and short duration of each work load. In clinical practice this type of almost continuous increase in load was found to be particularly useful in patients with ischaemic heart disease. Comparative studies showed that the work per heart beat at equal loads is significantly higher in the test with continuous increase in load than in the test with steps of 6 minutes duration, both in normal subjects and in heart patients. The difference, however, is small (7%) and for practical purposes these tests have equal validity as a measure of the circulatory capacity.
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PMID:Design of exercise test, with special reference to heart patients. 125 43

The purpose of this study was to determine the reactions of the cardiovascular system with special reference to myocardial oxygen consumption (MVO2) after the administration of graded doses (up to 2.4 g/kg) of thiamine. The data obtained indicate that thiamine: 1. Decreases mean peripheral pressure up to 25%. 2. Decreases LVEDP, left ventricular pressure, and LV dP/dtmax up to 10%, 15%, and 20% respectively. 3. Reduces pulse rate up to 25%. 4. Reduces coronary sinus blood flow up to 31%. 5. Reduces myocardial oxygen consumption up to 45%. The reduction in LVEDP, LVP, and LV dP/dtmax could be antagonized by dextran or norepinephrine infusion. It is suggested that thiamine blocks alpha-receptors which leads to pooling of blood with a concomitant reduction in pre- and afterload of the heart. The effect on MVO2 suggests that thiamine, the essential coenzyme for the formation of high energy substrates reduced the metabolic needs of the heart. The drug warrants further investigation for the treatment of myocardial ischemia.
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PMID:Cardiovascular effects of high doses of thiamine (vit B1) in the dog with special reference to myocardial oxygen consumption. 126 44

Nicorandil is a new vasodilator agent. Efficacy and safety of nicorandil in the treatment of angina pectoris have been evaluated through an extensive clinical program with a total of 1,680 patients who received the product. Results of hemodynamic studies provide clear evidence of the vasodilatory effect of nicorandil. In a population of patients with normal left ventricular function, a reduction in preload was apparent from a decrease in left ventricular end-diastolic pressure from 7.4 +/- 1.7 to -3.2 +/- 1.5 mm Hg. Furthermore, nicorandil produced marked reductions in total peripheral resistance (19%) and aortic blood pressures with decreases in systolic pressure of 34% and in diastolic pressure of 21%. At antianginal doses, nicorandil has a coronary vasodilating effect as well as a balanced peripheral action that leads to decreases in both preload and afterload. Therefore, nicorandil affects two of the main hemodynamic determinants of oxygen demand without impairing myocardial contractility or atrioventricular conduction. In addition, its strong spasmolytic activity is of particular interest when dynamic coronary obstruction is considered. Nicorandil clearly has demonstrated K(+)-channel-opening activity. In addition, the range of plasma concentrations in humans at therapeutic doses is similar to that of experimental models in which the K(+)-channel activity has been determined. This mechanism of action may explain the different hemodynamic profiles of nicorandil and nitrates in humans. Nicorandil is an effective and potent antianginal agent at a dose of 10-40 mg, which in monotherapy controls 69-80% of patients with stable chronic angina. Comparative trials have shown that the efficacy of nicorandil compares with that of drugs from the main classes of antianginal drugs--beta-blockers (atenolol, propranolol) and a Ca2+ antagonist (diltiazem). Patients treated for as long as 3 months or 1 year have shown sustained efficacy with no evidence of development of tolerance to the drug. The long duration of action allows effective treatment with a well-tolerated b.i.d. regimen. At the recommended doses, the main side effects were limited to headaches. They usually occurred early in the course of treatment and can be diminished by a progressive titration. From the large safety data base, there is no evidence that nicorandil induced exacerbation of myocardial ischemia or abrupt withdrawal syndrome. Nicorandil does not adversely affect the lipid profile or the glucose level. As an antianginal drug with a novel mechanism of action, nicorandil provides a useful alternative to existing antianginal agents in the long-term management of patients with angina pectoris.
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PMID:Clinical profile of nicorandil: an overview of its hemodynamic properties and therapeutic efficacy. 128 84

Inhibition of fatty acid oxidation is an early event in myocardial ischemia that most likely contributes to tissue injury by the accumulation of potentially toxic intermediates such as acylCoA and acylcarnitine. After reperfusion both myocardial oxygen consumption and fatty acid oxidation may rapidly recover to preischemic levels, even when contractile function remains depressed. The mechanisms underlying the apparent dissociation between contractile function and oxidative metabolism early during reperfusion are still controversial. In isolated rat hearts subjected to 60 min of no-flow ischemia myocardial oxygen consumption and oxidation of palmitate were lowered during reperfusion by 3 mM of NiCl2 and by 6 microM of ruthenium red. The results provide indirect evidence for the hypothesis that intracellular calcium transport may be involved in the mechanisms responsible for the high oxidative metabolic rate early after reperfusion.
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PMID:Myocardial fatty acid oxidation during ischemia and reperfusion. 128 66

This article reviews the factors influencing myocardial oxygen supply and demand. The regulative mechanisms in coronary blood flow, especially in critical conditions, are explained. Myocardial oxygenation in coronary artery disease is discussed with special reference to pharmacological intervention. An extensive evaluation of the effects of hemodilution on both the healthy and diseased heart is presented. Effects of hemodilution with fluorocarbons for the treatment or prevention of myocardial ischemia are shown with the aid of intramyocardial oxygen partial pressure measurements.
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PMID:Myocardial oxygen supply under critical conditions, the effects of hemodilution and fluorocarbons. 128 70

Biochemical and morphometric methods were employed to study the effect of decimetric waves (460 MHz, 10 and 120 mW/cm2) in cardiac and thyroid exposure on oxygen metabolism, myocardial microcirculation and contractility, thyroid and adrenal hormonal activity, kallikrein-kinin system activity in rabbits with experimental myocardial ischemia. Hypoxia discontinued in all the treatment regimens, but the exposure of the heart (field density 10 mW/sm2) had the additional effect on lipid peroxidation which reduced in the serum and normalized in the myocardium, on myocardial contractility, kallikrein-kinin system and on the adrenal and thyroid hormones.
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PMID:[The effect of decimeter waves on the metabolism of the myocardium and its hormonal regulation in rabbits with experimental ischemia]. 129 12

Since the seventies, and in particular the eighties of this century, findings on pathogenetic mechanisms of ischaemic heart disease are expanding markedly and are becoming more accurate. This makes it possible to know and understand better factors which influence the genesis and development of myocardial ischaemia including the most serious clinical forms (unstable angina pectoris, acute myocardial infarction and sudden cardiac death). Diminution of the cardiac flow and/or increased oxygen demands of the heart muscle are not the only determinants of myocardial ischaemia which is influenced markedly also by neurohumoral, metabolic, prothrombotic (proaggregation and procoagulation) factors as well as antithrombotic and haemodynamic factors. Acute coronary syndromes have as a rule, in particular in patients with out severe atherosclerotic stenosis of the coronary arteries, a common pathophysiological mechanism of fissuration of the atherosclerotic plaque followed by different grades of dynamic coronary occlusion depending on vasoconstriction--spasm of the coronary arteries and thrombus formation. The coronary arteries, usually affected with atherosclerosis, may be due to the comprehensive action of various factors temporarily, intermittently or permanently occluded. In case of the development of acute coronary syndromes thrombosis plays a key role. Better knowledge of pathogenetic mechanism of IHD markedly changes views on treatment and management of patients with IHD in particular patients with acute coronary syndromes. The authors emphasize strategies focused (also preventively) on preventing progression of the disease with the aim to improve survival and the short-term and long-term prognosis.
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PMID:[Pathogenesis of myocardial ischemia and acute coronary syndromes]. 129 43


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