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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mitochondrial calcium uptake, but not binding, like microsomal calcium uptake in failing human hearts, was less than the control values for dog, rabbit, and hamster hearts. Decrease in mitochondrial calcium binding and uptake was observed in genetically myopathic hamsters (BIO 14.6) at early, moderate, and late stages of congestive heart failure. Inhibitors of mitochondrial calcium transport, Dicumarol, dinitrophenol, and sodium azide, were found to produce a rapid fall in contractility of the isolated rat heart. Inability of rat hearts to generate contractile force on perfusion with Na+- or K+-free medium was associated with an increase in mitochondrial calcium uptake. A dramatic increase in mitochondrial calcium uptake was observed on perfusing rat hearts with control medium after CA++-free medium. No change in mitochondrial calcium uptake was noted in acute ischemic dog myocardium or hypoxic rat heart in which contractile force was severely depressed. Both mitochondrial calcium transport and contractility were decreased on perfusing rat hearts with substrate-free medium; however, the change in calcium uptake was secondary to the fall in contractile force. Decrease in pH, ATP:ADP ratio, ATP6AMP ratio, and K+:Na+ ratio were found to reduce the dog heart mitochondrial calcium uptake. It is likely that various factors such as pH, ATP:ADP ration, ATP:AMP ratio, and K+ :Na+ ration, in addition to damage in mitochondrial structure, play an important role in inhibiting mitochondrial calcium transport in failing hearts. The results also suggest that alterations in mitochondrial calcium transport are dependent upon the degree and type of heart failure.
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PMID:Role of mitochondrial calcium transport in failing heart. 5 79

An investigation into the fractional composition of myocardial proteins and ATP-ase activity of myosine in 86 persons, who during their lifetime suffered from hypertensive disease and coronary incompetence, revealed significant changes therein. An increased content of actomyosine complex proteins in hypertensive disease was superseded by their considerable diminution in the event of developing cardiac insufficiency, which was at that accompanied by declining ATP-ase activity of myosine. The development of acute myocardial infarction led to a still drastically reduced concentration of sarcoplasmatic and contractile proteins of the heart muscle, as well as to their diminished enzymatic activity.
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PMID:[Contractile myocardial proteins and their enzymatic activity in hypertensive disease and coronary atherosclerosis]. 12 91

Myocardial adenine nucleotides (nicotinamide adenine nucleotides included), glutathione, catecholamines (DOPA, dopamine, noradrenaline, adrenaline) and some enzymes in correlation were investigated in dogs with cardiac failure induced by bilateral iliac arteriovenous fistulas, and unilateral (left) heart vagotomy was also studied for its influence on the changes in the myocardial amounts of these compounds occuring in this pathological circumstance. The cardiac failure in arteriovenous fistula was characterized by the following myocardial metabolic aspects: (I) no change in the amount of proteins (although an important cardiac hypertrophy was present); (II) decreases in the amounts of adenine nucleotides (especially ADP and ATP), without significant variations in the adenosine concentration, accompanied by increases in the concentrations of nicotinamide adenine nucleotides (in both their oxidized and reduced forms) in the heart mitochondria; (III) no change in the amounts of oxidized and reduced glutathione and in the activity of NADH2-dependent glutathione reductase; (IV) a very significant increase in the activity of MAO without significant influences on the levels of the studied catecholamines. The partial vagal denervation of the heart was found to attenuate substantially the changes in the amounts of adenine nucleotides and nicotinamide adenine nucleotides in the myocardial mitochondria and to facilitate the action of MAO on noradrenaline leading to a significant decrease in its myocardial level.
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PMID:Role of the vagus nerves and catecholamines in the production mechanism of the myocardial failure induced by arteriovenous fistulas. 21 43

The relationship between energy metabolism and the extent of irreversible ischemic damage was examined in an isolated perfused working rat heart. The amount of cardiac work recovered after reperfusion of hearts exposed to severe global ischemia was dependent upon both the duration of ischemia and the type of substrate provided (either 5 mM glucose or 5 mM glucose + acetate). There appear to be two distinct phases in the ability to recover mechanical function in the reperfused ischemic heart. The second phase corresponds to the onset of severe irreversible tissue damage. Irreversible mitochondrial damage was not found to correspond with the onset of heart failure since the ATP/ADP ratio remained constant in the reperfused myocardium. Furthermore, there does not appear to be a direct correlation between the total ATP content and the extent of irreversible damage, either during ischemia or following reperfusion. However, the total adenine nucleotide content during ischemia showed dramatic changes which correspond temporally with the initiation of the second phase of damage. The observation that the adenine nucleotide pool becomes further depleted during reperfusion suggests that alterations in the salvage pathway for adenine nucleotide synthesis have occurred. Loss of adenine nucleotides appears to be an excellent marker for irreversible heart failure. Acetate provides some protection the the ischemic myocardium. The mechanism by which acetate mediates this protective effect is discussed.
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PMID:Relationship between adenine nucleotide metabolism and irreversible ischemic tissue damage in isolated perfused rat heart. 44 6

In 53 patients with mitral- or aortic-mitral valve disease, the content of ATP and lactate of the papillary muscles resected at the time of valve replacement was investigated at the beginning of ischemic arrest and at the time of reperfusion. Profound body hypothermia (25 degrees C) and injection cardioplegia using magnesium-aspartate-procaine were applied for myocardial protection. In hypertrophic papillary muscles the myocardial ATP content decreased at a slower rate (ATP decay 12% of the initial value after 60 minutes of ischemia) than in normal papillary muscles obtained from patients with isolated mitral stenosis (ATP decay 33% of the initial value after 40 minutes of ischemia). 20% of the patients required temporary inotropic circulatory support postoperatively for 12 to 88 hours. The ATP content of the papillary muscles of these patients differed only little from those, in who no myocardial failure occurred. However the myocardial lactate levels were higher in patients in whom a low cardiac output state evolved.
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PMID:[Behaviour of ATP and lactate in human papillary muscle during profound hypothermia and injection cardioplegia with magnesium-asparatate-procaine (author's transl)]. 75 Dec 88

Myocardial blood flow, left ventricular performance, regional myocardial metabolites (ATP, CrP, lactate) and a-v differences of oxygen, lactate and pyruvate were determined in 6 open chest dogs with cannulated left coronary artery. A mean flow reduction from 92 to 43 ml/min/100 g heart weight resulted in marked heart failure accompanied by extensive flow reduction to the endocard with nearly 10 fold increase of lactate and a decrease of CrP content to 50% of control. In contrast, flow and metabolic parameters of the epicardial part changed only slightly. Furthermore, the DPTI/SPTI-ratio showed a good correlation with the subendocardial CrP content (r = 0.93, p less than 0.01).
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PMID:[Effect of coronary flow reduction on the coronary flow distribution, the myocardial metabolism and left ventricular hemodynamics]. 101 81

Tests conducted with adult (8--10 months) and old (26--28 months) rats brought evidence that in ageing the cardiac ejection, dp/dt max, contractility index, the ATP concentration, that of creatinophosphate, glycogen, pyruvate decline, the phosphorylation coefficient, the lactate content increase, while the level of water-soluble proteins and collagen diminishes and that of water-insoluble ones decreases. In adult rats hemodynamics and myocardial contractility change but unsignificantly on the 4--6th day after coarctation of the aorta, whereas in the old ones there occur functional and metabolic alterations in the heart that are indicative of a developing cardiac insufficiency. The age-specific differences persist also on the 14--16th day following coarctation of the aorta. During these periods the weight of the heart, the content of the myofribrillary proteins and collagen are on the rise, whereas in the old ones the weight of the heart remains unchanged and the level of water-soluble protein drops. Changes in the properties of the actomyosin complex, disruption of the calcium pump, shifts in the system of the energy generation, limitation of potential possibilities incident to the systems of protein biosynthesis in the myocardial cell, all this leads to the development of cardiac incompetence following loading in old age.
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PMID:[Mechanisms of development of cardiac insufficiency in old age]. 102 32

Overdoses of several volatile anesthetics (ether, chloroform, ethyl chloride, halothane, methoxyflurane) as well as of various barbiturates lead to severe contractile failure of the heart. In all cases it was found that at the stage of maximal failure the myocardial stores of ATP and phosphocreatine were increased, indicative of reduced high energy phosphate utilization. Barbiturate-induced failure can be fully reversed by the intravenous injection of CaCl2, isoproterenol, or strophanthin. Simultaneously ATP and phosphocreatine concentrations become normal. In contrast, cardiac failure caused by volatile anesthetics proved to be resistant to this therapy. Electron micrographs showed a normal structure of the transverse tubules in the case of barbiturate failure. On the other hand, after the application of volatile anesthetics, a striking dilatation of the transverse tubular system was observed. The irreversibility of this latter type of contractile failure is probably caused by permanent damage of myocardial ultrastructures involved in excitation-contraction coupling.
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PMID:Reversible and irreversible forms of contractile failure caused by disturbances by general anesthetics in myocardial ATP utilization. 118 70

Daunomycin, adriamycin and 5 semisynthetic anthracycline antibiotics inhibited oxygen consumption or ATP production of rat heart mitochondria in vitro. The no-effect levels varied depending on the substrate used and ranged from 1 nmole per mg mitochondrial protein. Mitochondrial functions were also studied in hearts of rats treated with repeated i.p. injections of the 7 antibiotics. Decrease in oxygen consumption without change in ATP production was observed with adriamycin and NSC-149584. Daunomycin, NSC-164011, NSC-143496 NSC-143114 affected primarily ATP production. The most potent compounds were daunomycin and adriamycin which damaged mitochondrial function at cummulative doses of approximately 10 mg/kg. ECGs were monitored in groups of equally treated rats. Cardiotoxicity manifested itself by progressive widening of the QRS complex often followed by the development of a S-wave trough. The most toxic compounds also induced intraventricular block, bradycardia and heart failure. The development of the ECG changes showed a good correlation with the impairment of mitochondrial function.
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PMID:Effects of seven anthracycline antibiotics on electrocardiogram and mitochondrial function of rat hearts. 121 14

Experimental hyperthyroidism was produced in guinea pigs by daily intraperitoneal injection of l-thyroxine (T4) in various doses (0.7, 0.35, 0.175, and 0.07 mg/kg/day) for 7 days. Controls received solvent only. The following metabolites were determined in heart muscle (freeze-stop technique, enzymatic tests): Pi, adenosine tri-, di-, and monophosphates (ATP, ADP, AMP), creatine phosphate (CP), glucose 6-phosphate (G-6-P), fructose diphosphate (FDP), pyruvate, and lactate. Thyroxine induced a dose-related decrease of CP and a corresponding increase of Pi even in the lowest dose used in this study (0.07 mg/kg) and became more pronounced with increased doses. No remarkable changes of adeninenucleotides (ATP, ADP, AMP) were observed. G-6-P and FDP levels were markedly elevated in all dosages. Besides other possible effects (thyroxine-induced activation and induction of enzymes) the dose-related decrease of CP and increase of Pi may be due to the increasing contractility. In the physiological and pathophysiological range of thyroxine doses (T4 less than 20 mug%) high energy phosphates stores are dose-related decreased but not to a critical level. In the toxic range heart failure as a consequence of a deficit of CP may occur.
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PMID:Dose-relation of thyroxine-induced changes in myocardial energy stores. 121 45


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