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

The isolated perfused working rat heart preparation has been used to study the effects of respiratory acidosis on myocardial metabolism and contractilly. Hearts were perfused with 5 mM glucose and 10(-2) U/ml of insulin in order to enhance metabolsim of glucose relative to that of fatty acids. After perfusion with Krebs bicarbonate medium at pH 6.6, hearts rapidly ceased performing external work and peak left ventricular pressure fell by 75% after 5 minutes. Oxygen consumption, rate of ATP generation and overall glycolytic flux also declined rapidly. After about 2 minutes of perfusion, the fall of glycolytic flux showed a partial reversal, which was largely accounted for by increased lactate production, so that glucose oxidation decreased further. The reversal of glycoltic flux could be accounted for by partial release of H+ inhibition of phospho-fructokinase by increased tissue levels of adenosine 5'-diphosphate (ADP), adenosine monophosphate (AMP) and P1 and decreased levels of adenosine triphosphate (ATP) and creatine phosphate. The increased proportion of glucose uptake converted to lactate together with an increase of the tissue lactate/pyruvate ratio could be accounted for by inhibition of the malate-aspartate cycle combined with tissue hypoxia. Lactate accumulated in the tissue as a result of a decreased permeability of the plasma membrane to lactate. Decreased oxygen delivery to the myocardium was caused by secondary constriction of the coronary vessels. In further experiments, the coronary flow was regulated by an external pump which delivered fluid at a controlled rate into the aortic cannula above the coronary arteries, and the degree of tissue hypoxia was monitored by measuring changes of pyridine nucleotide reduction state by surface fluorescence techniques. The effects of acidosis uncomplicated by possible hypoxia were compared directly with those produced by ischemic hypoxia. The effects of acidosis under these conditions were similar to those described above, and to those produced by ischemia. From these and other data it is concluded that the effects of ischemia are caused by a lowering of the intracellular pH, which decreases the rate of energy production relative to the rate of energy demand. However, it is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart. Possible causes of irreversible heart failure after prolonged ischemia are discussed.
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PMID:Contribution of tissue acidosis to ischemic injury in the perfused rat heart. 0 93

The paper sets forth materials reflecting the present-day views of morphologists concerning the problem of cardiac insufficiency. The current state of the problem relating to morphology of the myocardium in cardiac incompetence is characterized. It is suggested that cardiac incompetence cannot be approached as a unique issue, and in different affections the pathogenesis of the heart muscle debility may prove to be dissimilar. Ultrastructural changes in the left heart myocardium of the rabbit, at a distance from the ischemic area, in experimental myocardial infarction at the stage of compensatory hypertrophy and with developing acute cardiac incompetence are described. In the lastly named case the mitochondria of myocites were found to contain compact bodies, apparently made up of calcium phosphate. Their appearance comes as a proof of irreversibility of the supervened changes.
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PMID:[Cardiac insufficiency and its morphological expression]. 13 11

The concentrations of urea, urate, phosphate and creatinine were measured in the plasma of 30 consecutive patients admitted acutely with heart failure. On admission, 20 had a raised plasma urea, 21 had a raised plasma urate, but only 6 had a raised plasma phosphate and only 6 had a raised plasma creatinine. A further 9 of the patients developed a raised plasma urea after admission. The increase in plasma urea present on admission was greater than expected for the fall in GFR (as indicated by the increase in plasma creatinine). The results for plasma and urine taken together suggest that a major cause of the raised plasma urea was an increased urea production rather than a reduced glomerular filtration rate. There was no obvious relationship between plasma urea and clinical features, or diuretic therapy.
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PMID:The cause of the raised plasma urea of acute heart failure. 43 64

Two thirds of the patients with peripheral arterial occlusive disease have to be treated conservatively, for only up to 30% can be revascularized by operative methods. Using the pharmacological differential treatment the grade of compensation and localization of the obliterative process has to be considered. Ignoring the usual basic therapy (elimination of heart failure and pathological bradycardia, systemic walking-exercise, anticoagulation etc.) intrafemoral long-term application of energetic phosphate (i.e. nucleotid-nucleosid-mixtures) leads to a positive result in nearly two thirds (n = 97 legs) with a degree of II to IV of Fontaine. Whereas the snakes' encyme Ancrod with the effect of defibrination was successful in almost 70% of the patients with arterial insufficiency (n = 45) including the degree II B (painless walking-distance under 100 meters). Energetic phosphates, applied to the arteria femoralis, are most successful in degree II with claudication intermittens. Ancrod should be used respectively for patients with pain during rest. These results are discussed with respect to compensation and localization of arterial occlusive disease, acute and chronic measurements of the hemodynamics by use of Doppler ultrasound and strain gauge plethysmography and with respect to variation of the concentration of the metabolic parameters lactate and pyruvate--the latter when defibrination was performed.
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PMID:[Pharmacological treatment of chronic arterial occlusive disease (author's transl)]. 49 58

1 Reccurent paroxysmal atrial, atrioventricular and ventricular tachycardias in 50 patients without acute coronary insufficiency, heart failure or metabolic abnormlity were treated with disopyramide phosphate in a dose of 2 mg/kg body weight infused over 5 min. 2 Conversion to sinus rhythm within 10 min of the completed infusion occurred in 10 of 14 (71%) patients with paroxysmal 'lone' atrial fibrillation, 3 of 7 (43%) patients with paroxysmal atrial flutter, 6 of 9 (67%) patients with paroxysmal atrial tachycardia, 5 of 9 (56%) patients with paroxysmal atrioventricular tachycardia associated with the Wolff-Parkinson-White syndrome and 8 of 11 (73%) patients with paroxysmal ventricular tachycardia. 3 Side effects: significant systemic hypotension in 3, high grade AV block in 1, an increased ventricular response producing symptoms in 4, post conversion asystole in 1 land sinus bradycardia in 2. 4 The anti-arrhythmic effect and arrhythmogenic side effects may be related to both the direct membrane stabilizing effect and the anticholinergic effect of disopyramide.
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PMID:The effect of intravenous disopyramide phosphate on recurrent paroxysmal tachycardias. 50 48

Diurnal cycles of glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and of excretion rates of sodium, potassium, magnesium, chloride and phosphate were measured in a 22 year old man with moderately severe heart failure under standardized conditions. Cycles of GFR, ERPF and excretion of potassium, chloride, and phosphate were indistinguishable from those of normals. The phases of the sodium and probably the magnesium excretory cycles were reversed from normal. The significance of some of the observations is discussed.
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PMID:Diurnal circadian rhythms of renal function and electrolyte excretion in heart failure. 57 67

Four uremic patients on maintenance hemodialysis developed intractable heart failure and atrioventricular block. All had persistently high (over 60) calcium-phosphorus products. At autopsy, all had metastatic myocardial calcification. Their inability to take phosphate-binding agents orally is responsible for this fatal complication.
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PMID:Calcific cardiomyopathy in advanced renal failure. 113 76

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

The shifts in the myocardial electrolyte metabolism during secondary or primary cardiopathies in dogs and rats, respectively, are described. Major attention is paid to the changes of Ca in the myocardial tissue. The increase in the Ca level after ligation of ramus circumflex of the left coronary artery, or after F-COL + Na2HPO4, and vitamin D2 administration, is regarded as a triggering process for more profound successive changes in the metabolism of the myocardial cell, which eventually lead to depletion of the high energy phosphate reserves. In the dogs with experimental coronary occlusion, the normalization of the myocardial ionogram, i.e., the ratio of K, Na, Ca, and Mg, was achieved by means of the mechanical heart assist, using the original design of the blood pump, where bypass and counterpulsation principles work simultaneously. The normalization of the Ca level in this case was achieved on the basis of a marked reduction of the volume work of the left ventricle, which is secured by the bypass component; on the other hand, the counterpulsation component of the combined pump secures the reduction of pressure work placed upon the left ventricle (represented by the decrease fo the end-diastolic pressure) and helps in the opening of the collaterals in the infarcted area during early diastole. Thus, the oxygen supply to the ischemic zone is improved. On the basis of our experiments with the combined blood pump, the failing heart is supported, not only hemodynamically, but also from the metabolic point of view. A similar effect is achieved by the administration of K-Mg-aspartate, and K-L- or K-DL-aspartate in dogs with experimental infarction. In primary electrolyte steroid cardiopathies characterized by necrosis, K-Mg-aspartate or K-aspartate only prevents the Ca increase in the myocardial tissue, whereas Mg-L- or Mg-DL-aspartate remains without andy effect. The necrotic changes observed after vitamin D2 administration are always accompanied by extremely high Ca levels in the myocardium. It shown in our experiments that administration of K-Mg-aspartate or Fe-dextran decreases the Ca level and reduces the necrotic and myolytic changes in the cardiac tissue. The authors recommend as an effective means in the therapy of acute heart failure the combination of mechanical heart support with the causative pharmacological therapy.
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PMID:Electrolyte changes in myocardial injury. 119 95

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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