Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of prolonged (14 days) passive smoking on the respiration of isolated cardiomyocytes in rabbits using various substrates (pyruvate, glutamate, succinate) was studied. The endogenous respiration of cardiomyocytes was not affected whereas stimulated respiration as well as the ratio of stimulated to endogenous respiration significantly decreased. These results complement previous studies in which the effect of smoking on the metabolic processes of heart muscle mitochondria was measured. In conclusion, prolonged smoking may provoke myocardial dysfunction and in this way may contribute to the development of heart failure in chronic smokers.
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PMID:Effect of smoking on the oxidative processes of cardiomyocytes. 128 81

The pathodynamics of lethal intoxication in rats and mice by i.v. administration of enterotoxin of Clostridium perfringens type A was studied using whole animals and isolated organs. A lethal i.v. dose (50 micrograms/kg) of enterotoxin killed anesthetized rats and mice within 4-15 min. Rapid changes of ECG pattern suggestive of hyperpotassemia, rapid fall of blood pressure and transient hyperpnea followed by respiratory depression were observed. Analysis of plasma levels of cations revealed hyperpotassemia in both animal species. On the other hand, enterotoxin (up to 100 micrograms) showed little direct cardiotoxicity on the isolated heart. ECG changes produced by i.v. injection of KCl (0.5 ml of 50 mM) mimicked the ECG changes observed in the intoxicated rats injected with a lethal dose of enterotoxin. Perfusion of rat isolated organs showed that potassium concentration in the eluent from the liver (but not lungs or lower extremities) increased markedly within 1-2 min after the administration of enterotoxin. The amount of potassium liberated from a rat liver was about 133 mumoles, which is sufficient to increase the plasma level of potassium to more than 10 mM. In addition to potassium, cytoplasmic enzymes, such as glutamate oxalacetate transaminase, glutamate pyruvate transaminase and lactate dehydrogenase, were also liberated from the intoxicated liver, indicating that potassium was liberated from hepatocytes by the change in membrane permeability produced by enterotoxin. It is concluded that hyperpotassemia elicited by the cytotoxic action of enterotoxin on hepatocytes caused cardiac failure leading to the death of the intoxicated animals.
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PMID:Pathodynamics of intoxication in rats and mice by enterotoxin of Clostridium perfringens type A. 192 76

Eighty consecutive patients receiving maximum inotropic and intraaortic balloon support underwent emergency coronary artery bypass grafting 3.4 +/- 1 days (mean +/- standard error) after infarction for severe left ventricular power failure (stroke work index less than 25 gm-m, left atrial pressure greater than 20 mm Hg). All underwent induction of cardioplegia with a 37 degrees C glutamate/aspartate blood cardioplegic solution, multidose cold (4 degrees C) replenishment, and warm reperfusate. Viable areas were grafted first to ensure cardioplegic distribution. Left ventricular power failure was reversed in 94% of patients; 75 of 80 patients had discontinuation of inotropic drugs and intraaortic balloon support. The early mortality rate (less than 30 days) was only 7% (3/45) with early operation (less than 18 hours) and rose to 31% (11/35, p less than 0.05) if operation was delayed more than 18 hours. Six of 14 early deaths were due to progression of preoperative organ failure despite reversal of shock. Eighteen of 66 early survivors died of end-stage heart failure (21/80), a 26% late mortality rate. Nonsurvivors (early and late) had a higher incidence of extending versus evolving infarction (33/64 versus 2/16, p less than 0.05), a longer delay from shock to operation (11/45 versus 24/35, p less than 0.05), more preoperative organ failure (9/9 versus 26/71, p less than 0.05), and a greater incidence of previous infarction (22/43 versus 13/37, p greater than 0.05). Thirty of 45 late survivors (67%) remain physically active. We conclude that left ventricular power failure should be considered a medical/surgical emergency that necessitates prompt angiography and can be reversed in selected patients. Postoperative mortality (early and late) is due principally to delay of operation leading to progression of preoperative organ failure or progression of underlying cardiac disease if infarction becomes established.
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PMID:Studies on prolonged acute regional ischemia. VI. Myocardial infarction with left ventricular power failure: a medical/surgical emergency requiring urgent revascularization with maximal protection of remote muscle. 281 6

Intravenous infusion of L-glutamic acid results in the augmentation of the cardiac output and an improvement of the circulation in patients with postoperative cardiac failure. This effect is not accompanied by increased myocardial oxygen demand. Arterial plasma glutamate level rises 10-fold and arterial-coronary sinus plasma glutamate difference increases fivefold during intravenous L-glutamic acid infusion. This leads to cessation of ammonia release from the myocardium, probably due to augmentation of glutamine synthesis and to an increase in alanine formation coupled with a change from lactate release to lactate uptake by the myocardium. The data obtained suggest that the beneficial effect of L-glutamic acid on depressed cardiac function in postoperative patients is related to changes in myocardial metabolism. Glutamic acid may be useful in treatment of circulatory and metabolic disturbances in cardiac failure.
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PMID:Cardiac metabolism and performance during L-glutamic acid infusion in postoperative cardiac failure. 286 48

In a retrospective analysis of case reports of 115 patients with glutamate-dehydrogenase (GLDH) activity in serum of more than 100 U/l in 1979-1981, the most common causes of this increase were: acute right heart failure (28 patients), protracted septic-toxic circulatory failure (20), obstructive jaundice (18) and severe respiratory insufficiency (16), i. e. diseases causing perfusion or excretion disorders in the liver. The ratio of GLDH activity to transaminase activity provided a reliable separation of acute viral hepatitis, but not of different forms of perfusion disorders. The correlation between GLDH activity and death rate, especially in acute right-heart failure, is of prognostic value.
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PMID:[Diagnostic and prognostic significance of massively increased serum glutamate dehydrogenase activity]. 649 77

Postischemic derangement of myocardial metabolism that is further aggravated by the systemic neuroendocrine response to surgical trauma may explain reversible myocardial dysfunction after cardiac surgical procedures. Since 1991, all patients with signs of cardiac failure after operation for ischemic heart disease (45/515 patients) were treated according to our metabolic strategy. Sixteen patients in whom we previously would have considered use of an intraaortic balloon pump were treated by prolonged unloading of the heart with cardiopulmonary bypass, by glutamate infusion, and by high-dose glucose-insulin-potassium. Rapid improvement in hemodynamic performance was seen in the first hour and almost full recovery within 6 hours in the surviving patients (12/16). None of the 3 patients requiring mechanical assist survived. Our early clinical experience suggests that metabolic support with glutamate and high-dose glucose-insulin-potassium is a safe treatment with a high success rate in reversible cardiac failure.
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PMID:Glutamate and high-dose glucose-insulin-potassium (GIK) in the treatment of severe cardiac failure after cardiac operations. 784 Jun 95

The amino acid pattern in the ascites of 79 dogs was examined. The concentration of glutamine in neoplastic ascites is significantly lower than in cardial effusions. In contrast, glutamate is significantly higher in neoplastic ascites than in cardial ascites. Using an arbitrary discrimination value of 0.28 for the glutamate/glutamine ratio, purulent or cardial ascites are easily differentiated, with a sensitivity of 100% and a specificity of 94%. The differentiation is very distinct, with no overlap between the group of patients with liver cirrhosis on the one hand and the groups of patients with purulent peritonitis, heart failure, or malignant ascites on the other hand. There was no diagnostically unsable correlation between the concentrations of the other 20 amino acids and the underlying causes of ascites formation.
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PMID:Glutamine and glutamate in ascitic fluid of dogs. 809 69

Glutamate infusion has been shown to exert beneficial hemodynamic effects in patients with heart failure after cardiac surgery. To elucidate the underlying mechanism we studied the possibility that glutamate is a Krebs-cycle precursor in the human heart. Therefore [1-13C]glutamate was infused in order to show production of 13CO2 by the heart. In five patients a primed constant infusion of [1-13C]glutamate was started 2|h before the start of sampling from coronary sinus and arterial blood. Plasma concentrations of glutamate and glutamine were determined by high pressure liquid chromatography. Blood concentration of CO2 and enrichment of [1-13C]glutamate, [1-13C]glutamine and [1-13C]glutmaine and 13CO2 were measured by GC-IRMS. The results show that approximately 85% of [1-13C]glutamate taken up by the heart is released released as 13CO2. These results show that synthesis of Krebs-cycle intermediates is a major fate of the glutamate extracted by the human heart.
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PMID:Glutamate metabolism of the heart during coronary artery bypass grafting. 1020 20

There is increasing evidence that the availability of different metabolic substrates can influence post-ischemic functional recovery of the heart and the damage incurred during episodes of myocardial ischemia. Here we present the rationale for metabolic interventions, describe their mechanisms of action and suggest potential clinical applications. In cardiac surgery, basic research, studies of human myocardial metabolism after cardiac operations, and available experience with metabolic interventions provide a rationale for metabolic support with glutamate and/or high-dose glucose-insulin-potassium (GIK) in postoperative cardiac failure. In the treatment of acute myocardial infarction GIK deserves serious evaluation as recent randomized studies in diabetics with myocardial infarction and in patients undergoing reperfusion strategies demonstrate significant reductions in mortality. However, before large scale prospective randomized studies are undertaken, further studies of myocardial metabolism in acute myocardial infarction and the impact of different GIK regimes may be advisable in order to determine appropriate doses. A brief overview of metabolic modulation with pharmacological measures is given as it eventually may prove that we have to await the introduction of pharmacological agents which enhance full glucose oxidation at the expense of free fatty acids to create the commercial interest necessary to achieve widespread use of metabolic therapies.
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PMID:Metabolic intervention for the ischemic and post-ischemic heart. 1044 3

Vascular calcification is common and clinically significant in atherosclerosis and heart failure. It was long believed to be an end-stage process of "passive" mineral precipitation. However, there is now a growing awareness that vascular calcification is a biologically regulated phenomenon. It has many similarities to bone formation, and ectopic bone is a well-documented part of vascular calcification. This implies that alterations in vascular cell differentiation, extensive or localized, are an integral part of vascular calcification. Matrix gamma-carboxylated glutamate (GLA) protein (MGP)-deficient mice develop extensive vascular calcification with replacement of the media by progressively calcifying cartilage. A potential mechanism that explains these findings is MGP interference with bone morphogenetic proteins-potent inducers of cartilage and bone.
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PMID:Insights into the mechanism of vascular calcification. 1147 40


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