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 enzymatic activity of creatine kinase-MB isoenzyme (CK-MB), a sensitive and specific marker of myocardial damage, was measured in 32 children following scorpion envenomation. CK-MB activity, total creatine phosphokinase (CPK) and serum glutamine oxalacetic transaminase (SGOT) levels were examined for relationship with electrocardiographic (ECG) results and the clinical state of the children. Twenty-seven out of the 32 children had signs of systemic intoxication ("symptomatic" cases), while the other five children had only local signs ("asymptomatic" cases). Thirteen out of the 27 symptomatic children had enzymatic myocardial involvement characterized by high total CPK level, elevated CK-MB level and a CK-MB/CK ratio exceeding 6%. Six of these 13 children had ECG changes consistent with myocardial damage, and only one child had clinical signs of myocardial injury. None of the asymptomatic children, nor five healthy control children, had any evidence of myocardial damage as judged by CK-MB levels, clinical signs and ECG. Our study suggests that CK-MB activity is specific and highly sensitive in detecting myocardial damage in children following scorpion envenomation, and appears superior to ECG and clinical parameters. We speculate that the myocardial lesions are too small to cause heart failure in most cases, but they may account for the cardiovascular changes frequently seen in scorpion envenomation.
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PMID:Myocardial injury without heart failure following envenomation by the scorpion Leiurus quinquestriatus in children. 204 53

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

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

Acute post-ischemic cardiac failure was studied in isolated rat hearts. Xylitol, glutamine, aspartic acid and glycine were added during reperfusion, resulting in no inotropic effect. Concanavalin A had a moderate inotropic effect. When concanavalin A added with xylitol, glutamine, aspartic acid and glycine, a rapid recovery of myocardial function and high-energy phosphate was achieved.
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PMID:Concanavalin A enhances ATP resynthesis via de novo pathway in postischemic rat hearts. 834 Nov 30

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

Conditionally essential nutrients (CENs) are organic compounds that are ordinarily produced by the body in amounts sufficient to meet its physiological requirements. However, in disorders, such as cardiovascular disease (CVD), and in other physiologically stressful conditions, their biosynthesis may be inadequate. Under these circumstances, CENs become essential nutrients, comparable to vitamins. The CENs of primary importance in CVD, based on the quantity and quality of human clinical studies, are l-arginine, l-carnitine, propionyl-l-carnitine, and coenzyme Q10. Controlled studies of these CENs are reviewed in depth. Taurine is a CEN of secondary importance caused by a limited human database. Other putative CENs include alpha-lipoic acid, betaine, chondroitin sulfate, glutamine, and d-ribose, each of which is mentioned in passing. Collectively, CENs have demonstrated favorable clinical effects in CVDs, including chronic heart failure, myocardial infarction, angina pectoris, and in CVD risk factors, such as hypertension, hyperlipidemia, and lipoprotein(a). Limited research has pointed to possible benefits in CVD therapy accruing from supplementation with several CENs in combination. Additional controlled clinical studies of CENs in CVD are urgently needed. In view of the efficacy and safety of appropriate supplementation with CENs, it is strongly suggested that healthcare professionals become knowledgeable of these potentially important additions to the CVD therapeutic armamentarium.
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PMID:Supplemental conditionally essential nutrients in cardiovascular disease therapy. 1640 31

Obesity is a risk factor for heart failure through a set of hemodynamic and hormonal adaptations, but its contribution at the molecular level is not clearly known. Therefore, we investigated the kinetic cardiac transcriptome and metabolome in the Spontaneous Hypertensive Heart Failure (SHHF) rat. The SHHF rat is devoid of leptin signaling when homozygous for a mutation of the leptin receptor (ObR) gene. The ObR-/- SHHF rat is obese at 4 months of age and prone to heart failure after 14 months whereas its lean counterpart ObR-/+ is prone to heart failure after 16 months. We used a set of rat pangenomic high-density macroarrays to monitor left ventricle cardiac transcriptome regulation in 4- and 10-month-old, lean and obese animals. Comparative analysis of left ventricle of 4- and 10-month-old lean rat revealed 222 differentially expressed genes while 4- and 10-month-old obese rats showed 293 differentially expressed genes. (1)H NMR analysis of the metabolome of left ventricular extracts displayed a global decrease of metabolites, except for taurine, and lipid concentration. This may be attributed to gene expression regulation and likely increased extracellular mass. The glutamine to glutamate ratio was significantly lower in the obese group. The relative unsaturation of lipids increased in the obese heart; in particular, omega-3 lipid concentration was higher in the 10-month-old obese heart. Overall, several specific kinetic molecular patterns act as a prelude to heart failure in the leptin signaling deficient SHHF obese rat.
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PMID:NMR and cDNA array analysis prior to heart failure reveals an increase of unsaturated lipids, a glutamine/glutamate ratio decrease and a specific transcriptome adaptation in obese rat heart. 1722 24

Beta-adrenergic receptor (betaAR) blockade is a standard therapy for cardiac failure and ischemia. G protein-coupled receptor kinases (GRKs) desensitize betaARs, suggesting that genetic GRK variants might modify outcomes in these syndromes. Re-sequencing of GRK2 and GRK5 revealed a nonsynonymous polymorphism of GRK5, common in African Americans, in which leucine is substituted for glutamine at position 41. GRK5-Leu41 uncoupled isoproterenol-stimulated responses more effectively than did GRK5-Gln41 in transfected cells and transgenic mice, and, like pharmacological betaAR blockade, GRK5-Leu41 protected against experimental catecholamine-induced cardiomyopathy. Human association studies showed a pharmacogenomic interaction between GRK5-Leu41 and beta-blocker treatment, in which the presence of the GRK5-Leu41 polymorphism was associated with decreased mortality in African Americans with heart failure or cardiac ischemia. In 375 prospectively followed African-American subjects with heart failure, GRK5-Leu41 protected against death or cardiac transplantation. Enhanced betaAR desensitization of excessive catecholamine signaling by GRK5-Leu41 provides a 'genetic beta-blockade' that improves survival in African Americans with heart failure, suggesting a reason for conflicting results of beta-blocker clinical trials in this population.
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PMID:A GRK5 polymorphism that inhibits beta-adrenergic receptor signaling is protective in heart failure. 1885 42

Chronic physical exercise with adequate intensity and volume associated with sufficient recovery promotes adaptations in several physiological systems. While intense and exhaustive exercise is considered an important immunosuppressor agent and increases the incidence of upper respiratory tract infections (URTI), moderate regular exercise has been associated with significant disease protection and is a complementary treatment of many chronic diseases. The effects of chronic exercise occur because physical training can induce several physiological, biochemical and psychological adaptations. More recently, the effect of acute exercise and training on the immunological system has been discussed, and many studies suggest the importance of the immune system in prevention and partial recovery in pathophysiological situations. Currently, there are two important hypotheses that may explain the effects of exercise and training on the immune system. These hypotheses including (1) the effect of exercise upon hormones and cytokines (2) because exercise can modulate glutamine concentration. In this review, we discuss the hypothesis that exercise may modulate immune functions and the importance of exercise immunology in respect to chronic illnesses, chronic heart failure, malnutrition and inflammation.
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PMID:Importance of exercise immunology in health promotion. 2097 9

Swim-training exercise in mice leads to cardiac remodeling associated with an improvement in contractile function. Protein O-linked N-acetylglucosamine (O-GlcNAcylation) is a posttranslational modification of serine and threonine residues capable of altering protein-protein interactions affecting gene transcription, cell signaling pathways, and general cell physiology. Increased levels of protein O-GlcNAcylation in the heart have been associated with pathological conditions such as diabetes, ischemia, and hypertrophic heart failure. In contrast, the impact of physiological exercise on protein O-GlcNAcylation in the heart is currently unknown. Swim-training exercise in mice was associated with the development of a physiological hypertrophy characterized by an improvement in contractile function relative to sedentary mice. General protein O-GlcNAcylation was significantly decreased in swim-exercised mice. This effect was mirrored in the level of O-GlcNAcylation of individual proteins such as SP1. The decrease in protein O-GlcNAcylation was associated with a decrease in the expression of O-GlcNAc transferase (OGT) and glutamine-fructose amidotransferase (GFAT) 2 mRNA. O-GlcNAcase (OGA) activity was actually lower in swim-trained than sedentary hearts, suggesting that it did not contribute to the decreased protein O-GlcNAcylation. Thus it appears that exercise-induced physiological hypertrophy is associated with a decrease in protein O-GlcNAcylation, which could potentially contribute to changes in gene expression and other physiological changes associated with exercise.
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PMID:Swim-exercised mice show a decreased level of protein O-GlcNAcylation and expression of O-GlcNAc transferase in heart. 2149 20


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