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)

Glucagon is a counter-regulatory hormone that is classically used to treat hypoglycemia. However, it can elicit the generation of cAMP within the myocardium to cause positive inotropic and chronotropic effects without the need for beta-1 adrenoceptor stimulation. Glucagon has been used extensively to treat beta-blocker overdose and has evidence for use in verapamil and imipramine overdose as well. Glucagon has been used as adjunctive therapy in shock situations and heart failure but is inferior to catecholamines. An interesting potential indication for glucagon is in treating postcountershock asystole.
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PMID:A review of potential cardiovascular uses of intravenous glucagon administration. 1023 90

Hypoglycemia is a clinical and biological syndrome, caused by an abnormal decrease in plasma glucose levels to below 0.55 g/l (3.0 mmol/l). Hypoglycemia is responsible for non-specific signs and symptoms which should be noted in a particular pathological context, and for secretion of counterregulatory hormones (mainly glucagon and catecholamines). Difficulty in identifying the etiology is variable, based upon history and physical examination, and hormonal investigations or imaging procedures, according to the results. Drug-related hypoglycemia is the most frequent observed cause (mainly in insulin-treated diabetic patients, but many drugs may be involved), followed par toxicity (alcohol mainly). Tumor-induced hypoglycemia is secondary to inappropriate insulin secretion by a beta-cell pancreatic tumor (insulinoma), and, rarely to an extrapancreatic mesenchymal large tumor secreting IGF-II. Hypoglycemia is present in other diseases, such as hormonal deficiencies, hepatic, or renal failure, or acute cardiac insufficiency. Multifactorial hypoglycemia seems to be underdiagnosed, mainly in hospitalized, underfed older patients with severe disease or sepsis. Autoimmune hypoglycemia is rare, due to insulin or insulin-receptor autoantibodies. Reactive hypoglycemia is observed after gastrectomy, but true primitive hypoglycemia appears to be rare, with false excess diagnosis in the majority of the cases.
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PMID:Hypoglycemia in adults. 1063 72

During the past 20 years, several bioactive peptides have been identified in teleost fishes that subsequently have been shown to play important regulatory roles in mammalian physiology. The urophysis, corpuscles of Stannius and Brockmann body are anatomical structures particular to fish that have no obvious counterpart in mammals. Extracts and/or cDNA libraries prepared from these tissues have been used to identify for the first time urotensin II (U-II), urotensin-I (U-I), stanniocalcin and glucagon-like peptide-1 (GLP-1). Although U-II and U-I were originally regarded as exclusively the products of the teleost urophysis, the peptides have a wide phylogenetic distribution across the vertebrate lineage, including mammals. U-II is localized to motor neurones in the human spinal cord and is a potent vasoconstrictor that may be implicated in the pathogenesis of heart failure. The human ortholog of urotensin-I is urocortin which is synthesized in selected regions of the brain and is the endogenous ligand for the CRF type 2 receptor. Urocortin is believed to important in mediating the effects of stress on appetite. Stanniocalcin is involved in maintaining calcium and phosphate homeostasis in teleost fish. An ortholog of stanniocalcin has a widespread distribution in mammalian tissues and is postulated to regulate renal phosphate excretion and to protect neurons against damage during cerebral ischemia. The biological actions and therapeutic potential of GLP-1 in humans are now fully appreciated but the peptide was first identified as a domain in a preproglucagon cDNA prepared from anglerfish Brockmann bodies. In contrast to mammalian preproglucagons, GLP-1 is present in anglerfish preproglucagon as the bioactive, truncated sequence [corresponding to human GLP-1(7-37)] rather than the inactive, N-terminally extended form [corresponding to GLP-1(1-37)]. Failure to appreciate the significance of this fact retarded progress in the field for several years.
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PMID:Singular contributions of fish neuroendocrinology to mammalian regulatory peptide research. 1103 47

L-Arginine (Arg) is the substrate for the synthesis of nitric oxide (NO), the endothelium-derived relaxing factor essential for regulating vascular tone and hemodynamics. NO stimulates angiogenesis, but inhibits endothelin-1 release, leukocyte adhesion, platelet aggregation, superoxide generation, the expression of vascular cell adhesion molecules and monocyte chemotactic peptides, and smooth muscle cell proliferation. Arg exerts its vascular actions also through NO-independent effects, including membrane depolarization, syntheses of creatine, proline and polyamines, secretion of insulin, growth hormone, glucagon and prolactin, plasmin generation and fibrinogenolysis, superoxide scavenging and inhibition of leukocyte adhesion to nonendothelial matrix. Compelling evidence shows that enteral or parenteral administration of Arg reverses endothelial dysfunction associated with major cardiovascular risk factors (hypercholesterolemia, smoking, hypertension, diabetes, obesity/insulin resistance and aging) and ameliorates many common cardiovascular disorders (coronary and peripheral arterial disease, ischemia/reperfusion injury, and heart failure). Dietary Arg supplementation may represent a potentially novel nutritional strategy for preventing and treating cardiovascular disease.
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PMID:Arginine nutrition and cardiovascular function. 1105 97

A case of acute poisoning with amlodipine with deep hypotension, transient oliguria and clinical signs of acute heart failure was described. A woman of 23 years swallowed intentionally 60 tablets of amlodipine (600 mg). After eleven hours of ingestion she was admitted to Warsaw Poison Control Centre. She was in severe clinical condition; tachycardia and deep hypotension were the prominent signs of poisoning. There was not CNS depression. Intensive treatment with i.v. catecholamines (dopamine, norepinephrine), crystalloids (with continuous control of central venous pressure), and i.v. calcium salts (with control of plasma calcium concentration) was started immediately. The patient did not improve but got worse. Acute heart failure developed, especially of left ventricle, so i.v. crystalloids were stopped and dubutamin, morphine, nitroglycerin and glucagon were introduced. Because of oliguria and insufficient effect of high doses of furosemide four-hours hemodiafiltration was set in. The patient's condition slowly improve after third and forth day of hospitalization. The systolic blood pressure rose, heart work was really better and on sixth day--the stabilization of diastolic blood pressure was definitely achieved. The patient was discharge in good condition with heart ejection fraction of 65% measured echocardiographically.
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PMID:[Deep hypotension with transient oliguria and severe heart failure in course of acute intentional poisoning with amlodipine]. 1186 80

Combined poisoning with calcium channel blockers (CCBs) and beta-blockers is usually associated with severe hypotension and heart failure. Due to the block of the beta receptors, treatment with adrenergic agonists, even at high doses, can be insufficient, and beta-independent inotropes, such as glucagon, may be required. Phosphodiesterase III (PDEIII) inhibitors represent a possible alternative to glucagon in these cases as they have an inotropic effect which is not mediated by a beta receptor.
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PMID:Successful treatment with enoximone for severe poisoning with atenolol and verapamil: a case report. 1519 15

The firm association of diabetes mellitus with congestive heart failure (CHF) has been undoubtedly established. Recent reports support the presence of the reciprocal interrelationships between CHF and glucose abnormalities. The present review provides an overview of some aspects of the multifactorial interrelationships between heart failure and diabetes mellitus. Patients with heart failure are generally at higher risk of developing type 2 diabetes mellitus. Several factors may be involved, such as a lack of physical activity, hypermetabolic state, intracellular metabolic defects, poor muscle perfusion, and poor nutrition. Serum levels of inflammatory cytokines and leptin are elevated in patients with heart failure. Activation of the sympathetic system in CHF not only increases insulin resistance but also decreases the release of insulin from the pancreatic beta cells, increases hepatic glucose production by stimulating both gluconeogenesis and glycogenolysis, and increases glucagon production and lipolysis. People who develop type 2 diabetes mellitus usually pass through the phases of nuclear peroxisome proliferator-activated receptor modulation, insulin resistance, hyperinsulinemia, pancreatic beta-cell stress and damage leading to progressively decreasing insulin secretion, and impaired fasting and postprandial blood glucose levels. Once hyperglycemia ensues, the risk of metabolic and cardiovascular complications also increases. It is possible that the cornerstone of diabetes mellitus prevention in patients with CHF could be controlled by increased physical activity in a cardiac rehabilitation framework. Pharmacologic interventions by some medications (metformin, orlistat, ramipril and acarbose) can also effectively delay progression to type 2 diabetes mellitus in general high risk populations, but the magnitude of the benefit in patients with CHF is unknown. In patients with CHF and overt diabetes mellitus, ACE inhibitors may provide a special advantage and should be the first-line agent. Recent reports have suggested that angiotensin receptor antagonists (angiotensin receptor blockers), similar to ACE inhibitors, provide beneficial effects in patients with diabetes mellitus and should be the second-line agent if ACE inhibitors are contraindicated. Treatment with HMG-CoA reductase inhibitors should probably now be considered routinely for all diabetic patients with CHF, irrespective of their initial serum cholesterol levels, unless there is a contraindication.
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PMID:Impaired glucose metabolism in patients with heart failure: pathophysiology and possible treatment strategies. 1544 70

We describe a case of severe heart failure due to the combined effect of verapamil and enalapril overdose in a patient treated regularly with metoprolol. The patient was dependent for 2 days on glucagon and dopamine infusion but remained oliguric, with deteriorating renal function. Marked improvement in all hemodynamic parameters was noted a short time after initiation of treatment with low-dose insulin infusion (1-2 units/h), which allowed the prompt withdrawal of glucagon and dopamine. We discuss the efficacy of glucose-insulin treatment in toxic cardiac depression and suggest that a low dose may be beneficial in similar cases.
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PMID:The use of low-dose insulin in cardiogenic shock due to combined overdose of verapamil, enalapril and metoprolol. 1668 30

Acute poisonings with cardiotoxicants are responsible of significant morbidity and incompressible mortality, mainly among youths. Their incidence is increasing. Death mainly results from cardiac failure refractory to pharmacological treatments as well as sudden cardiac arrest refractory to cardiopulmonary resuscitation. Determination of the exact mechanism of shock is essential to guide adequate treatments. Treatment is supportive including high-dosage catecholamines and may require antidotes. Administration of other inotropic agents (including glucagon, phosphodiesterase inhibitors, calcium salts, and euglycemic insulin) may be discussed, although their efficacy is still not clearly established. Extracorporeal life support allows organ perfusion until reversal of cardiac dysfunction and elimination of the toxicant. Several cases of survival using this exceptional technique were reported in the literature. Thus, based on these reports, extracorporeal life support has gained a recognized place in the therapeutic arsenal of acute poisonings.
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PMID:[Extracorporeal life support for poisonings with cardiotoxicants]. 1863 Aug 23

Endothelial dysfunction is a major characteristic of the atherosclerotic process and can be used to predict the outcome of cardiovascular disease in humans. Together with obesity and insulin resistance, such dysfunction is common among patients with type 2 diabetes and may explain their poor prognosis in connection with such a disease. Insulin resistance in skeletal muscle, adipose tissue, and the liver, a well-characterized feature of obesity and type 2 diabetes, contributes to the impairment of glucose homeostasis. Furthermore, the myocardial muscle can also be resistant to insulin, which might, at least in part, explain the frequent development of heart failure in individuals suffering from type 2 diabetes. The relationship between insulin resistance and endothelial dysfunction has prompted investigations, which reveal that regular exercise, dietary changes, and/or pharmacological agents can both increase insulin sensitivity and improve endothelial function. Glucagon-like peptide-1, an incretin, lowers blood levels of glucose and offers a promising new approach to the treatment of type 2 diabetes mellitus. Its extensive extra-pancreatic effects, including a favorable influence on cardiovascular parameters, are extremely interesting in this connection. The potential pharmacological effects of glucagon-like peptide-1 and its analogues on the endothelium and the heart are discussed in the present review.
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PMID:The potential beneficial role of glucagon-like peptide-1 in endothelial dysfunction and heart failure associated with insulin resistance. 1879 70


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