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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of variations in the volume conductor properties of the torso on the electrocardiogram were studied by means of a theoretical eccentric spheres model. The model includes a blood cavity, cardiac muscle layer, pericardium, lung region, skeletal muscle layer, and subcutaneous fat. The source of the field is a double-layer spherical cap located within the myocardium. The following effects regarding the electrocardiogram (ECG) potentials were determined: (1) blood augments the potential, but less than predicted by simpler published models; (2) in anemia, high potentials are expected, whereas in polycythemia, voltages are reduced; (3) abnormally low lung conductivity (emphysema) causes low surface potentials whose magnitude is controlled by the low conductivity skeletal muscle layer; (4) low voltages result both from low and high pericardial conductivities; (5) the surface potential increases with increasing myocardial conductivity; (6) low skeletal muscle conductivity (Pompe's disease) causes high surface potentials; (7) obesity lowers the potential only slightly; (8) a thick myocardium, protruding into the lung region, slightly augments the potential; (9) an increase in the thickness of the myocardium at the expense of the blood cavity causes a decrease in potential; (10) the potential increases with increasing heart size; and (11) the location of the heart within the torso has a very significant effect on the surface potential distribution.
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PMID:The effects of variations in conductivity and geometrical parameters on the electrocardiogram, using an eccentric spheres model. 75 26

Echocardiography was studied in 83 uremic patients on maintenance hemodialysis and 18 normal subjects. Cardiac systolic and diastolic functions were evaluated according to Yamaguchi's method. Systolic functions such as ejection fraction and fractional shortening decreased in the patients receiving hemodialysis for less than 3 months. However, they remained within normal range in the patients under hemodialysis for more than 3 months. There were no significant correlations between systolic functions and mean blood pressure or various serum biochemical parameters such as urea nitrogen, creatinine, Na, K, Ca, P, hematocrit and PTH-C. Diastolic functions such as rapid filling rate/endosystolic volume, mean velocity of circumferential fiber lengthening during rapid filling, diastolic descent rate and diastolic posterior wall velocity also decreased in the patients receiving hemodialysis for less than 3 months. However, they increased slightly in the patients under hemodialysis for more than 3 months, although they were still lower than those in normal subjects. They were not related to mean blood pressure or various serum biochemical parameters. Hemodialysis patients had left ventricular hypertrophy regardless of duration of hemodialysis. Diastolic dysfunction in hemodialysis patients seemed to be due to systolic dysfunction, left ventricular hypertrophy and diminished ventricular compliance with myocardial degeneration. It was also suggested that increasing slow filling and atrial contraction in diastole might be related to diastolic dysfunction. These cardiac changes may be compensatory reactions of cardiac muscle to various uremic environments such as anemia, hypertension, fluid retention, electrolytes disturbance or uremic toxins.
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PMID:[An echocardiographic study of cardiac function in chronic hemodialysis patients]. 258 30

The clinical signs and lesions of Nubian goats and Desert sheep orally dosed with fresh and dry leaves and stems of Ipomoea carnea at 2.5, 5 and 10 g/kg/day were studied. The signs of Ipomoea poisoning were inappetence, depression, weakness of the hind limbs, dyspnea, staggering, and pallor of the visible mucous membranes. The main lesions were focal necrosis and fatty vacuolation of centrilobular hepatocytes, accumulation of fibroblasts in hepatic portal tracts, degeneration or necrosis of the cells of the renal proximal convoluted tubules, hemorrhage in renal cortices, in renal medullas and in cardiac muscle fibers, focal pulmonary edema, and emphysema and straw-colored fluid in serous cavities. Increased serum aspartate amino transferase and ammonia concentrations, and decreased concentrations of total protein, calcium and magnesium in the serum of Ipomoea-poisoned animals were detected. Hematological changes indicated the development of normocytic normochromic anaemia.
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PMID:The effects of Ipomoea carnea on goats and sheep. 362 12

This study examined the effect of long-term administration of reserpine, an adrenergic blocking agent, on cardiac hypertrophy in animals with severe iron deficiency anaemia. This condition was induced by feeding rats on an iron-deficient diet for 30 days from the time of weaning. Anaemia was indicated by lowering of blood haemoglobin levels. Reserpine was administered i.p. (0.15 mg/kg body wt) every day during the experiment. Marked cardiac hypertrophy, as indicated by increase heart weight and increased size of cardiac muscle cells, was evidenced in iron-deficient rats, while the heart weights and myocardial cell size of drug-treated anaemic rats were in the normal range. The successful prevention of cardiac hypertrophy in anaemic iron-deficient rats by reserpine administration supports the hypothesis that noradrenaline plays a key role in the cardiac-hypertrophy process in iron deficiency anaemia.
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PMID:Pathogenesis of cardiac hypertrophy in iron deficiency anaemia: the role of noradrenaline. 621 77

Noradrenaline levels and heart morphology were studied in animals with severe iron deficiency anaemia. This condition was induced by feeding rats an iron-deficient diet for 30 days from the time of weaning. Anaemia was indicated by the lowering of blood haemoglobin levels. Statistically significant decreases in myocardial noradrenaline levels associated with cardiac hypertrophy, as revealed by increased wet heart weight and increased size of cardiac muscle cells, were observed in anaemic rats compared with controls.
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PMID:The effect of iron deficiency anemia in the rat on catecholamine levels and heart morphology. 645 88

Physical exercise increases metabolic rate, and induces both adaptational biogenesis of mitochondria in skeletal muscle and an increase in antioxidant capacity. The onset of experimental anorexia and cachexia can be delayed by voluntary exercise. As skeletal muscle is the main target for cancer cachexia, we determined the levels of coenzymes Q9 and Q10 in skeletal muscle from tumour-bearing exercising rats, and compared them to those of sedentary tumour-bearers and controls. Both tumour-bearing groups had increased levels of coenzymes Q9 and Q10 in the anterior tibial muscle (P < 0.05 for exercised animals). In the soleus muscle, only the tumour-bearing exercising animals demonstrated an increase in the levels of both coenzymes (P < 0.05). In cardiac muscle, the presence of tumour and exercise reduced the levels of coenzymes below that of sedentary controls. Exercise counteracted the anaemia in the tumour-bearing host (P < 0.05). In conclusion, the increase in antioxidant capacity in skeletal muscle indicates a defence mechanism in the tumour-bearing hosts which is augmented by physical exercise.
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PMID:Coenzymes Q9 and Q10 in skeletal and cardiac muscle in tumour-bearing exercising rats. 750 6

Hemoglobin concentration, iron parameters and cardiac status of 25 patients with beta thalassemia/hemoglobin E disease were measured. Two-dimensional echocardiography was employed to evaluate chamber size, ejection fraction and muscle fiber shortening. The seventeen patients who had a mean hemoglobin concentration of less than 7.7 g/dl were found to have significantly larger cardiac chambers and higher cardiac output than the patients with higher hemoglobin concentrations. A statistically significant difference in ejection fraction and per cent of fractional shortening of cardiac muscle fibers was not found. A comparison of subjects with ferritin concentrations above and below 1,500 micrograms/L showed no significant difference in chamber sizes, ejection fraction and in per cent fractional shortening. However, a comparison of 14 patients with transferrin saturation > or = 80 per cent with those less than 80 per cent showed a significant decrease in both ejection fraction and fiber fractional shortening in the more highly saturated subjects. By using stepwise multiple regression analysis, the hemoglobin level was shown to significantly determine cardiac enlargement, while ejection fraction and percentage fractional shortening were significantly associated with transferrin-iron saturation. Thus, anemia leads to chamber enlargement, while high transferrin iron saturation is associated with cardiac muscle dysfunction. The findings in the individual patient reflect the integration of these two effects.
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PMID:Echocardiographic features in patients with beta thalassemia/hemoglobin E: a combining effect of anemia and iron load. 779 36

Different tissues display distinct sensitivities to defective mitochondrial oxidative phosphorylation (OXPHOS). Tissues highly dependent on oxygen such as the cardiac muscle, skeletal and smooth muscle, the central and peripheral nervous system, the kidney, and the insulin-producing pancreatic beta-cell are especially susceptible to defective OXPHOS. There is evidence that defective OXPHOS plays an important role in atherogenesis, in the pathogenesis of Alzheimer's disease, Parkinson's disease, diabetes, and aging. Defective OXPHOS may be caused by abnormal mitochondrial biosynthesis due to inherited or acquired mutations in the nuclear (n) or mitochondrial (mt) deoxyribonucleic acid (DNA). For instance, the presence of a mutation of the mtDNA in the pancreatic beta-cell impairs adenosine triphosphate (ATP) generation and insulin synthesis. The nuclear genome controls mitochondrial biosynthesis, but mtDNA has a much higher mutation rate than nDNA because it lacks histones and is exposed to the radical oxygen species (ROS) generated by the electron transport chain, and the mtDNA repair system is limited. Defective OXPHOS may be caused by insufficient fuel supply, by defective electron transport chain enzymes (Complexes I - IV), lack of the electron carrier coenzyme Q10, lack of oxygen due to ischemia or anemia, or excessive membrane leakage, resulting in insufficient mitochondrial inner membrane potential for ATP synthesis by the F0F1-ATPase. Human tissues can counteract OXPHOS defects by stimulating mitochondrial biosynthesis; however, above a certain threshold the lack of ATP causes cell death. Many agents affect OXPHOS. Several nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit or uncouple OXPHOS and induce the 'topical' phase of gastrointestinal ulcer formation. Uncoupled mitochondria reduce cell viability. The Helicobacter pylori induces uncoupling. The uncoupling that opens the membrane pores can activate apoptosis. Cholic acid in experimental atherogenic diets inhibits Complex IV, cocaine inhibits Complex I, the poliovirus inhibits Complex II, ceramide inhibits Complex III, azide, cyanide, chloroform, and methamphetamine inhibit Complex IV. Ethanol abuse and antiviral nucleoside analogue therapy inhibit mtDNA replication. By contrast, melatonin stimulates Complexes I and IV and Gingko biloba stimulates Complexes I and III. Oral Q10 supplementation is effective in treating cardiomyopathies and in restoring plasma levels reduced by the statin type of cholesterol-lowering drugs.
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PMID:Mitochondrial medicine--molecular pathology of defective oxidative phosphorylation. 1131 62

Clinical-and-hemodynamic manifestations of heart failure were studied in 28 patients with iron deficiency anemia (IDA). Half of the IDA patients have been found out to develop the heart failure syndrome of both systolic and diastolic variant. Decrement in exercise tolerance in the above patients is due to anemia as well as to development and progression of the cardiac muscle dysfunction, which fact warrants an in-depth diagnostic quest together with an optimum treatment.
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PMID:[Clinical and hemodynamic characteristics of heart dysfunction in patients with iron deficiency anemia]. 1207 49

Despite being relatively recent, a growing and significant accumulation of experimental and clinical evidence has been observed that points to a gradual state of immune-inflammatory activation in patients with heart failure (HF). High levels of several cytokines are found in the circulation and cardiac muscle of individuals with HF, and invariably correlate with the severity of the disease. These cytokines act on endothelial dysfunction, oxidative stress, induction of anemia, myocyte apoptosis, and on the progressive loss of skeletal muscle mass which is conventionally called the inflammatory paradigm of HF. Not only the myocardium, but also several tissues seem to synthesize these cytokines and perpetuate this continuous inflammatory state at a low degree, including leukocytes, monocytes, skeletal muscle cells and endothelial cells in response to hemodynamic and infectious stimuli, to hypoxia, to oxidative stress, to neurohumoral activation, and others. Thus, a network of molecules that interact with each other is formed, and connections with other axes that effectively contribute to the clinical deterioration of the patients are also established which fits into the pathophysiological model of multisystemic involvement that has been increasingly attributed to HF. Although the determination of these biomarkers in peripheral blood provides solid evidence of prognostic power, the results of therapeutic trials that modulated the immune-inflammatory loop in the clinical phase have been, so far, hardly encouraging. Therefore, we believe that a better understanding of the inflammatory activation and its multifaceted relation with the axes of decompensation of the disease is key for new therapeutic perspectives with a relevant impact to be established in the near future.
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PMID:Immune-inflammatory activation in heart failure. 1790 20


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