UMLS:C0018801 - FACTA Search

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

The purpose of this study is to evaluate the efficiency of energy metabolism in the myocardium by means of the activities of creatine kinase (CK) and CK isoenzyme following age-related change in the heart and experimental heart failure. Wistar strain male rats aged from 3 weeks to 57 weeks after birth were used. The main experimental results obtained are as follows. (1) There were differences in the compositions of CK isoenzyme of the ventricular, atrial, and papillar muscles. No apparent variation, however, was noted among the basal portions of the left and right ventricular muscles, free wall of the left ventricle, and apex. (2) Compositions of CK isoenzyme analyzed from the ventricle and atrium were clearly different. The level of CK-B subunit activity of the ventricular muscle was highest level in the 5-week-old rat, and subsequently dropped significantly in the 24-week-old rat. Thereafter, the level gradually increased with aging. Dramatic change in the energy metabolism in the myocardium occurred in rats more than 3 weeks old. (3) Decrease in activity of m-CK but increase in activity of succinate dehydrogenase analyzed from the ventricular muscle of experimental heart failure induced by monocrotaline was recognized. From these results, the author assumed that the trend of the composition of CK isoenzyme is one of the indices in the determination of the regulation of energy metabolism of the myocardium.
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PMID:[Evaluation of energy metabolism on the myocardium analyzing of creatine kinase isoenzymes in rats]. 151 14

A 5-month-old boy died of progressive heart failure that started at the age of 3 months. Autopsy revealed a mitochondrial cardiomyopathy and a mitochondrial myopathy of the limb muscle and diaphragm. Cytochemically random defects of cytochrome c oxidase were visualized by light and electron microscopy in the diaphragm and especially the heart muscle, the limb muscle showing a diffuse attenuation whereas the liver and kidneys reacted normally. The activities of NADH-dehydrogenase (complex I) and cytochrome c oxidase (complex IV) were severely diminished (20% residual activity of controls) in the skeletal and heart muscle. In the heart, succinate cytochrome c reductase (complex II/III) was additionally decreased to the same degree. Loss of cytochrome c oxidase activity was based on a reduction of both mitochondrial and nuclear derived subunits in the heart and diaphragm as revealed by immunohistochemical analysis, whereas the limb muscle showed a normal immunoreactive protein content. The results illustrate heterogeneous tissue expression of respiratory chain enzyme defects and demonstrate that a cardiomyopathy may be the leading presentation of a mitochondrial disorder in early infancy.
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PMID:Fatal infantile mitochondrial cardiomyopathy and myopathy with heterogeneous tissue expression of combined respiratory chain deficiencies. 165 34

A reduction in exercise capacity is a common feature of congestive heart failure. We hypothesized that depressed aerobic enzyme activity of skeletal muscle may contribute to this exercise intolerance. Biopsy samples of vastus lateralis muscle were obtained from seven patients with severe chronic heart failure and analyzed for aerobic enzyme activity. Compared with normal laboratory controls, the patients with heart failure had a moderate reduction (greater than 60%) in skeletal muscle citrate synthase and a marked reduction (greater than 90%) in succinate dehydrogenase and cytochrome oxidase (all p less than 0.001). Depression of aerobic enzyme activity of skeletal muscle is associated with severe chronic heart failure and is likely one of the contributory factors for impaired exercise capacity seen in the advanced stages of this condition.
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PMID:Depressed aerobic enzyme activity of skeletal muscle in severe chronic heart failure. 185 Apr 46

The activity of human myocardial enzymes in sudden coronary death (SCD) was quantitatively histochemically examined. The activity of succinate dehydrogenase (SDH), lactate dehydrogenase (LDH), beta-oxybutyrate dehydrogenase (beta-OBDH), alpha-glycerolphosphate dehydrogenase (alpha-GPDH), NAD-diaphorase (NAD-ase), and glucose-6-phosphate dehydrogenase (G-6-PDH) was measured on prompt autopsies (up to 3 hours of death onset). beta-OBDH and LDH showed an increase in activity in the myocardium from the subjects who had suddenly died from coronary heart disease without evident changes in the heart. In SCD in the presence of small cardiosclerosis, the activity of the enzymes characterizing the major processes of energy generation was also enhanced, which was caused by moderately severe myocardial hypertrophy. In the myocardium from the subjects who had died from coronary heart disease in the presence of large postinfarction cardiosclerosis, the activity of the enzymes was directly related to the degree of myocardial hypertrophy and the signs of chronic heart failure. As myocardial hypertrophy progressed, the enzymatic activity rose, but there were signs of chronic heart failure, it fell. The findings suggest that the changes in myocardial enzymatic activity in SCD are heterogeneous and associated with the type of prior abnormalities in the cardiovascular system.
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PMID:[Disorders of myocardial metabolism in sudden coronary death in the presence of coronary atherosclerosis: findings of quantitative histoenzymologic studies]. 221 37

Recent studies in patients with long-term heart failure have suggested that intrinsic abnormalities in skeletal muscle can contribute to the development of early lactic acidosis and fatigue during exercise. The present study provides an analysis of substrate and enzyme content, fiber typing, and capillarization in skeletal muscle biopsy samples obtained at rest from the vastus lateralis in 11 patients with long-term heart failure (left ventricular ejection fraction, 21 +/- 8%) and nine normal subjects. Patients demonstrated a reduced peak exercise oxygen consumption (13.0 +/- 3.3 ml/kg/min) when compared with normals (30.2 +/- 8.6 ml/kg/min, p less than 0.001) and had an accelerated rise in blood lactate levels during exercise. In mixed fiber skeletal muscle, total phosphorylase and glycolytic enzyme activities were not different in the two groups, whereas mitochondrial enzymes involved in terminal oxidation were decreased in patients as compared with normal subjects as indicated by reductions in succinate dehydrogenase (51 +/- 15 vs. 81 +/- 17 microM/g protein/min, p less than 0.001) and citrate synthetase (26 +/- 7 vs. 43 +/- 20 microM/g protein/min, p less than 0.05). 3-Hydroxyacyl-CoA-dehydrogenase, an important enzyme mediating beta-oxidation of fatty acids, was also reduced in patients as compared with normals (18 +/- 7 vs. 27 +/- 10 microM/g protein/min, p less than 0.05). There was no difference in high-energy phosphagens or lactate concentration of mixed muscle in the two groups, whereas glycogen content was decreased in patients (262 +/- 29 vs. 298 +/- 35 microM glucosyl units/kg dry wt, p = 0.01). Patients demonstrated a reduced percentage of slow twitch type I fibers (36 +/- 7% vs. 52 +/- 22%, p less than 0.05) and had a higher percentage of type IIb fast twitch fibers (24 +/- 9% vs. 11 +/- 12%, p = 0.02), which were smaller than the type IIb fibers seen in normal subjects (p less than 0.05). In patients, the number of capillaries per fiber was decreased for type I and type IIa fibers (both, p less than 0.03), but the ratio of capillaries to cross-sectional fiber area was not different for the two groups. These data demonstrate major alterations in skeletal muscle histology and biochemistry in patients with long-term heart failure, including fiber atrophy, a decrease in percentage of composition of type I fibers, and an increase in type IIb fibers accompanied by a decrease in oxidative enzyme capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure. 229 59

The response to exercise was investigated in trained and sedentary rats with moderate compensated heart failure produced by myocardial infarction (MI) and in rats that underwent sham operations. Trained rats ran on a treadmill (10% grade at 20 m/min) for 60 min/day, 5 days/week for 10 to 12 weeks, whereas sedentary rats had only limited activity. Maximal oxygen consumption normalized for body weight (ml kg-1 min-1) was determined for each rat and found to be (1) greater in trained rats when compared with sedentary rats and (2) greater in sham-operated rats when compared with their counterparts that suffered infarction. In addition, skeletal muscle succinate dehydrogenase activities were greater and the blood lactic acid response to submaximal exercise was lower in trained rats compared with sedentary rats. Left ventricular infarct size for sedentary and trained rats with infarction was 36 +/- 3% and 34 +/- 3% of the total endocardial circumference, respectively, and resulted in (1) elevated left ventricular end-diastolic pressures at rest and during exercise, (2) lower mean arterial pressures at rest, and (3) lower maximal heart rates when compared with those in their sham-operated counterparts. However, normalization of mean arterial pressures during submaximal and maximal exercise was found along with a trend toward normalization of maximal heart rate when trained rats with infarction were compared with their sedentary counterparts. Blood flows to the kidneys, organs of the gut, and skeletal muscle during both submaximal and maximal exercise were unaffected by either myocardial infarction or training; no differences between sedentary and trained rats with infarction and sedentary and trained sham-operated rats were found. These results demonstrate that an exercise training program of moderate intensity produces beneficial hemodynamic and metabolic effects in rats with moderate compensated heart failure.
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PMID:Endurance training in rats with chronic heart failure induced by myocardial infarction. 373 31

The timing of surgery in chronic aortic regurgitation remains a difficult problem. To identify variables predictive of postoperative haemodynamic improvement, changes in left ventricular mass, volume, morphology, and histochemistry were analysed in 67 patients undergoing surgery for chronic aortic regurgitation. Patients were divided into two groups: those in whom the left ventricular echo diameters returned to normal after operation (51 patients, group A), and those with postoperative dilatation (16 patients, group B). A preoperative biopsy was obtained in all patients; postoperative tissue samples were available in 13 patients (five from group A, eight from group B). Data were correlated with the postoperative clinical, haemodynamic state over a follow-up period of three years. Regression of hypertrophy was usually incomplete. Echocardiographic and angiographic data could not define the type and degree of dysfunction which was irreversible. Massive fibre hypertrophy (mean 34.1 micrometers), moderately or severely increased interstitial fibrous tissue, reduced levels of the myofibrillar and mitochondrial enzymes adenosine triphosphates and succinate dehydrogenase in pre- and post-operative tissue samples correlated with persistent dilation, cardiac failure, and early death (group B). Irreversible morphological and functional changes contributed to a depressed cardiac function after operation. Preoperative ventricular biopsies are thus of prognostic importance in volume overload.
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PMID:Irreversible morphological changes contributing to depressed cardiac function after surgery for chronic aortic regurgitation. 621 5

Defects of the mitochondrial respiratory chain in cardiac muscle are an important, yet still overlooked cause of heart failure. In 16 of 32 endocardial biopsies from infants affected by "idiopathic" hypertrophic cardiomyopathy we demonstrated a remarkable decrease of activity of either complex I, or complex IV, or both, relative to complex II + III activity which was taken as an index of mitochondrial proliferation. At the molecular level, several mtDNA mutations have been associated with cardiomyopathy. For instance, MIMyCa is a maternally inherited syndrome presenting with a variable combination of skeletal and heart muscle failure associated with a heteroplasmic A3260G transition in the tRNALeu(UUR) gene. To study the effects of the mutation in a controlled system, we prepared clones of transmitochondrial cybrids by fusing mutant cytoplasts with mtDNA-less tumor cells. Two groups of clones were identified: nearly 100% mutant (M group) and nearly 100% wild-type (WT group). The means of complex I and IV in the M group were 63% and 67% relative to the WT group. The O2 consumption in the M group was 36%, and the lactate production was 218% of that in the WT group. MtDNA-specific translation was defective in M clones. The study of transmitochondrial cybrids is an important clue to test the pathogenicity of mtDNA mutations.
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PMID:OXPHOS defects and mitochondrial DNA mutations in cardiomyopathy. 760 20

Ilexonin A (IA), a pentacyclic triterpene, has been semisynthesized in china for the first time. It is extracted from the root of Ilicis pubescentis, a commonly used herbal medicine in Guangdong for the treatment of cardiovascular, cerebrovascular and peripheral vascular diseases and heart failure with satisfactory effects. The pharmacokinetic studies indicated that the elimination half-life after oral and i.v. dosing were 17.7 +/- 2.4 h and 22.5 +/- 2.9 h respectively. The total clearance was 4.6 +/- 0.51/h. The bioavailability of IA capsules was 0.39 +/- 0.14 and LD50 was 234 mg/Kg. We have adopted modern techniques, including cellular electrophysiology, isotope tracing methods, molecular biology, electromicroscopy, etc., to probe into the pharmacologic mechanisms of the effects of IA on cardiovascular system. The results indicated that IA can increase the contractility of isolated guinea pig auricular myocardium, attenuate vascular smooth muscle tension induced by noradrenaline in the rabbit aorta. IA can exert a biphasic regulatory effect on arterial blood pressure. IA also can prolong A-V duration of Hiss bundle electrograph (HBE) in rabbits and prolong the action potential duration and the effective refractory period (ERP) of myocardial cells in guinea pigs. The results showed that IA can increase the cAMP content in the smooth muscle of aorta and exert a calcium-blockade effect. Therefore, the peripheral resistance vessels are relaxed and the cardiac afterload is lowered. IA-blocked calcium channels are correlated with both the potential-dependent channel and the receptor operated channel in vascular smooth muscles. IA also increases the cAMP content of myocardium and accelerates the cellular calcium influx and efflux, and this may be responsible for the direct mechanism of the positive inotropic action of IA. Under electron microscopy, it is observed that IA can alleviate the defect of succinate dehydrogenase in the myocardial mitochrondria of rabbit chronic congestive heart failure (CF) model and reduce the microstructural damage of the failed myodardium, therefore the anoxic tolerance of myocardium is increased, the effect of IA on the platelet stretching activity and microstructure in the patients with CF is also studied. It is found that IA can reduce the hypercoagulability of blood, decrease the severity of blood stagnation and improve the status of microcirculation. Effects of IA introventricular and cardiovascular central microinjection (nucleus tractus solitarius, paraventricular nucleus) on arterial blood pressure and heart rate were studied. It demonstrated that IA possess circulatory neuroregular effects by the medium of alpha-receptor and beta-receptor of cardiovascular motoneurons.
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PMID:Effects of Ilexonin A on circulatory neuroregulation. 761 16

Congestive heart failure is often associated with skeletal muscle abnormalities that contribute to early fatigue and acidosis. Up to the present time, however, the mechanisms responsible for these changes are unclear. Myocardial infarctions were produced by coronary ligation in adult Sprague-Dawley rats. At 20 weeks, 10 control rats, and 15 animals with heart failure [defined by elevated LVEDP (26.1 +/- 3.1 v 2.5 +/- 0.5 mmHg) and RV hypertrophy (300 +/- 21 g v 158 +/- 9 mg)] underwent in vivo measurements of total body, and soleus total protein and myosin heavy chain (MHC) synthesis by [3H]leucine constant infusion. Soleus muscle was also analysed for protein content, and MHC isoenzyme content by SDS-PAGE. Northern blotting also was used to determine levels of the mRNA's encoding type I, IIa, IIb, and IIx MHC, alpha-skeletal actin, COX III, SDH and GAPDH. Soleus muscles in heart failure rats were smaller than controls (112 +/- 6 v 126 +/- 5 mg) and the degree of atrophy was significant when corrected for body mass (0.38 +/- 0.02 v 0.46 +/- 0.02 mg/g. P = 0.007). Although there was no significant difference in plasma leucine flux (an index of whole-body protein synthesis), soleus muscle total and MHC synthesis was reduced in heart failure animals. Whereas the Type I MHC isoenzyme (beta MHC) was the only MHC detected in the soleus of control animals, type II MHC isoenzyme comprised 11.8 +/- 3.1% of the MHC in the heart failure group. Furthermore, steady-state mRNA levels encoding beta MHC were significantly depressed in the heart failure rats, where those encoding Types IIb and IIx MHC were increased. Steady-state mRNA levels of alpha-skeletal actin, cytochrome C oxidase (COX III) and succinate dehydrogenase (SDH) were also significantly depressed. This animal model of chronic heart failure is associated with quantitative and qualitative alterations in skeletal muscle gene expression that are similar to those reported in skeletal muscle of patients with chronic heart failure. The altered phenotype and impaired metabolic capacity may contribute to exercise intolerance in CHF.
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PMID:Alterations in skeletal muscle gene expression in the rat with chronic congestive heart failure. 887 78

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