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)

Leukotoxin (9,10-epoxy-12-octadecenoate) biosynthesised from linoleate by neutrophils is highly toxic to cellular function. Its cardiovascular effects were studied in dogs together with the effects of various fatty acids. Aortic flow, left ventricular peak dP.dt-1, and aortic pressure were measured in 60 anaesthetised dogs, which were divided into 10 groups of six animals each--namely, control group (10 ml of physiological saline), three leukotoxin groups (5, 10, and 50 mg.kg-1), two linoleic acid groups (10 and 50 mg.kg-1), two oleic acid groups (10 and 50 mg.kg-1), and two stearic acid groups (10 and 50 mg.kg-1). Leukotoxin injected intravenously depressed cardiac function in a dose dependent manner. Administration of leukotoxin 5 mg.kg-1 showed no significant cardiotoxic effect. However, 10 mg.kg-1 of leukotoxin significantly decreased aortic flow from 0.74(0.04) to 0.40(0.07) litre.min-1 (mean(SEM], left ventricular peak dP.dt-1 from 2040(205) to 1140(217) mmHg.s-1, and aortic pressure from 106(7.1)/67(6.3) to 75(9.2)/48(6.5) mmHg 5 min after injection. Dogs given leukotoxin 50 mg.kg-1 showed more pronounced cardiodepressive effects; aortic flow was decreased to 0.19(0.06), left ventricular dP.dt-1 to 560(134), and aortic pressure to 72(15.1)/41(10.6) 5 min after injection. All dogs in this group were dead within 45 min. Administration of 10 mg.kg-1 of linoleic acid, oleic acid, or stearic acid caused no significant haemodynamic changes. Administration of linoleic acid 50 mg.kg-1 had cardiotoxic effects, but the effect was less than that of leukotoxin. Since leukotoxin appears to be a potent cardiodepressive agent it may be an important factor in the development of heart failure observed in patients with severe burns.
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PMID:Cardiovascular effects of leukotoxin (9, 10-epoxy-12-octadecenoate) and free fatty acids in dogs. 316 45

Histological findings on repeat endomyocardial biopsy and changes in left ventricular ejection fraction early during immunosuppressive treatment were studied in 20 patients with documented myocarditis. All patients presented with heart failure of less than six months' duration and a left ventricular ejection fraction of less than or equal to 0.40. Repeat biopsy and assessment of ventricular function were performed at a mean (SEM) of 79 (17) days after the initial biopsy. At repeat biopsy eight patients had evidence of ongoing myocarditis and 12 showed resolved myocarditis. In eight (66%) of the 12 patients with resolved myocarditis ventricular function had improved significantly. Left ventricular ejection fraction also improved significantly in four of eight patients during treatment despite ongoing myocardial inflammation. Regardless of the histological findings on repeat biopsy, early improvement in ejection fraction was associated with an excellent long term prognosis--that is 83% survived for at least three years. Histological resolution of myocarditis during immunosuppressive treatment is not a prerequisite for improvement in ventricular function; and changes in left ventricular ejection fraction during the first three months of treatment are predictive of clinical outcome.
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PMID:Relation between histological findings on early repeat right ventricular biopsy and ventricular function in patients with myocarditis. 319 Sep 62

Approximately 32% of the rats used as animal models showed an elevated heart weight/body weight ratio (0.432[SEM 0.022] g.100 g-1 compared to 0.293[0.009] g.100 g-1 for sham-operated rats), a hydrothorax, pulmonary and liver congestion, and specific histological changes 82-93 weeks after surgically induced aortic constriction. The histological changes were comparable to those observed in hearts of people suffering from long term hypertension. Cardiac failure was also confirmed by depressed contractility as measured by maximum and minimum dP/dt (first derivative of left ventricular pressure), which were 4604(346) and 3627(526) mm Hg.sec-1, respectively, compared with 9165(745) and 5835(268) mm Hg.sec-1 respectively in rats that did not develop left ventricular hypertrophy and failure (CLIP rats). Systolic and left ventricular blood pressures measured under anaesthesia were also decreased: 71.6(5.0) and 88.1(6.3) mm Hg respectively in rats with congestive heart failure, compared with 83.6(2.4) and 109.5(3.6) mm Hg in CLIP rats. Except for a prolonged mean PQ interval associated with a lower heart rate and for a slightly shorter QRS interval in the conscious state, the electrocardiograms of rats with congestive heart failure did not show any major abnormalities specific to ventricular hypertrophy and/or failure. This model could be useful for studying the pathology and adaptative mechanisms in compensated pressure overload induced congestive heart failure as well as in studies comparing pathological changes and means of treatment of congestive heart failure with different aetiologies encountered in the human population.
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PMID:A pressure overload model of congestive heart failure in rats. 259 Sep 29

Adverse pulmonary reactions to some nitrofuran antibiotics are thought, in part, to involve production of reactive oxygen radicals. Furazolidone, a nitrofuran antibiotic, causes a dilated cardiomyopathy in domestic turkeys. The mechanism of this drug induced cardiomyopathy is unknown. We investigated the possible role of free radical injury in this heart failure model. Left ventricular lipid peroxidation capacity, assessed by two methods (the thiobarbituric acid reactive substances and lipid hydroperoxides assays respectively), was investigated in five 5-8 week old cardiomyopathic turkeys with severe cardiac dilatation, left ventricular dysfunction and systemic hypotension, and in five control birds. Superoxide dismutase activity, total and manganese, was also measured in the crude left ventricular homogenates. Both lipid peroxidation products were reduced in the myopathic hearts: thiobarbituric acid reactive substances (malondialdehyde) 70(SEM 4) v 86(3) nmol.100 mg protein-1 in controls, p less than 0.02; and lipid hydroperoxides 29(7) v 74(14) nmol.100 mg protein-1, p less than 0.02. Total superoxide dismutase activity was similar in cardiomyopathic and control hearts: 670(26) v 657(105) nitrite units.100 mg protein-1. Although total superoxide dismutase activity was unchanged, we found decreased manganese superoxide dismutase in the dilated hearts compared with controls (54% v 84% of total activity, p less than 0.02). In separate in vitro experiments furazolidone (2-10 mg.g wet weight-1) did not increase malondialdehyde production in turkey (or rat) left ventricular homogenates. These results indicate that cardiomyopathy induced by furazolidone is associated with decreased myocardial lipid peroxidation. Although as yet unexplained, the decrease may be due to a diminished amount of heart lipid susceptible to peroxidation accompanying the process of cardiac hypertrophy and dilatation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced lipid peroxidation in dilated hearts of cardiomyopathic turkeys. 325 24

The influence of age on cardiac allograft rejection was studied in 57 consecutive recipients. Twenty-one subjects were 54 years of age or older (mean, 57.7 +/- 0.6 years [+/- SEM]; range, 54 to 63 years) and 36 subjects were 52 years of age or younger (mean, 39.9 +/- 1.8 years; range, 16 to 52 years; p less than 0.001). The older recipients had fewer rejection episodes during the first four months following cardiac transplantation (0.24 +/- 0.05 episodes per month versus 0.72 +/- 0.09 episodes per month; p less than 0.001) and during the total duration of follow-up (0.20 +/- 0.03 episodes per month versus 0.40 +/- 0.07 episodes per month; p = 0.045), and experienced their first rejection episode later (50.4 +/- 4.0 days versus 27.7 +/- 8.5 days; p = 0.008). Younger age was found to add significantly as a predictor of rejection in a multivariate analysis that controlled for sex, immunosuppressive agents, cause of heart failure, and pretransplantation lymphocyte cross-match status (r = 0.64, p less than 0.05). Decreased rejection frequency occurred without a concomitant increase in the serious infection rate (67 percent in both groups). The 12-month actuarial survival was 100 percent in the older group and 94 percent in the younger group (p = NS). Decreased rejection in the older recipients is likely a manifestation of an age-associated decline in immune function and might represent an advantage in transplantation for carefully selected older patients.
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PMID:Age-associated decline in cardiac allograft rejection. 331 Jun 19

To determine the prevalence of unrecognized brain dysfunction accompanying chronic severe cardiac disease, we examined 20 clinically stable consecutive admissions to a cardiac rehabilitation service who were free of known stroke or dementia. Age range was 47 to 85 years (mean +/- SEM, 72.5 +/- 2.1 years), the male: female ratio was 10:10. Multiple cognitive deficits including significant memory impairment and disorientation were present in eight patients (40%), and seven of these eight patients were unable to administer their own medications reliably. An additional six patients (30%) showed milder impairments. One patient was found to be normal after neurological examination, four showed evidence of a single brain lesion, and 15 of 20 (75%) had multiple neurological abnormalities suggesting multifocal brain disease. The mechanism of cognitive deficits in cardiac patients is unclear, and it may be related to multiple infarcts, or acute or chronic hypoxic damage secondary to arrhythmias, cardiac failure, or small vessel disease of the brain. The term "circulatory dementia" is proposed to describe patients with vascular disease and non-Alzheimer type dementia. Patients with cardiac disease should undergo cognitive screening, as early identification of patients at risk of progressive intellectual loss may allow early use of preventive therapy.
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PMID:Unrecognized cognitive impairment in cardiac rehabilitation patients. 333 26

Beta agonist therapy for heart failure has been disappointing, perhaps because of renin induced aldosteronism. To investigate this possibility we measured plasma renin activity (PRA) in 23 patients (17 male, 6 female, age 41-70) with New York Heart Association stage III heart failure due to ischaemic heart disease in a placebo controlled trial over one month. All patients received constant doses of digoxin and diuretics throughout the trial. Compliance was confirmed in all patients by digoxin and prenalterol assay. In a preliminary (dose titration) study of 9 patients there was a progressive, but non-significant rise of mean PRA from 14.8 to 17.6 and 27.7 ng/ml per h with doses of 20, 50 and 100 mg of prenalterol, respectively. After one month of treatment with prenalterol (n = 11), PRA was 12.8 +/- 2.4 (SEM) ng/ml per h which was not significantly different from the initial level of 14.4 +/- 2.3 ng/ml per h (n.s.). The placebo group (n = 12) results were 13.8 +/- 4.2 ng/ml per h at entry and 14.4 +/- 5.2 ng/ml per h at one month (n.s.). These results indicate that PRA is elevated by acute treatment with the partial beta agonist prenalterol but stimulation of renin secretion does not appear to occur with chronic therapy.
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PMID:Effect of the partial beta-agonist prenalterol on plasma renin activity in patients with left ventricular failure. 354 8

To evaluate the effects of dobutamine on myocardial function in newborns, left ventricular systolic time intervals (STI) - normalized pre-ejection period (PEPI), normalized left ventricular ejection time (LVETI) and pre-ejection period to left ventricular ejection time ratio (PEP/LVET) - were assessed by echocardiography in 18 newborns treated with dobutamine for clinically diagnosed heart failure. Examinations were performed prior to and 30 min after starting dobutamine infusion (7.5 or 10 micrograms/kg per min). Patients were assigned to two groups according to their PEP/LVET prior to dobutamine administration: group I (n = 9) with pre-treatment PEP/LVET less than or equal to 0.35 and group II (n = 9) with pre-treatment PEP/LVET greater than 0.35. While there was no change of STI in group I, dobutamine infusion resulted in a significant decrease in PEPI (from 102 +/- 4.8 to 87.8 +/- 4.2; mean +/- SEM; P less than 0.01) and of PEP/LVET (from 0.56 +/- 0.05 to 0.45 +/- 0.05; mean +/- SEM; P less than 0.01) and in a significant increase of LVETI (from 237.6 +/- 5.6 to 253.3 +/- 5.2; mean +/- SEM; P less than 0.01) in group II. Heart rate increased significantly in both groups. Left ventricular end-diastolic dimension, also assessed by echocardiography, did not change in the eight studies performed. An increase in mean arterial pressure was found in three out of five newborns of group II and in one out of four patients in group I. It is concluded that dobutamine can improve cardiac performance in newborns with impaired left ventricular function. This effect is probably due to an improvement in myocardial contractility.
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PMID:Effects of dobutamine on left ventricular performance in newborns as determined by systolic time intervals. 356 49

Germ cell degeneration during spermatocytogenesis and meiosis was investigated to explain the age-related decline in daily sperm production (DSP). Numbers of Types A-dark, A-pale, and B-spermatogonia, potential daily sperm production per g parenchyma (PDSP) based on type B-spermatogonia, early primary spermatocytes, and late primary spermatocytes, and DSP per g based on early spermatids were determined in 15 men aged 20 to 48 yr (mean +/- SEM, 33 +/- 2 yr) and 15 men aged 52 to 90 yr (65 +/- 3 yr). Testes obtained within 15 h of death (largely due to trauma or heart failure) were perfused vascularly with glutaraldehyde. The number of each cell type per g parenchyma was calculated as the product of the percentage of nuclei in the parenchyma times a correction factor for section thickness and nuclear diameter divided by the volume of a single nucleus of that cell type. Paired testicular weight was lower (p less than 0.01) in older men (33 +/- 3 g) than in the younger men (49 +/- 3 g). Younger and older men had similar numbers of A-dark, A-pale, and B-spermatogonia per g parenchyma. PDSP based on late primary spermatocytes and DSP based on early spermatids were lower (p less than 0.01) in older men than in younger men. In younger men, PDSP was similar (p greater than 0.05) between B-spermatogonia and late primary spermatocytes, whereas DSP measured at the spermatid level was abruptly lower than that estimated from younger cell types. Older men showed reduction in PDSP between early and late primary spermatocytes, with further reduction occurring in DSP at the spermatid level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantification of human spermatogenesis: germ cell degeneration during spermatocytogenesis and meiosis in testes from younger and older adult men. 367 17

Plasma catecholamine concentrations were measured in 15 patients (six male) aged 14-63 years attending the casualty department with acute severe asthma (peak expiratory flow 27% (SEM 3%) of predicted). Nine patients were admitted and six were not. The plasma noradrenaline concentration, reflecting sympathetic nervous discharge, was two to three times normal in all patients and was significantly higher in those who required admission compared with those discharged home (mean 7.7 (SEM 0.6) v 4.7 (0.5) nmol/l (1.3 (SEM 0.1) v 0.8 (0.08) ng/ml); p less than 0.001). Plasma adrenaline concentration, however, was not increased in any patient. This surprising failure of the plasma adrenaline concentration to increase during the stress of an acute attack of asthma was unexplained and contrasts with the pronounced rise in plasma adrenaline and noradrenaline concentrations in acute myocardial infarction, heart failure, and septicaemia. The failure of plasma adrenaline concentration to increase in acute asthma is unlikely to be explained by adrenal exhaustion, but it may be another example of impaired adrenaline secretion in asthma.
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PMID:Circulating catecholamines in acute asthma. 391 81


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