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  • 1
    ISSN: 1432-1440
    Keywords: Coronary angioplasty ; Excercise ; Atrial natriuretic factor ; Pulmonary artery pressure ; Right atrial pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary According to several reports of close correlations between pulmonary artery pressure and ANF plasma levels it would be convenient to replace invasive pressure monitoring by ANF determination. Mean pulmonary artery and right atrial pressures and pulmonary artery as well as peripheral venous ANF plasma concentrations were measured in 24 patients before and after coronary angioplasty (PTCA) continuously at rest and during exercise: At rest, both pressure and ANF-values remained unchanged before and after PTCA. At exercise, there was a decrease of mean pulmonary artery pressure (from 41.3±8.6 to 31.5±7.4 mmHg,p〈0.001), mean right atrial pressure (from 11.9±3.0 to 9.0±2.3 mmHg,p〈 0.001), pulmonary artery (282.5±191.0 to 207.3±157.2 pg/ml,p〈0.05) and peripheral venous (112.7±48.0 to 97.1±53.2 pg/ml, n.s.) ANF concentration after PTCA. We found no correlation between PTCA-induced changes of right arterial pressures and ANF concentrations, while changes of pulmonary artery pressures were significantly correlated to changes of peripheral venous (r=0.79,p〈0.001) as well as pulmonary artery (r=0.59,p〈0.01) ANF concentrations at exercise. In 6 of the 24 patients, however there was an inverse relationship between changes of pulmonary artery pressures and ANF concentrations. — Our data demonstrate a significant correlation between changes of ANF plasma level and pulmonary artery pressure values at exercise after PTCA. In the individual case however invasive pressure monitoring cannot be replaced by determination of ANF plasma levels.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1435-1803
    Keywords: alcoholic cardiomyopathy ; enzymes ; nicotinamide adenine dinucleotide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We investigated in rat hearts if chronic alcohol consumption causes an enzymatic adaption of the energy-supplying metabolism and/or of the alcohol-aldehyde metabolizing system. 16 rats were pair-fed with a liquid diet for 10 weeks. Ethanol was added to this diet to amount for 35% of calories in eight rats and was isocalorically replaced by saccharose in the control group. Selected enzyme activities of the glycolysis, the glycogenolysis, the β-oxidation of fatty acids, the citric acid cycle and the alcohol-aldehyde oxidizing system were determined in the supernatants of the homogenized hearts. The intracellular redox state was assessed by measurement of the myocardial nicotinamide coenzymes. Enzyme activities of the alcohol-aldehyde metabolizing system did not alter after chronic alcohol intake. As we found that the capacity to oxidize acetaldehyde was much higher than the ability to oxidize ethanol we must question the role of acetaldehyde in inducing alcoholic cardiomyopathy. Chronic ethanol treatment significantly increased the activity of glyceraldehyde-3-phosphate dehydrogenase and decreased the activity of glycogen phosphorylase. The impairment of the hydroxyacylCoA dehydrogenase was not significant. The other measured enzyme activities did not alter, nor the intracellular redox state. The enzymatic adaption indicates an impaired glycogenolysis, an increased glycolysis, and probably a diminished β-oxidation of fatty acids. We expect that the measurement of the responding enzyme activities in human endomyocardial biopsies should be a good tool to further classify cardiomyopathies according to biochemical criteria.
    Type of Medium: Electronic Resource
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