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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 71 (1993), S. S124 
    ISSN: 1432-1440
    Keywords: Ubiquinone ; ATP ; Heart failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The pathophysiological basis for the use of metabolic therapy in the treatment of heart failure is analyzed. Bioenergetical processes related to ATP bioavailability play a central role in regulating myocardial contractility at rest and on effort. Furthermore, a significant correlation has been demonstrated in diseased heart between ATP content, revealed at endomyocardial biopsy, and systolic and diastolic left ventricular indexes evaluated with invasive and noninvasive methods. Several international investigations demonstrate the beneficial effects of ubiquinone (coenzyme Q10) in the treatment of heart failure. Here the results of a study are reported that was conducted on patients with heart failure treated with ubiquinone. After 7 months of oral drug administration (100 mg/day), a significant improvement was observed in echocardiographic indexes of systolic function, cardiothoracic ratio, and clinical signs and symptoms of congestive heart failure. In conclusion, the introduction of metabolic drugs, such as ubiquinone, in the treatment of heart failure opens new horizons in the therapeutic approach to an ailment that entails substantial human and social costs.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The actions of lidocaine on cardiac pacemaker rhythms were studied in anaesthetized dogs and in Purkinje fibres from hearts of the same animals.2. In vivo, lidocaine (1 mg/ kg, intravenously) slowed the sino-atrial (SA) node rhythm (– 5.0%), and (during vagal stimulation) prolonged ventricular standstill by + 25.1% and slowed the idioventricular rhythm (– 16.7%). A higher dose (4 mg/kg) had more pronounced effects.3. Propranolol also slowed sinus (– 26.2%) and idioventricular (– 27.2%) rhythms, and prolonged ventricular standstill (+ 36.8%). In the presence of propranolol, the effects of lidocaine on idioventricular rhythm were exaggerated.4. In Purkinje fibres driven in vitro, lidocaine (10 μmol/L) decreased contractile force (– 47.9%) and (during the interruption of drive) prolonged the suppression of (+ 53.2%) and slowed the escape rhythm (– 67.0%).5. In the presence of lidocaine the threshold potential was shifted to less negative values and diastolic depolarization slope was decreased (– 23.6%).6. Lidocaine slowed spontaneously active Purkinje fibres, abolished early afterdepolarizations in low [K]0 and slow responses in high [K]0 (by shifting the threshold to less negative values), and antagonized strophanthidin arrhythmias.7. TTX reduced the hyperpolarization by lidocaine in low [K]0 and vice versa.8. We conclude that lidocaine enhances vagally-induced ventricular standstill by depressing the idioventricular rhythm far more than the sinus rhythm, an action enhanced by beta-blockade. Furthermore, lidocaine depresses normal and different types of abnormal automaticity through direct and indirect effects of the blockade of the fast sodium channel.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-7241
    Keywords: angiotensin converting enzyme ; quinapril ; left ventricular hypertrophy ; glomerular filtration rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Of 17 patients with mild to moderate essential hypertension, 8 showed echocardiographic evidence of left ventricular hypertrophy. Cardiac and renal function evaluated by glomerular filtration rate (GFR) were studied in all patients before and after 20 weeks of quinapril treatment. Systolic pressure decreased from 174.7±16.7 to 131.7±7.7 mmHg (p〈.0001) and diastolic pressure decreased from 101.8±9.8 to 80±4.3 mmHg (p〈.0001). Left ventricular mass index decreased in the eight patients with left ventricular hypertrophy (p〈.01). Basal values of GFR were lower than normal in 41% of all patients; GFR increased significantly after 20 weeks of treatment (from 96.5±32.3 to 108.6±31.12 ml/min, p〈.01); it decreased in only one patient. Patients reported few adverse effects to quinapril, and no important clinical laboratory abnormality was observed. Quinapril not only lowered arterial pressure, but it had a distinct effect on regression of left ventricular hypertrophy and favorable effects on renal function.
    Type of Medium: Electronic Resource
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