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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
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Journal of Molecular and Cellular Cardiology 17 (1985), S. 1043-1053 
    ISSN: 0022-2828
    Keywords: Cardiac Purkinje fiber ; Cellular calcium ; Contractile force ; Digitalis ; Intracellular sodium activity ; Na-Ca exchange ; Positive inotropy
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of biomedical science 1 (1993), S. 28-42 
    ISSN: 1423-0127
    Keywords: Norepinephrine ; High [Ca]o ; Strophanthidin ; Na/K pump ; Na/Ca exchange
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The role of intracellular sodium activity (a Na i ) in the control of force was studied in sheep cardiac Purkinje fibers exposed to norepinephrine (NE) and high [Ca]o in the absence and presence of overdrive or of a low concentration of strophanthidin. Both NE and high [Ca]o decrease a Na i and increase force, while overdrive increases and low strophanthidin decreases both parameters. In the presence of NE, overdrive increases a Na i less than force and is followed by a more pronounced undershoot in a Na i and force. In contrast, in high [Ca]o overdrive increases a Na i more than force and is followed by a less pronounced undershoot in a Na i and force than in NE. High [Ca]o increases force to a peak, but then the decreasing a Na i reduces force. In all these conditions, a Na i determines force changes during recovery from overdrive. NE and high [Ca]o decrease a Na i less and increase force more in low strophanthidin. Thus, changes in a Na i modulate the increase in force due to increased Ca influx and control force development when Ca influx is either unchanged (low strophanthidin) or has reached a steady state (high [Ca]o, recovery from overdrive).
    Type of Medium: Electronic Resource
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