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  • 1
    Electronic Resource
    Electronic Resource
    Nicainoprol (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Cardiovascular drug reviews 9 (1991), S. 0 
    Details
    ISSN: 1527-3466
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1527-3466.1991.tb00413.x
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  • 2
    Electronic Resource
    Electronic Resource
    Prevention of Ventricular Fibrillation by Cilostazol, an Oral Phosphodiesterase Inhibitor, in a Patient with Brugada Syndrome (2002)
    Oxford, UK : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 13 (2002), S. 0 
    Details
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Cilostazol and Brugada Syndrome. We report the case of 67-year-old man with Brugada syndrome, in whom daily episodes of ventricular fibrillation (VF) occurred every early morning for 4 days. The episodes of VF were completely prevented by an oral administration of cilostazol, a phosphodiesterase inhibitor. This effect was confirmed by the on-and-off challenge test, in which discontinuation of the drug resulted in recurrence of VF and resumption of the drug again prevented VF. This effect may be related to the suppression of Ito secondary to the increase in heart rate and/or to an increase in Ca2+ current (ICa) due to an elevation of intracellular cyclic AMP concentration via inhibition of phosphodiesterase activity. This drug might have an anti-VF potential in patients with Brugada syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1540-8167.2002.00698.x
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  • 3
    Electronic Resource
    Electronic Resource
    Ataxia with isolated vitamin E deficiency is caused by mutations in the α–tocopherol transfer protein (1995)
    [s.l.] : Nature Publishing Group
    Nature genetics 9 (1995), S. 141-145 
    Details
    ISSN: 1546-1718
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Ataxia with isolated vitamin E deficiency (AVED) is an autosomal recessive neurodegenerative disease which maps to chromosome 8q13. AVED patients have an impaired ability to incorporate α–tocopherol into lipoproteins secreted by the liver, a function putatively attributable to the ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/ng0295-141
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  • 4
    Electronic Resource
    Electronic Resource
    Resolvin E1 and protectin D1 activate inflammation-resolution programmes (2007)
    [s.l.] : Nature Publishing Group
    Nature 447 (2007), S. 869-874 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Resolution of acute inflammation is an active process essential for appropriate host responses, tissue protection and the return to homeostasis. During resolution, specific omega-3 polyunsaturated fatty-acid-derived mediators are generated within resolving exudates, including resolvin E1 ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature05877
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  • 5
    Electronic Resource
    Electronic Resource
    Effects of cibenzoline, a new class Ia antiarrhythmic drug, on various membrane ionic currents and action potentials of guinea-pig ventricular cells (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 167-173 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Cibenzoline – Ventricular myocytes – Membrane currents – Action potential duration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. We examined the effects of cibenzoline, a new class Ia antiarrhythmic drug, on various membrane ionic currents and action potentials of guinea-pig single ventricular cells, using patch clamp techniques in whole-cell configuration. Action potentials and the membrane currents were evoked at a clamping rate of 0.2 Hz, and all experiments were performed at 32–33°C.   1) Cibenzoline (5, 10 and 30 μM) decreased the Na+ current (INa), in a concentration-dependent manner. The concentration of the half-maximal inhibition (Kd) for INa was estimated to be 7.8 μM.   2) In addition to the inhibition of INa, this drug (5, 10, and 30 μM) decreased, in a concentration-dependent manner, all other membrane currents examined, such as L-type Ca2+ current (ICa), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1). The Kd (apparent dissociation constant) values were 14.4 μM for ICa, 23.0 μM for IK, and 33.7 μM for IK1 respectively.   3) Cibenzoline (5, 10, and 30 μm) significantly shortended the action potential duration measured at both 30% and 90% repolarization without altering the resting membrane potential.   From these findings, we conclude that apart from potent inhibitory effects on INa, cibenzoline possesses multiple blocking effects on other currents, e.g., ICa, IK and IK1, with a different potency (INa〈ICa〈IK〈IK1) and with essentially the same efficacy. These effects may explain, at least in part, the alleged, potent antiarrhythmic effects of this drug.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00241092
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  • 6
    Electronic Resource
    Electronic Resource
    Magnesium restores high K-induced inactivation of the fast Na channel in guinea pig ventricular muscle (1982)
    Springer
    Pflügers Archiv 395 (1982), S. 78-80 
    Details
    ISSN: 1432-2013
    Keywords: Magnesium ; Ventricular muscle ; Maximum rate of rise ; Na inactivation curve ; Surface charge
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of extracellular magnesium concentration (Mgo) on the upstroke of the action potential was studied in guinea pig ventricular muscle under various K+ concentrations (2.7–19mM). Increased Mgo shifted the steady state inactivation curve of the fast Na channel in the depolarizing direction and this effect was concentration-dependent (0–20mM). Such an effect could explain the Mg-induced increase in maximum rate of rise of the action potential which Späh and Fleckenstein (1979) proposed to be due to a “Mg channel”.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00584973
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  • 7
    Electronic Resource
    Electronic Resource
    Modification of cardiac sodium current by intracellular application of cAMP (1994)
    Springer
    Pflügers Archiv 426 (1994), S. 146-154 
    Details
    ISSN: 1432-2013
    Keywords: Sodium current ; cAMP-dependent protein kinase ; Guinea-pig ventricular myocyte ; Intracellular perfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the effects of intracellular perfusion of cyclic adenosine monophosphate (cAMP) on the sodium current (I Na) of guinea-pig ventricular myocytes, using the whole-cell clamp technique. I Na was elicited by depolarizing voltage steps (−20 mV) from a variety of holding potentials (−120 to −50 mV), under conditions of 60 mM extracellular Na+ concentration ([Na+]0) and at the temperature of 24–26°C. Intracellular perfusion of cAMP decreased the I Na elicited from the holding potentials less negative than −90 mV. In the presence of 1 mM cAMP, for example, the peak I Na elicited from −80 mV decreased from 6.0±2.0 nA to 4.0±2.2 nA (mean±SD, P〈0.02, n=7) within 3–6 min. In the presence of extracellular 3-isobutyl-1-methylxanthine (IBMX, 20 μM), much lower concentrations of cAMP (0.2 mM) yielded a comparable effect. On the other hand, intracellular perfusion of cAMP increased the I Na elicited from very negative holding potentials (〈−100 mV). For instance, the application of cAMP (1 mM) increased the I Na elicited by step depolarizations from −120 mV (to −20 mV), from 9.9±2.1 nA to 11.0±3.1 nA (P〈0.05, n=5). The former effect was attributed to a marked shift of the steady-state inactivation curve of I Na to the negative direction; the voltage of half-inactivation shifted from −77.9±1.0 to −83.5±1.4 mV, or by −5.6 mV. The latter effect may be explained by increases in maximum available conductance of I Na. Extracellular application of isoproterenol (1 μM) also decreased the I Na evoked from a holding potential of −80 mV, whereas it increased the I Na elicited from more negative potentials of −120 mV. These effects of isoproterenol were reversible and markedly attenuated in the presence of a specific inhibitor of cAMP-dependent protein kinase, H-89 {N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulphonamide}, an isoquinolinesulphonamide derivative, in the extracellular medium (2–10 μM) and a protein kinase inhibitor (Walsh inhibitor) in the pipette solution (40 μM). H-89 (10 and 30 μM) affected neither the adenylate cyclase activity prepared from rabbit ventricular muscles, nor the isoproterenol-mediated increases in the cAMP content in guinea-pig ventricular muscles. Our observations suggest that the increase in intracellular cAMP modulates the function of cardiac Na channels, preferentially by stimulating cAMP-dependent protein kinase, with subsequent phosphorylation of the channel protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374682
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  • 8
    Electronic Resource
    Electronic Resource
    Inhibitory effects of palmitoylcarnitine and lysophosphatidylcholine on the sodium current of cardiac ventricular cells (1992)
    Springer
    Pflügers Archiv 420 (1992), S. 94-100 
    Details
    ISSN: 1432-2013
    Keywords: Guinea-pig ventricular cell ; Patch clamp ; Palmitoylcarnitine ; Lysophosphatidylcholine ; Cardiac sodium current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the effects of ischemia-related amphipathic compounds, palmitoylcarnitine (PamCar, 0.5–50 μM) and lysophosphatidylcholine (lysoPtdCho, 5–50 μM) on sodium current (I Na) of guinea-pig ventricular myocytes. The cells were perfused with low-Na+ (60 mM) Tyrode's solution, and Ca2+ and K+ currents were blocked by external Co2+ (3 mM) and internal Cs+ (140 mM), respectively. I Na was elicited by depolarizing voltage steps from a holding potential of −100mV at a temperature of 33 °C. PamCar (5 μM) decreased the peak I Na (attained at −20mV or −30mV) from 6.1±2.1 nA to 3.9±1.4 nA (n=11), or by 36.1% within 2 min, and shifted the curve of steady-state I Na inactivation by 5.4 mV in the positive direction (from −76.3±4.6 mV, control to −70.9±4.0 mV, in PamCar, n=4). Partial restoration of the amplitude and the shift of the steady-state inactivation curve of I Na was attained after washout of PamCar. In contrast, lysoPtdCho at concentrations over 10 μM irreversibly depressed the I Na within 0.5–3 min and the reduction of IinNa was followed by cell contracture or cell death (n=9). The survival time, defined as a period from the start of lysoPtdCho application to the time of the last successful recording of the I Na (before evolution of sudden changes in the holding current), depended on the concentrations of lysoPtdCho. Both PamCar and lysoPtdCho retarded the time course of activation and inactivation of I Na. These findings are compatible with the idea that PamCar and lysoPtdCho decrease the maximum Na+ conductance and alter the surface negative charge of the membrane, perhaps via amphiphilic intervention in the phospholipid bilayers. However, PamCar had an additional effect that indicates more direct but reversible incorporation of this agent with the Na+ channels or integral membrane proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00378647
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  • 9
    Electronic Resource
    Electronic Resource
    Effects of lysophosphatidylcholine on resting potassium conductance of isolated guinea pig ventricular cells (1986)
    Springer
    Pflügers Archiv 406 (1986), S. 296-302 
    Details
    ISSN: 1432-2013
    Keywords: Single ventricular cell ; Guinea pig heart ; Patch clamp ; Lysophosphatidylcholine ; Inward rectifier K channel ; Transient inward current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We studied the effects of lysophosphatidylcholine (LPC), a toxic metabolite of ischemia, on the inward rectifier potassium channel current in isolated guinea pig ventricular cells. 1) LPC (10–50 μM) added to the external solution decreased the resting membrane potential and occasionally induced repetitive action potential discharges, with or without loss of repolarization. 2) In voltage clamp studies, LPC (20 μM) decreased the conductance at the levels of resting potentials (≃ −80 mV) from 26±8 nS to 16±3 nS (mean and SD,n=4) within 10 min. Prolonged application of LPC (〉12 min) produced transient inward currents after depolarizing clamp pulses, thereby suggesting that the LPC elevated intracellular Ca2+ concentrations. 3) The effect of LPC on the single inward rectifier K channel current was examined using the patch clamp technique in a cell-attached mode. LPC decreased the single channel conductance, depending on the concentration (5–100 μM). The slope conductance in the presence of 150 mM K+ in the pipette decreased from 45±7 pS (control) to 32±17, 20±19, and 14±10 pS for 5, 20 and 100 μM LPC, respectively. LPC induced little change with regard to probability of the channel opening. These results suggest that LPC depolarizes membrane by decreasing single channel conductance of the inward rectifier K channel. This reduction partially contributes to the alleged LPC-induced abnormal automaticities and conduction disturbances in the heart.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00640917
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  • 10
    Electronic Resource
    Electronic Resource
    Effects of cibenzoline, a new class Ia antiarrhythmic drug, on various membrane ionic currents and action potentials of guinea-pig ventricular cells (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 350 (1994), S. 167-173 
    Details
    ISSN: 1432-1912
    Keywords: Cibenzoline ; Ventricular myocytes ; Membrane currents ; Action potential duration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the effects of cibenzoline, a new class Ia antiarrhythmic drug, on various membrane ionic currents and action potentials of guinea-pig single ventricular cells, using patch clamp techniques in whole-cell configuration. Action potentials and the membrane currents were evoked at a clamping rate of 0.2 Hz, and all experiments were performed at 32–33°C. 1) Cibenzoline (5, 10 and 30 μM) decreased the Na+ current (INa), in a concentration-dependent manner. The concentration of the half-maximal inhibition (Kd) for INa was estimated to be 7.8 μM. 2) In addition to the inhibition of INa, this drug (5, 10, and 30μM) decreased, in a concentration-dependent manner, all other membrane currents examined, such as L-type Ca2+ current (ICa), delayed rectifier K+ current (IK), and inward rectifier K+ current (IK1). The Kd (apparent dissociation constant) values were 14.4 μM for ICa, 23.0 μM for IK, and 33.7 μM for IK1 respectively. 3) Cibenzoline (5,10, and 30 μm) significantly shortended the action potential duration measured at both 30% and 90% repolarization without altering the resting membrane potential. From these findings, we conclude that apart from potent inhibitory effects on INa, cibenzoline possesses multiple blocking effects on other currents, e.g., ICa, IK and IK1, with a different potency (INa 〉 ICa 〉 IK 〉 IK1) and with essentially the same efficacy. These effects may explain, at least in part, the alleged, potent antiarrhythmic effects of this drug.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00241092
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