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  • Transient inward current  (2)
  • Atypical pulmonary stenosis  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Hypertrophic obstructive cardiomyopathy as a manifestation of a cardiocutaneous syndrome (Noonan syndrome) (1991)
    Springer
    Journal of molecular medicine 69 (1991), S. 932-936 
    Details
    ISSN: 1432-1440
    Keywords: Noonan syndrome ; Turner phenotype ; Single gene mutation ; Atypical pulmonary stenosis ; Hypertrophic cardiomyopathy ; Cardiocutaneous syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The case of a 50-year-old patient with hypertrophic obstructive cardiomyopathy is reported. The patient demonstrated somatic signs of the Turner phenotype, but a cytogenetically normal karyotype was shown. These findings were compatible with the diagnosis of Noonan syndrome. The most commonly diagnosed cardiac disease in this syndrome is pulmonary stenosis, followed by hypertrophic cardiomyopathy. The patient's prognosis is limited by the natural history or the typical complications of the underlying cardiac lesion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01798545
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Alterations of ionic currents after reoxygenation in isolated cardiocytes of guinea-pigs (1991)
    Springer
    Pflügers Archiv 418 (1991), S. 238-247 
    Details
    ISSN: 1432-2013
    Keywords: Isolated cardiocytes ; Whole cell recording ; Reoxygenation ; Increased net current ; Transient inward current ; Ca current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Single myocytes were isolated from ventricles of adult guinea-pig hearts. The patch-clamp technique in the whole-cell configuration was used to study ionic currents. Experiments were performed in an experimental chamber that allowed the cells to be exposed to a sufficiently low O2 pressure to cause metabolic inhibition after 4–35 min (mean 14.1 min, n=20), which was indicated by the appearance of a large time-independent K current. Reoxygenation about 1 min after the first extra outward current was observed caused this current to vanish completely within 2–6 s if the calcium inside the pipette was buffered to negligible values with 20 mmol/l EGTA. With only 10 μM EGTA in the pipette, reoxygenation was followed by an arrhythmogenic period of 10–150 s duration, which was dominated by three types of event: (a) transient inward currents (I ti) developed during the first 5–10 s (26 cells); (b) the net current was increased by a factor of 1.9±0.4 (mean±SD, n=17) yielding a reversal potential for the increased component of −77±4 mV (mean±SD, n=4); and (c) the Ca current decreased by 20%–100% within the first 5–10 s. At the end of the arrhythmogenic period, I ti vanished, the net current recovered completely, and the Ca current recovered partially. At −45 mV, increasing preceding depolarization enlarged the amplitude of both the I ti and the net current, Iti being about four times more increased than the net current. The suppression of the Ca current was independent of the phase of the preceding I ti. We conclude that in isolated cardiocytes, after the induction of an anoxia-induced K current, reoxygenation causes a period of up to 150 s of cytosolic Ca overload, during which I ti is triggered, the net current is enhanced, and the Ca current is suppressed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370522
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Reoxygenation-induced arrhythmogenic transient inward currents in isolated cells of the guinea-pig heart (1991)
    Springer
    Pflügers Archiv 418 (1991), S. 248-260 
    Details
    ISSN: 1432-2013
    Keywords: Isolated cardiocytes ; Transient inward current ; Current-voltage relationship ; Kinetics ; Na/Ca exchanger
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Transient inward currents (I ti), activated by a rise in intracellular Ca concentration, are believed to trigger cardiac arrhythmias in reperfused hearts. In this report, I ti in isolated cardiocytes from the guinea-pig were evoked by reoxygenation following a period of anoxia of between 4 min and 35 min. Reoxygenation was performed 1 min after the full development of an anoxia-induced time-independent K current. This current disappeared within 2–6 s and in the following 10 s I ti developed to maximum amplitude. I ti were evoked using a constant pulse pattern (holding potential V h=−45 mV; test potential V t=+10 mV; pulse duration 350 ms; frequency 1 Hz). In more than 95% of the cells, I ti at the holding potential I ti (−45 mV) declined with a time constant of τ=670±240 ms (mean±SD, n=17). In two cells, undamped oscillatory currents were observed. The amplitude of I ti (-45 mV) was proportional to the amplitude and duration of the preceding depolarizing test pulse. Test pulses of long duration (500 ms and 1000 ms, mean ± SD) to potentials positive to +10 mV produced slowly decaying tail currents (τ=391±51 ms, mean ± SD), which superimposed with I ti (−45 mV). The current/voltage relationship of I ti peaked between −30 mV and −10 mV and approximated zero at the most positive potentials, i.e. no reversal of I ti was found up to +80 mV. Using double-pulse protocols (prepulse potential +40 mV), I ti were enhanced at potentials negative to −30 mV and were also present in the range of the normal resting potential of ventricular heart cells. The instantaneous current-voltage relationship was monotone between −50 mV and +40 mV. Because of the dependence of I ti on the preceding depolarization, the instantaneous current-voltage relationship provides more reliable information on the voltage dependence of I ti. The interval between two subsequent I ti (−45 mV) values was 237±35 ms (mean ± SD, n=27) and depended on the amplitude of I ti (−45 mV) to increase by 5.2±0.5% (mean ± SD) per 100 pA decrease in I ti (−45 mV). A simple noise analysis showed that if one assumes that ionic channels are responsible for the generation of I ti (−45 mV), their unitary conductance cannot exceed 0.36 pS. We conclude that reoxygenation-induced I ti are triggered by a cyclic release of Ca from the sarcoplasmic reticulum and provide evidence that they are mediated by the electrogenic Na/Ca exchanger. The arrhythmogenic potency of reoxygenation-induced I ti is demonstrated under current-clamp conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370523
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    Paper (German National Licenses)
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