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  • 1
    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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  • 2
    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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  • 3
    Electronic Resource
    Electronic Resource
    Effects of anoxia on K and Ca currents in isolated guinea pig cardiocytes (1990)
    Springer
    Pflügers Archiv 416 (1990), S. 207-209 
    Details
    ISSN: 1432-2013
    Keywords: Isolated cardiocytes ; Anoxia ; AP shortening ; K current ; Ca current
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Whole cell currents were measured in isolated cardiocytes of guinea pig under anoxic conditions (pO2 〈0.5 torr). After 2 to 32 (mean 11.2) minutes of anoxia, time independent outward currents developed gradually which had a linear current-voltage relation between -100 and +20 mV and reversed at the resting potential of the cells (-82 to -90 mV). After 20 to 170 (mean 38) seconds, the amplitude of these outward currents saturated (3.6±0.5 nA at +10 mV, n=23). Reoxygenation within one minute after the appearance of the first extra outward currents led in most cells (〉90%) to their complete disappearance in 2 to 4 (mean 2.87, n=15) seconds. Ca currents were not affected at the time when the first extra outward currents occurred. It is concluded that (i) the anoxia-induced outward current is carried by K+ ions probably through KATP channels which open at intracellular ATP concentrations below 1 mmol/l (Noma and Shibasaki 1985) and (ii) this degree of ATP depletion does not affect normal Ca channel function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370244
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    Paper (German National Licenses)
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