Complete ischemia in mammalian hearts leads to a progressive deterioration of intracellular electrical activity, including shortened action potentials and reduced resting potentials, which persist for up to 20 minutes.
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Prolonged electrical activity during anoxia may define intervention windows; leaves open translation to human ischemic arrhythmias.
Spontaneous ventricular electrical potentials of whole mammalian hearts subjected to complete ischemia were investigated by means of the intracellular microelectrode. Spontaneous membrane action potentials persist for 20 min, following the onset of anoxia. Early, the duration of the action potential shortens, followed by a progressive fall in the amplitude of the spike. The resting potential shows a diminution to 65 per cent of the control value. The relationship of these effects to change in membrane ionic transports and metabolic processes are discussed.
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Kardesch et al. (1958) studied this question.
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