Abstract
Ventricular and Purkinje action potentials were recorded with a microelectrode in a strip of human papillary muscle. Lowering the K-content of the superfusing solution from 5.9 to 0.5 mmol·litre−1 at 37°C hyperpolarised ventricular diastolic potential steadily as long as [K+]o was low (up to 70 min tested). Ventricular action potentials were transiently lengthened and then shortened. A positive inotropic effect was noted and attributed to Na-K pump inhibition since it was reversed by the addition of 2 mmol·litre−1 thallous chloride to the low [K+]o solution. Beyond 40 min, transient depolarisations and after-contractions were found. During the first minutes in low [K+]o, Purkinje diastolic potential was hyperpolarised and the action potential was lengthened at all levels of repolarisation. Afterwards, the Purkinje diastolic potential suddenly depolarised by 30 mV. Restoration of the control solution caused a slow repolarisation and then a sudden return of the diastolic potential to near control value. This was reproduced during drive (38 stim·min−1) and at rest. At the depolarised level of potential, stimulation elicited slow action potentials with diastolic slow depolarisation and spontaneous oscillations of potential appeared at rest. In Purkinje cells, increasing concentrations of tetrodotoxin from 10−7 to 8 x 10−6 mol·litre−1 in the control solution shifted the diastolic potential in negative direction by a few mV and shortened the action potential duration at all levels of repolarisation. The possible implications of these phenomena in the genesis of some cardiac arrhythmias is discussed.

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