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Biomedical subjects

J Wiemer

Publications and source records attributed to J Wiemer.

22 records · Page 2Linked to original sources
PubMed1982

Tl+-ions: effects on the automaticity of sinoatrial tissue and dV/dtmax and iK2 of cardiac Purkinje fibres.

The disrhythmic effects of thallium were investigated in various cardiac tissues to determine the primary site of intoxication with respect to ensuing arrhythmias. In isolated cardiac tissue Lameijer and van Zwieten [1] had contended that arrhythmias arise from the sinus node after thallium poisoning. To test this hypothesis we administered concentrations of Tl+ between 10(-7) and 10(-4) M to guinea pig sinoatrial preparations, to guinea pig papillary muscles and to sheep cardiac Purkinje fibres. In sinoartial preparations thallium provoked increases and decreases of spontaneous beat frequency which were not linked to corresponding changes in contractile force. In conductive tissue, Purkinje fibres, the inactivation kinetics of the fast sodium current and the pacemaker current iK2 were investigated by voltage clamp experiments. Here, thallium was seen to be essentially without toxic effects which could account for arrhythmias. In ventricular muscle actions potentials and contractile force were recorded simultaneously. Here again, ventricular arrhythmias are not to be expected from thallium intoxication in rather high concentrations. The findings support the view that arrhythmogenic effects of thallium are restricted to the sinus node.

Animals↗
PubMedDate not supplied

Excitation-contraction coupling in voltage-clamped cardiac myocytes.

Myocytes isolated from guinea pig ventricles were voltage-clamped using patch pipettes in the whole-cell configuration. For proper voltage control fast Na+ current was blocked by TTX or inactivated by an appropriate prepulse. Zero-load cell shortening was monitored by a photoelectric device. The mechanical response to a short depolarizing clamp was mainly a phasic (transient) contraction. Long-lasting depolarizations caused a tonic (sustained) shortening of a cell. Different clamp patterns were used to study the mode of activation of phasic contraction. 1) With a constant Ca2+ preload established by a train of conditioning pulses, the shortening-voltage relation measured with test pulses of varying height was a bell-shaped curve reflecting the slow inward current (ICa)-voltage relation. The test pulse had a striking influence on the first contraction of the following conditioning series, resulting in an S-shaped relation between post-test contraction and test potential. 2) With series of identical clamps of varying height, steady-state contraction was maximal around 40 mV and not in proportion to ICa. In these measurements Ca2+ preload was likely to increase with increasing potential. It is concluded that ICa initiates phasic contraction by inducing a release of Ca2+ from internal stores while replenishment of the stores is largely determined by an electrogenic transsarcolemmal Na+-Ca2+ exchange. The data suggest that Na+-Ca2+ exchange is not only involved in long-term changes of cardiac contractility but also in beat-to-beat regulation.

Action Potentials↗
PubMedDate not supplied

A voltage clamp study of the effects of AR-L 115 BS on the pacemaker current of cardiac Purkinje fibres.

The new cardiotonic agent AR-L 115 BS was investigated by means of the double-micro-electrode voltage clamp technique on sheep cardiac Purkinje fibres. Clinical and pharmacological studies show that AR-L 115 BS increases heart rate as a side effect at medium to high therapeutic doses. The classical analysis of the pacemaker current was therefore performed to study the possible mechanism of this effect at a cellular level. The kinetic parameter s infinity and the reversal potential of the pacemaker current were shifted in the depolarizing direction after exposure to AR-L 115 BS. Peak values of the fully activated pacemaker current were either increased or diminished, while potassium leakage was slightly increased. These results are not related to the action of AR-L 115 BS on beta-adrenergic receptors but possibly due to enhanced intracellular calcium (see third paper in this series). Despite its tendency to increase heart rate, high concentrations of AR-L 115 BS should not be expected to promote arrhythmias in the Purkinje system since the electrophysiological effects tend to counteract each other.

Animals↗