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W Boldt

Publications and source records attributed to W Boldt.

29 records · Page 2Linked to original sources

[Pacing-interval-dependent changes of action potentials in the heart atrium of the warm-blooded animal].

Investigated are the cellular post rest action potentials of the rabbit atrial trabeculae (length 2-4 mm, diameter 150-800 micrometers). The first action potential (A.P.) after a pacing pause develops a characteristic configuration: (1) a rapid early repolarization up to -30 to -60 mV within 4 to 8 ms, (2) an extremely decelerated repolarization phase or a secondary depolarization, (3) a prolongation of the A. P. duration at 90% repolarization. During Ca++ excess perfusion the secondary depolarization is increased, shifted to more positive potentials and an earlier maximum value. It disappears during zero Ca++ and verapamil perfusion. Elevating the Ca++ concentration and shortening the pacing intervals before the period of rest increases the A. P. duration at 90% repolarization. Prolonging the pacing pause and decreasing the external Ca++ concentration delays the restitution of the steady state A. P. configuration after the rest By Ca++ excess the post rest A. P. restitution is accelerated. To explain the experimental findings, the possible role of a Ca++-sensitive K+ conductivity a poststimulatory variation of the slow inward current and the time-dependent K+ currents as well as processes of accumulation are discussed.

Action Potentials↗

[Existence and properties of a chloride-sensitive conductivity in atrial myocardium].

Investigated are the intracellularly recorded action potentials (A. P.) of the rabbit atrial trabeculae (length 2-4 mm, diameter 150-800 micrometers). After a pacing pause the first A. P. shows a rapid initial repolarization (I. R.) up to -40 mV within 4-6 ms. By increasing the duration of the pacing pause the I. R. is accentuated. It is diminished by repetitive stimulation after the pause and disappears within 2-4 s. At variation of the extracellular Ca++ concentration and under verapamil, tetraethyl ammonium chloride load (TEA load) the I. R. is unchanged. On the other hand, the I. R. is very sensitive to the variation of the external Cl- concentration. When decreasing the external Cl- concentration, the I. R. is diminished. At 10 mmol x 1(-1) the I. R. disappears. Assuming a Cl- current ICl the experimental findings are modelled. During the A. P. a Cl- conductivity gCl is activated instantaneously and inactivated slowly (rate constant 5.09 s-1). Because of the repriming of gCl the I. R. disappears after the post rest pacing. During the pacing pause a recovery of gCl takes place (rate constant 0.06 s-1). The gCl recovery induces the post rest I. R. Estimation of the maximum gCl yields 0.24 mmho . cm-2.

Action Potentials↗

[Effects of intracellular 4-aminopyridine and tetraethylammonium load on action potentials in the rabbit atrial myocardium].

Investigated are rabbit atrial trabeculae (2-4 mm length, 150-800 micrometers diameter). When using a standard microelectrode technique, the action potentials after an intracellular 4-AP and TEA load are prolonged. Only the TEA load significantly diminishes the resting potential of the beating preparations. The typical configuration of the action potential following a period of rest (rapid initial repolarization, secondary depolarization and a late retarded repolarization) is not changed qualitatively. During a repetitive stimulation after a pacing pause the action potentials' restitution is accelerated at 4-AP. After 4-AP and TEA load the secondary depolarization of the first post rest action potential is more accentuated. By reconstructing the post rest action potentials a 4-AP sensitive current is determined. At constant drive this current shows a threshold potential at -40 and a reversal potential at -10 mV. The current is inward directed between -40 and -10 mV and is outward directed at more positive potentials than -10 mV. After a pacing pause the current-voltage relation is shifted to more negative potentials. The 4-AP sensitive current is modelled by consideration of a slow activated (during the action potential) and deactivated (during the pacing pause) conductivity. Processes of accumulation are discussed.

4-Aminopyridine↗

Rate-related changes of the transmembrane potential in the rabbit atrial myocardium.

We studied changes of the transmembrane resting and steady state action potentials in the rabbit atrial trabecular preparations (length 2-4 mm, diameter 150-800 micrometers, standard microelectrode techniques). Following cessation of rapid drive the transmembrane potential shows an initial depolarization and a terminal hyperpolarization. Increasing the stimulation frequencies before the cessation of driving the initial depolarization and the terminal hyperpolarization are more accentuated. When the stimulation frequency is abruptly reduced, the enddiastolic ("resting") potential increases (steady state resting potential - 82 +/- 3 mV at 1.0 s, -73 +/- 6 mV at 0.25 s driving interval). Decreasing the rate of stimulation the duration of the steady state action potential shortens at 25% and prolongs at 90% repolarization. A calculated background conductivity is diminished using a slower drive. From the experimental findings ensue some considerations about a K+ accumulation, the rate dependent sodium pump and the rate related shifts of the steady state outward current-voltage relationships.

Action Potentials↗

[Effect of cesium ions on the electrotropic actions of acetylcholine in the rabbit atrium].

Cs+ (15-20 mM) decreases the electrotropic vagal effects on an isolated vagal innervated rabbit atrium. By means of investigating the action potentials and the phase plane trajectories of trabeculae from the rabbit atrium using a modified single sucrose gap technique the anomalous rectification disappears and also the effect of acetylcholine (ACh) on action potential duration. We presume that the anomalous rectification should be a necessary condition of electrotropic vagal (ACh) action on the rabbit atrium.

Acetylcholine↗

[Action of acetylcholine on the mammalian auricle influenced by verapamil].

The action of acetylcholine (ACh) and verapamil (VePa) on the action potential (V(t)), phase plane trajectories of V(t) (dV/dt--V(t) -- plot) and isotonic contractions were investigated using an isolated vegal innervated preparation from rabbit atrium (method I) and investigating action potentials from atrial trabeculae by means a modified sucrose gap technique (method II). If the VePa-concentration increases to 4 mg/1 the duration of the action potential decreases at 20 and 90% repolarization (driving frequencies 2 s-1). In the VePa-solutions phase plane trajectories of the action potential did not change significantly. ACh application favours the disappearance of a region in the repolarization phase plane plot showing anomalous rectification (d(--dV/dt)/dV less than 0) both by control conditions and verapamil. The electrotropic ACh-and vagal effects will be unchanged by verapamil. The inotropic ACh-and vegal action (method I) increases by VePa (2 mg/1). The action of ACh and verapamil will be analysed using a mathematical model for reconstructing the repolarization phase of mammalian atrial myocardium action potentials.

Acetylcholine↗

[Electrotropic acetylcholine action on the mammalian auricle by means of the "phase plane" trajectories of the action potential].

A single sucrose gap techniques has been used to study action potentials and phase plane trajectories of them in atrial trabeculae of the rabbit. Using polynomial representations of current-voltage relationships a model of membrane action potential of atrial myocardial fibres is described and allows an interpretation of recording data from the phase plane trajectories. Our findings show: 1. Increasing extracellular calcium concentration increases a potassium conductivity of the atrial membrane. 2. An anomalous rectification concerning repolarizing currents in atrial fibres decreases with increasing extracellular calcium. 3. Acetylcholine (3.10(-4) g.cm-3) abolishes the anomalous rectification. These results are discussed in relation to previous electrophysiological studies of negative electrotropic effects of acetylcholine in cardiac muscle.

Acetylcholine↗

[Effects of hypertrophy on the behavior of potentials in isolated ventricular strips of the rat].

Potentiation of right-ventricular strips obtained from normal rats (NT-group) and from rats showing hypertrophic hearts as a result of long-time swimming (HT-group) has been investigated. Strength-interval relationships, poststimulation potentiation and the potentiation by paired stimulation has been tested. The behavior of the action potential in both groups showed no significant differences. Standardized strength-interval relationships of HT-group were steeper than those of the NT-group. Maximal potentiation in the HT-group occurred at shorter delay-intervals. Potentiation after long-time pauses was greater in the HT-group. The results are discussed on the basis of model considerations of electro-mechanical coupling.

Action Potentials↗