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E Luckmann

Publications and source records attributed to E Luckmann.

10 recordsLinked to original sources

[Clinical physiology and physiopathology of the atrioventricular node].

The functional behaviour of the healthy and sick human AV-node under various clinical-experimental conditions is described with special reference to (1) AV-nodal conduction, (2) AV-nodel refractoriness, (3) influence of autonomic tone and (4) role of the AV-node in the initiation of rhythm disturbances.

Adolescent

[The influence of frequency and blockade of the autonomic nervous system on the functional behaviour of the human conduction system. Part B: Refractory periods (author's transl)].

32 patients were studied by His-bundle-electrocardiogram and programmed atrial stimulation to examine to which extent frequency and autonomic tone participate in influencing the effective (ERP) and functional (FRP) refractory periods of the atrium and AV-node. The measurements were performed during three electrically induced atrial frequencies before and after intravenous injection of 1 mg Atropine (15 patients) and 0.4 mg Visken (17 patients). For the atrium, frequency dominates the blockade of both components of the autonomic nervous system in influencing both refractory periods. Increase in frequency shortens both ERP and FRP of the atriu. The blockade of parasympathicus and sympathicus does not significantly influence the changes in atrial ERP and FRP induced by atrial pacing. The AV-node responses most sensitive to both pacing induced cycle length shortening and blockade of the autonomic tone. Cycle length shortening prolongs the nodal ERP. the FRP is either shortened or prolonged. Blockade of the parasympathicus shortens both nodal ERP and FRP. Blockade of the sympathicus lengthens both parameters. This behaviour of both refractory periods in response to atrial pacing and blockade of the autonomic tone are discussed with respect to the "gate mechanism" in the conduction system. In the majority of patients blockade of the parasympathicus shifts the "gate" from the AV-node to the atrium. Blockade of the sympathicus has the opposite effect in some cases.

Adrenergic beta-Antagonists

[The adaptation of AV-nodal conduction time on gliding increase and decrease of atrial frequency before and after autonomic blockade (author's transl)].

In 19 patients with healthy AV-nodes the adaptation of the intranodal conduction time (A-H time) to gliding increase and decrease in atrial frequency and to the blockade of the autonomic nervous system was investigated using His bundle electrograms. The measurements were performed during right atrial stimulation with three frequencies, each with a duration of one minute, before and after blockade of the parasympathetic (8 pat.; 1 mg atropine i.v.) and the sympathetic (11 pat.; 0.4 mg Visken i.v.) nervous system. Gliding increase and decrease in atrial frequency results in a staircase pattern of A-H-adaptation in 18 of the patients. The height of the steps was identical in both phases of stimulation in each individual patient. One patient showed functional dissociation of intranodal conduction which was different during increase and decrease of atrial frequency. With parasympathetic blockade the staircase behavior of the A-H time basically remained unchanged with the exception of shorter A-H intervals resulting in lower steps. Atropine abolished the functional dissociation of intranodal conduction; thus the drug might prevent reentrytachycardias due to functional dissociation in the AV-node. Sympathetic blockade lengthens the intranodal conduction time; thus shifting the staircase pattern of the A-H time to higher levels. The results are discussed with respect to the electrophysiological characteristics of AV nodal cells as slow response fibers, and to the changes caused by atrial stimulation, acetylcholine and adrenaline.

Atrioventricular Node

[Influence of cycle length shortening, atropine and beta-receptor blockage on sinus node recovery time (SRT) in patients with healthy sinus node (author's transl)].

Sinus node recovery time (SRT) was measured in 30 patients with healthy sinus nodes to examine the influence of the increase in atrial frequency, atropine and beta-receptor blockade. The measurements were performed following pacing with 3 atrial frequencies before and after administration of 1 mg atropine i.v. (13 patients) and 0.4 mg prindolol (Visken) i.v. (17 patients). Total group; Increase of frequency alone caused prolongation of the SRT in 17 patients and shortening in 13 patients. Atropine group: Blockade of the parasympathicus alone induced a highly significant reduction in the SRT. Simultaneous increase in frequency and blockade of the parasympathicus led to greater SRT-shortening during low frequency than with high frequency. This interrelationship of frequency and blockade of the parasympathicus influencing the SRT is statistically significant. Visken-group: Blockade of the sympathicus causes a highly significant prolongation of the SRT. Simultaneous increase in frequency and blockade of the sympathicus led to greater SRT-prolongation during low frequency than with high frequency. This interrelationship of frequency and blockade of the sympathicus influencing the SRT has slight statistical significance. The results are discussed in respect to the electrophysiological influences of atrial cycle length shortening, acetylcholine and catecholamines on the sinus node, the perinodal atrial fibres and the atrial working myocardium.

Atropine

[The influence of frequency and blockade of the autonomic nervous system on the functional behaviour of the human conduction system. Part A: Conduction velocity (author's transl)].

32 patients were studied by His-bundle recordings to examine the extent to which frequency and autonomic nervous system influence the conduction velocity in the subdivisions (atrium, AV-node, His-Purkinje system) of the normal PR-interval. The measurements were performed during sinus rhythm and three electrically induced atrial frequencies before and after intravenous administration of 1 mg Atropine (15 patients) and 0.4 mg Visken (17 patients). In influencing the atrial conduction velocity frequency dominates the blockade of both components of the autonomic nervous system. Increase in frequency lengthens the intraatrial conduction time. Blockade of parasympathicus and sympathicus does not significantly influence the changes in intraatrial conduction velocity induced by increase of frequency. Patients with prolonged intraatrial conduction respond in the same way to cycle length shortening and blockade of the autonomic tone as patients with normal conduction. The results are discussed with respect to acetylcholine and catecholamine influence on the electrophysiological properties of the atrial myocardium. The AV-node is the part of the conduction system most sensitive to the influence of both cycle length shortening and blockade of the autonomic nervous system. Artificially induced cycle length shortening prolongs the intranodal conduction time to a different individual level for each patient. Blockade of the parasympathicus not only shortens this interval but also reduces the steepness of the AH-time induced by atrial pacing. Blockade of the sympathicus has the opposite effect. The most likely explanation for these results is the abolishing of the functional dissociation within the AV-node by blocking the autonomic influence on this structure. The conduction velocity in the His-Purkinje system is influenced neither by atrial pacing nor by blockade of both components of the autonomic nervous system.

Adrenergic beta-Antagonists