Effect of disopyramide and disobutamide on conduction in perfused rabbit hearts

1981 ◽  
Vol 59 (11) ◽  
pp. 1192-1195
Author(s):  
Peter E. Dresel ◽  
Keith D. Cameron
Keyword(s):  
Antiarrhythmic Agent ◽  
Conduction System ◽  
Atrioventricular Conduction ◽  
Cardiac Conduction ◽  
Conduction Time ◽  
Related Effect ◽  
Av Node ◽  
His Bundle ◽  
Time Changes ◽  
His Bundle Recording

The effects of disopyramide (DP) and a new antiarrhythmic agent, disobutamide (DB) on cardiac conduction were studied using His bundle recording from modified rabbit Langendorff preparations electrically driven at 3 and 4 Hz. Both disopyramide (4–16 μg/mL) and disobutamide (1–30 μg/ml) slowed conduction throughout the atrioventricular conduction system, i.e., SA, AH, and HV intervals were increased in a dose-related manner. Conversion of the conduction time changes to percent changes indicates that disobutamide has a relatively equal effect on each part of the system whereas disopyramide exhibited significantly less effect on AV nodal conduction. Slowing of conduction in the AV node by DP was clearly related to rate. Changes in SA and HV intervals were rate related to a lesser degree. No such rate-related effect was evident with disobutamide. Block of atrial conduction occurred in two out of six hearts when the rate was increased at 8 μg/mL of DP and in three additional hearts at 16 μg/mL. This was interpreted to indicate a change in atrial excitability such that 2 × threshold currents no longer excited the tissues. This was not observed at any concentration of DB.

Regional distribution of ECS in contractile and conductive elements of rat and rabbit heart

1992 ◽  
Vol 263 (1) ◽  
pp. H168-H176
Author(s):  
K. G. Lurie ◽  
J. Dutton ◽  
P. Wiegn
Keyword(s):  
Regional Differences ◽  
Regional Distribution ◽  
Rabbit Heart ◽  
Conduction System ◽  
Cardiac Conduction ◽  
Ventricular Muscle ◽  
Av Node ◽  
His Bundle ◽  
Ventricular Tissue ◽  
Left And Right

By adaptation of recently developed quantitative microanalytic techniques, the size of the extracellular space (ECS) was measured regionally in the rat and rabbit cardiac conductive and contractile tissues. When inulin and sucrose were measured as extracellular markers in rabbit heart, the ECS in the atrioventricular (AV) node was found to be, respectively, 2.4 and 2.2 times larger than that of adjacent ventricular muscle. By use of inulin, the ECS in the rabbit His bundle was found to be 1.8 times larger than the adjacent ventricular tissue. Similarly, when inulin was used in rat, the ECS of the AV node, His bundle, right bundle branch, and right atrium was found to be, respectively, 2.5, 1.9, 1.8, and 1.2 times larger than that of left and right ventricular muscle. Similarly, significant regional differences in ECS were also observed in rat heart with sucrose. By use of glucose as an ECS marker, these results also revealed a 2.5-2.9 times larger ECS in rat and rabbit AV node compared with contractile elements. In contrast, ATP content, measured as an intracellular marker, was the same in both AV nodal and ventricular muscle tissue from both rat and rabbit. These data demonstrate that there are significant regional variations in ECS within the cardiac conduction system. Collectively, the data obtained with all extracellular markers indicate that the size of the ECS of the conduction system is markedly larger than the adjacent contractile muscle.

Modulation of AV nodal and Hisian conduction by changes in extracellular space

1999 ◽  
Vol 276 (3) ◽  
pp. H953-H960
Author(s):  
Keith G. Lurie ◽  
Atsushi Sugiyama ◽  
Scott McKnite ◽  
Paul Coffeen ◽  
Keitaro Hashimoto ◽  
...  
Keyword(s):  
Extracellular Space ◽  
Left Ventricular ◽  
Conduction Time ◽  
Av Node ◽  
Total Blood ◽  
His Bundle ◽  
Induced Changes ◽  
Total Blood Flow ◽  
Dose Dependent Increase ◽  
Dose Dependent

Previous studies have demonstrated that the extracellular space (ECS) component of the atrioventricular (AV) node and His bundle region is larger than the ECS in adjacent contractile myocardium. The potential physiological significance of this observation was examined in a canine blood-perfused AV nodal preparation. Mannitol, an ECS osmotic expander, was infused directly into either the AV node or His bundle region. This resulted in a significant dose-dependent increase in the AV nodal or His-ventricular conduction time and in the AV nodal effective refractory period. Mannitol infusion eventually resulted in Wenckebach block ( n = 6), which reversed with mannitol washout. The ratio of AV nodal to left ventricular ECS in tissue frozen immediately on the development of heart block ( n = 8) was significantly higher in the region of block (4.53 ± 0.61) compared with that in control preparations (2.23 ± 0.35, n = 6, P < 0.01) and donor dog hearts (2.45 ± 0.18, n = 11, P < 0.01) not exposed to mannitol. With lower mannitol rates (10% of total blood flow), AV nodal conduction times increased by 5–10% and the AV node became supersensitive to adenosine, acetylcholine, and carbachol, but not to norepinephrine. We conclude that mannitol-induced changes in AV node and His bundle ECS markedly alter conduction system electrophysiology and the sensitivity of conductive tissues to purinergic and cholinergic agonists.

Separate parasympathetic control of heart rate and atrioventricular conduction of dogs

1990 ◽  
Vol 259 (2) ◽  
pp. H536-H542 ◽  
Author(s):  
D. W. Wallick ◽  
P. J. Martin
Keyword(s):  
Vena Cava ◽  
Atrioventricular Conduction ◽  
Conduction Time ◽  
Fat Pad ◽  
Av Node ◽  
Parasympathetic Ganglia ◽  
Anesthetized Dogs ◽  
Parasympathetic Control ◽  
The Right ◽  
Electrical Stimuli

In open-chest, autonomically decentralized, anesthetized dogs, a brief burst of electrical stimuli was delivered at various time delays to the right pulmonary vein (RPV) fat pad. This fat pad contains parasympathetic ganglia that innervate the sinoatrial (SA) node. Each burst elicited a bimodal increase in the cardiac cycle length (CCL) without eliciting a significant change in atrioventricular conduction time (AVCT). A similar burst was applied to the inferior vena cava-inferior left atrial fat pad. This fat pad contains nerves that innervate the AV node. This latter stimulation elicited a bimodal increase in AVCT without eliciting any change in the CCL. When the cervical vagi were stimulated in a similar manner, a bimodal increase in the CCL was elicited that was similar to the response we observed when the RPV fat pad was stimulated. In contrast, the dromotropic response was quite variable. In conclusion, we could, for the most part, elicit selective parasympathetic control of either the SA or the AV node, respectively.

scholarly journals PROPEDEUTICS ASPECTS OF UNDERSTANDING OF ATRIOVENTRICULAR CONDUCTION AND ITS ELECTROCARDIOGRAPHIC REFLECTION

2016 ◽  
pp. 7-13
Author(s):  
L. I. Druyan ◽  
A. L. Kalinin ◽  
N. B. Krivelevich
Keyword(s):  
Conduction System ◽  
Atrioventricular Conduction ◽  
Cardiac Conduction ◽  
Cardiac Conduction System

The work offers two variants of explanation and understanding of atrioventricular conduction while teaching students how to interpret electrocardiography and considers the electrocardiographic reflection of the transmission of the excitation impulse throughout the cardiac conduction system and the myocardium.

Differential effect of verapamil isomers on sinus node and AV junctional region

1983 ◽  
Vol 244 (1) ◽  
pp. H80-H88
Author(s):  
H. O. Gloor ◽  
F. Urthaler
Keyword(s):  
Sinus Rhythm ◽  
Sinus Node ◽  
Conduction Time ◽  
Av Node ◽  
Junctional Rhythm ◽  
His Bundle ◽  
Sinus Node Artery ◽  
Rate Dependent ◽  
Av Conduction ◽  
Differential Responsiveness

The l- and d-isomers of verapamil were selectively perfused into the sinus node artery and atrioventricular (AV) node artery of 48 dogs. Injection of l-verapamil into the sinus node artery during sinus rhythm and into the AV node artery during AV junctional rhythm depresses both sinus rhythm and AV junctional rhythm significantly more than does the d-isomer. l-Verapamil is three to four times more powerful than d-verapamil. Injection of the isomers into the AV node artery during sinus rhythm rapidly impairs AV conduction. Increments in conduction time are measured exclusively at the level of the A-H interval of the His bundle electrogram, and l-verapamil is six times more powerful than d-verapamil. Neither d- nor l-verapamil in concentrations that exert a profound negative chronotropic effect or cause AV block, has any significant effect on transatrial or His bundle conduction. Thus these concentrations of d-verapamil have little or no significant effect on the fast sodium channel, but both verapamil isomers affect the slow channel. The main difference in action between l- and d-verapamil appears to be only quantitative in nature. The sinus node is significantly more sensitive to the negative chronotropic action of verapamil than is the AV junctional pacemaker, and this differential responsiveness appears to be related to the different intrinsic rates of the two pacemakers. During sinus rhythm (either in the presence or absence of atropine) sinus node automaticity is less affected than AV conduction when verapamil is given parenterally. We propose that this greater negative dromotropic effect of verapamil is also in part due to a rate-dependent process, since during sinus rhythm AV junctional cells have to be depolarized at frequencies significantly higher than their intrinsic rates.

The effect of propranolol and dimethylpropranolol on cardiac conduction

1979 ◽  
Vol 57 (6) ◽  
pp. 637-641 ◽  
Author(s):  
Peter E. Dresel ◽  
Pamela Potter
Keyword(s):  
Heart Rate ◽  
Quaternary Ammonium ◽  
Cardiac Conduction ◽  
Conduction Time ◽  
Av Node ◽  
Heart Rates ◽  
Ammonium Derivative ◽  
Quaternary Derivative ◽  
Quaternary Ammonium Derivative ◽  
Ventricular Conduction

Isolated dog hearts perfused with blood from a donor dog and driven at two heart rates were used to compare the effects of propranolol with those of its quaternary ammonium derivative on atrial, atrioventricular (AV) nodal, and His-Purkinje conduction. Propranolol slowed only AV-nodal conduction, increasing the minimal conduction time and the effect of prematurity, without affecting fatigue. Practolol did not have this effect. Dimethylpropranolol had similar but not identical effects on the AV node, but also slowed atrial and ventricular conduction. In contrast with the quaternary derivative of lidocaine, dimethylpropranolol's effect on atrial and ventricular conduction was not dependent on the heart rate. The effect of dimethylpropranolol on ventricular conduction was observed at doses lower than those reported by others to be antiarrhythmic.

Morphology and electrophysiology of the mammalian atrioventricular node

1988 ◽  
Vol 68 (2) ◽  
pp. 608-647 ◽  
Author(s):  
F. L. Meijler ◽  
M. J. Janse
Keyword(s):  
Mammalian Species ◽  
Conduction Block ◽  
Atrioventricular Node ◽  
Conduction Delay ◽  
Conduction Time ◽  
Av Node ◽  
Crista Terminalis ◽  
His Bundle ◽  
Transitional Cells ◽  
Av Bundle

The AV node of those mammalian species in which it has been thoroughly investigated (rabbit, ferret, and humans) consists of various cell types: transitional cells, midnodal (or typical nodal cells), lower nodal cells, and cells of the AV bundle. There are at least two inputs to the AV node, a posterior one via the crista terminalis and an anterior one via the interatrial septum, where atrial fibers gradually merge with transitional cells. The role of a possible third input from the left atrium has not been investigated. Since the transition from atrial fibers to nodal fibers is gradual, it is very difficult to define the "beginning" of the AV node, and gross measurements of AV nodal length may be misleading. Histologically, the "end" of the AV node is equally difficult to define. At the site where macroscopically the AV node ends, at the point where the AV bundle penetrates into the membranous septum, typical nodal cells intermingle with His bundle cells. A conspicuous feature, found in all species studied, is the paucity of junctional complexes, most marked in the midnodal area. The functional counterpart of this is an increased coupling resistance between nodal cells. An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart. In those studies in which activation patterns, transmembrane potential characteristics, and histology have been compared, a good correlation has been found between AN and transitional cells, N cells and the area where transitional cells and cells of the beginning of the AV bundle merge with midnodal cells, and NH cells and cells of the AV bundle. Dead-end pathways correspond to the posterior extension of the bundle of lower nodal cells and to anterior overlay fibers. During propagation of a normal sinus beat, activation of the AN zone accounts for at least 25% of conduction time from atrium to His bundle, the small N zone being the main source of AV nodal delay. Cycle length-dependent conduction delay is localized in the N zone. Conduction block of premature atrial impulses can occur both in the N zone and in the AN zone, depending on the degree of prematurity. Several factors determining AV nodal conduction delay have been identified.(ABSTRACT TRUNCATED AT 400 WORDS)

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