The effect of propranolol and dimethylpropranolol on cardiac conduction

1979 ◽  
Vol 57 (6) ◽  
pp. 637-641 ◽  
Author(s):  
Peter E. Dresel ◽  
Pamela Potter

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.

1988 ◽  
Vol 254 (4) ◽  
pp. H651-H657
Author(s):  
J. M. Loeb ◽  
J. M. deTarnowsky

Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.


1986 ◽  
Vol 251 (6) ◽  
pp. H1126-H1133 ◽  
Author(s):  
M. R. Warner ◽  
J. M. Loeb

We examined the integration of heart rate and neural influences at the atrioventricular (AV) node in conscious dogs. Animals were anesthetized and, under sterile conditions, instrumented to chronically record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded on a beat-by-beat basis, and heart rate and AV interval were plotted graphically as a function of time. Resting animals exhibited both respiratory sinus arrhythmia and marked oscillations in AV conduction time associated with respiration. During inspiration AV interval was shortened, and during expiration AV interval was prolonged. To obviate the effect of cyclic changes in heart rate, atrial pacing was used to increase heart rate over a wide range both abruptly and linearly. Regardless of the pattern of heart rate change, AV interval oscillated at the respiratory frequency at pacing rates 10-100 beats/min above control. Higher levels of atrial pacing resulted in AV conduction patterns that were correlated with changes in blood pressure. Thus in the conscious dog variations in AV conduction time occur on a beat-by-beat basis in conjunction with respiration; oscillatory activity of AV conduction is not dependent on simultaneous changes in heart rate; and during atrial pacing, autonomic neural activity associated with respiration and blood pressure appears to dynamically modulate AV conduction with respiratory effects predominating at low heart rates and blood pressure effects at high heart rates.


1988 ◽  
Vol 7 (3) ◽  
pp. 335-351 ◽  

Polyquaternium-10 is a polymeric quaternary ammonium derivative of hydroxyethyl cellulose that is used in cosmetics as a conditioner, thickener, and emollient at concentrations of ≤0.1%–5%. Polyquaternium-10 has, at most, only a low potential to penetrate the stratum corneum but is adsorbed by keratinous surfaces. The oral LD50 of Polyquaternium-10 was not obtained at 16 g/kg in rats. Inhalation, dermal, and ocular animal test data indicated, at most, only a low degree of toxicity at test concentrations of Polyquaternium-10 greater than that used in cosmetic products. Polyquaternium-10 with and without metabolic activation was not a mutagen in three separate assay systems. Polyquaternium-10 was neither an irritant nor a human sensitizer when tested at 2.0%. Cosmetic products containing up to 1% Polyquaternium-10 were not human irritants, sensitizers, or photosensitizers. On the basis of the information presented, it is concluded that Polyquaternium-10 is safe as a cosmetic ingredient in the present practices of use.


1981 ◽  
Vol 59 (11) ◽  
pp. 1192-1195
Author(s):  
Peter E. Dresel ◽  
Keith D. Cameron

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.


2017 ◽  
Vol 80 (3) ◽  
pp. 517-526 ◽  
Author(s):  
Imen Miladi ◽  
Magali Vivier ◽  
Marie-Mélanie Dauplat ◽  
Morgane Chatard ◽  
Sophie Besse ◽  
...  

2010 ◽  
Vol 345 (1) ◽  
pp. 120-123 ◽  
Author(s):  
Shaoli Yang ◽  
Zhanyong Guo ◽  
Yuling Zhou ◽  
Lili Zhou ◽  
Qinzhao Xue ◽  
...  

1995 ◽  
Vol 83 (6) ◽  
pp. 1293-1301 ◽  
Author(s):  
G. K. Wang ◽  
C. Quan ◽  
M. Vladimirov ◽  
W. M. Mok ◽  
J. G. Thalhammer

Abstract Background Use of long-acting local anesthetics that elicit complete neural blockade for more than 3 h often is desirable in pain management. Unfortunately, clinically available local anesthetics are in general not suitable for prolonged analgesia. This report describes the organic synthesis and functional testing of a lidocaine derivative that appears to fulfill the criteria of long-acting local anesthetics.


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