Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties.

Abstract

Recent work has shown that alterations in the dynamic atrioventricular (AV) nodal response to changes in heart rate can significantly modify AV nodal function. The present study was designed to evaluate the nature and potential importance of sympathetic regulation of the rate-dependent properties of the AV node. Selective stimulation protocols and mathematical formulations were used to independently quantify AV nodal recovery, facilitation, and fatigue in 12 morphine-chloralose-anesthetized dogs. Vagal effects were prevented by bilateral vagal transection and intravenous atropine, and the sinus node was crushed to allow a broader range of pacing cycle lengths. In seven dogs with sympathetic nerves intact, beta-adrenergic receptor blockade increased the recovery time constant (tau rec) for the conduction of premature test beats from 47 +/- 2 (mean +/- SEM) msec (control) to 62 +/- 1 msec (p less than 0.001), whereas isoproterenol decreased tau rec to 38 +/- 1 msec (p less than 0.001). In addition, beta-blockade increased the maximum amount of rate-dependent AV nodal fatigue from 7 +/- 1 msec (at a cycle length of 198 +/- 9 msec [control]) to 17 +/- 2 msec (p less than 0.001). In five dogs with decentralized stellate ganglia, tau rec was decreased from 71 +/- 3 msec (control) to 57 +/- 4 msec and 48 +/- 2 msec (p less than 0.001 for each) by left stellate ganglion stimulation at 5 and 10 Hz, respectively. Maximum fatigue was similarly reduced from 16 +/- 1 msec (control) to 12 +/- 2 msec (p = NS) and 8 +/- 1 msec (p less than 0.01), respectively. Stellate ganglion stimulation, isoproterenol, and beta-blockade did not alter AV nodal facilitation. A mathematical model incorporating quantitative indexes of AV nodal function accurately accounted for tachycardia-dependent increases in the atrial-His activation interval, which were enhanced by beta-adrenergic receptor blockade and reduced by isoproterenol. Furthermore, this model showed that beta-adrenergic effects were increased by increasing heart rate, with the majority of the rate-dependent action being due to changes in the time course of AV nodal recovery. We conclude that beta-adrenergic receptor stimulation alters functional properties that govern the AV nodal response to changes in heart rate. These changes in functional properties alter the ability of the AV node to conduct impulses during tachycardia and, as such, could play a major role in the ability of sympathetic stimulation to promote and beta-adrenergic receptor blockade to prevent the occurrence of AV nodal reentrant arrhythmias.

Rate‐Related and Autonomic Effects on Atrioventricular Conduction Assessed Through Beat‐to‐Beat PR Interval and Cycle Length Variability

“…4), The statistical procedure applied for the LF, MF, and HF bands in Table 1 was also applied to the 0.06-0. 10 by standing was significant for the RR spectra (n = 10, area ratio = 1.61, P = 0.03) but not for the PR spectra (n = 10, area ratio = 1.30, P > 0.05). Atropine with propranoloi (Fig.…”

The electrocardiogram of the Beagle dog: reference values and effect of sex, genetic strain, body position and heart rate

“…The relationship between HR and PQ probably originates mainly from the dependence of both parameters on the autonomic system. The sympathetic system increases the HR and velocity of atrioventricular conduction, and therefore shortens PQ interval, whereas the parasympathetic system has the opposite effects (O'Toole et al 1984, Nayebpour et al 1992, Furukawa et al 1997. However, an increase in HR results in a prolongation of atrioventricular conduction time due to an increase in the atrioventricular nodal refractoriness (Warner & Loeb 1986).…”

Electrophysiological remodeling in heart failure

“…In the AV node, sympathetic nerve activation accelerates pacemaker function (due to increases in I Ca ), enhances excitability, heightens action potential amplitude, increases conduction velocity, and decreases the effective refractory period of AV nodal cells, which together facilitate both antegrade slow conduction and retrograde fast conduction through the AV node[31]. In failing human ventricle, adrenergic over-activation is accompanied by down-regulation of β1-adrenergic receptors with preservation of β2-adrenoceptors, which shifts the β1:β2 ratio towards the β2-subtype.…”