Parasympathetic control of right atrial pressure in anesthetized dogs

Abstract

We investigated whether the intracardiac parasympathetic ganglia for sinoatrial (SA) nodal pacemaker cells control the right atrial contractility selectively and totally in the autonomically decentralized heart of the open-chest anesthetized dog. Stimulation of the intracardiac parasympathetic nerves to the SA nodal area (SAP Stim) decreased the right atrial pressure (a wave pressure) and its first pressure derivative (dP/dt) as well as the atrial rate but did not change the atrioventricular (AV) conduction time. Stimulation of right and left cervical vagosympathetic complexes (CV Stim) decreased the a wave pressure, dP/dt, and atrial rate and prolonged the AV conduction time. When SAP and CV Stim decreased the atrial rate similarly, the decreases in a wave pressure and dP/dt in response to SAP Stim were less than those to CV Stim in unpaced and paced hearts. When treatment with hexamethonium bromide or tetrodotoxin into the SAP Stim locus abolished the decreases in atrial rate evoked by SAP and CV Stim, each treatment abolished the decrease in a wave pressure response to SAP Stim but only slightly attenuated the pressure response to CV Stim. These results demonstrate that right atrial pressure is modified by efferent parasympathetic neurons, which are located in a region that differs from that of efferent parasympathetic neurons controlling heart rate.

Inotropic, chronotropic, and dromotropic effects mediated via parasympathetic ganglia in the dog heart

“…The parasympathetic neural elements controlling sinus rate also exist in the fatty tissue overlying the right pulmonary veins of the human hearts (3). However, clustered parasympathetic ganglionic cells controlling atrial contractile force have not been identified yet in the mammalian heart, although stimulation of the parasympathetic neural elements at the SA fat pad increases spontaneous sinus cycle length (SCL) and partly decreases the atrial contractile force in the dog heart (9). Recently, Chiou et al (4) have reported that there are ganglionic cells in the fat pad located between the medial superior vena cava and aortic root (SVC-Ao fat pad) and that radiofrequency catheter ablation to the SVC-Ao fat pad led to complete vagal denervation or attenuation of vagally induced effective refractory period (ERP) shortening of the right and left atria of the dog.…”

New arguments for positive inotropic vagal influence on cardiac contractility in cats

“…Our data indicate that VN does not inhibit ventricular contractility directly, but reduced it indirectly via the rhythmoinotropic effect [ 14], reduction of preand afterload [5,11], and suppression of the trophic mechanisms [7,8]. The combination of these factors usually prevails over the opposite (positive) effect of VN manifested by cardiac escape from the effect of stimulated nerve and postvagal potentiation of heart automaticity and contractility.…”

“…However, extrapolation of this phenomenon to the whole myocardium [9,12,13] can be erroneous, because heart ventricles are practically devoid of vagal terminals [10] and insensitive to acetylcholine [2]. The reason of this possibly erroneous although widespread view can be indirect decrease of ventricular contractility produced by vagal stimulation accompanied by vagal inhibition of sympathetic influences on the heart [7], cholinergic constriction of coronary vessels [8], moderation of the atrial pumping function [5,11], and bradycardia [14] associated with decreased afterload [5]. However, all these phenomena do not agree with escape rhythm under conditions of vagal stimulation [5,10] and postvagal potentiation of myocardial automaticity and contractility [5,10].…”

Vagal Stimulation Prior to Atrial Rapid Pacing Protects the Atrium From Electrical Remodeling in Anesthetized Dogs.

“…Tetrodotoxin, when applied to the fatty tissue overlying the right atrial side of the right pulmonary vein junctions, blocked this protective effect of VS (Fig 2). Tetrodotoxin is a selective axonal conduction blocker 18 and the fatty tissue overlying the right atrial side of the right pulmonary vein junctions contains the parasympathetic neuronal pathway to the right atrial musculature. 10 Therefore, we concluded that this protective effect was not mediated by muscarinic receptors, even though it was still the result of VS. We do not know the mechanism of the protective effect exerted by VS against the shortening of ERP induced by atrial rapid pacing.…”

“…Electrical stimulation of the fatty tissue overlying the right atrial side of the junctions of the right pulmonary veins elicited a marked slowing of the sinus rate, together with nonuniform shortening of the atrial ERP, thus identifying the parasympathetic neuronal pathway to the sinoatrial node and right atrial musculature in this fatty tissue. 10 At the start of the experiment, tetrodotoxin (3 g/0.01 ml) was applied topically to the fatty tissue in order to block parasympathetic axonal conduction, 18 and then we followed the same protocol as that used in the second series of the present experiments.…”