Several investigators have documented immaturity of cardiac autonomic innervation in neonates. To evaluate the integrity of afferent and efferent responses and to determine the role of circulating catecholamines in newborns, 50 puppies and 24 adult dogswere studied with the use of chloralose anesthesia. Interventions were: bilateralvagotomy, bilateral carotid occlusion, central vagus stimulation, stellate stimulation, bilateral adrenalectomy, infusion of norepinephrine or isoproterenol, and intravenoustyramine. Newborns exhibited supersensitivity to exogenous norepinephrine, isoproterenol, and stellate stimulation; responses to carotid occlusion and central vagal stimulation were comparable in both groups. Newborns had less resting vagal tone. After adrenalectomy, newborns exhibited a more marked decline in systemic pressureand heart compared to adults. Myocardial catecholamine content in newborns was 1/10 that in adults, whereas plasma catecholamine concentration in newborns was 30-fold greater than in adults. These data demonstrate functional integrity of afferent and efferent cardiac autonomic pathways in the newborn, define in vivo supersensitivity to the sympathetic neurotransmitter, and suggest a dominant role of circulating catecholamines in modulation of cardiovascular events in neonates.
In dogs with unilaterally sympathectomized hearts, the remaining intact stellate ganglion was electrically stimulated 14–58 days following sympathectomy. Pressures were simultaneously recorded from all four chambers of the heart and the resulting responses compared with those observed in similarly stimulated but nonsympathectomized animals. Augmentor responses were markedly decreased in some animals but relatively unchanged in others, and it is evident that considerable variation exists in the distribution of sympathetic fibers in different animals. A common finding was markedly delayed augmentation in which responses were practically absent during the initial periods of stimulation. Chronotropic responses appeared to be largely dependent upon intact connections via the right sympathetic nerves. It may be concluded that the sympathetic cardiac nerves from the right side go primarily to the atria and nodal tissue, with a variable supply to the ventricles. In some animals the latter supply is very large while in others it is minimal. The left sympathetic cardiac nerves furnish the major supply to the ventricles, with variable but generally lesser distribution to the atria.
Recently it has been suggested that the parasympathetic innervation of the ventricles is by way of postganglionic axones that emanate from ganglion cells in the atria, reaching the ventricles by traversing the atrioventricular (AV) groove. We designed a series of experiments to test this hypothesis. Phenol (89%) was applied to the AV groove and surrounding 5 mm of epicardium in 21 dogs on cardiopulmonary bypass. The effects of intracoronary acetylcholine (ACh; 1-5 micrograms) and intracoronary nicotine (NIC; 25-100 micrograms) on cardiac isovolumic pressures were evaluated after beta-blockade. In another series of experiments, eight dogs were exposed to phenol in the same way and allowed to recover for 7-10 days. Atrial and ventricular responses to NIC were unaffected by phenol application to the AV groove in the acute animals when compared with application of saline alone. However, in the chronic animals, pretreatment with phenol 7-10 days previously reduced the ventricular responses to NIC by 70% while leaving the atrial responses intact. These data indicate that the intrinsic cardiac nerves (ICN) of the canine ventricles consist primarily of postganglionic parasympathetic axones which arise from supraventricular ganglia and cross the AV groove.
Experiments were designed to determine whether the canine mitral valve actively contracts and, if so, if its mechanical activity can be modulated by the autonomic nervous system. A miniature displacement gauge was sutured to the atrial (muscular) surface of the septal leaflet in 65 dogs under pentothal sodium anesthesia during total cardiopulmonary bypass. During bypass, with blood constantly drained from the left ventricle (LV), the leaflet deflected into the LV during ventricular systole as would be expected with active contraction. With blood present in the LV, leaflet deflection was reversed, indicating a passive displacement. After application of 85% phenol to the atrial surface, ventricular displacement of the leaflet was abolished, whereas the atrial displacement was significantly augmented. There was a positive inotropic effect during sympathetic stimulation and a negative inotropic effect with parasympathetic stimulation, i.e., increased and decreased ventricular deflection, respectively. These effects of autonomic stimulation were abolished by application of phenol to the leaflet muscle. During simultaneous electrical and mechanical recordings from the valve, activation appeared to originate from the atrium, before ventricular depolarization. It was concluded that the valvular muscle actively contracts to assist in bringing the valve leaflets into early apposition. This contraction imparts a measurable level of active "stiffness" to the valve, reducing atrial displacement during ventricular systole. This "stiffness" can be modified by autonomic input and may contribute to dysfunction of morphologically normal mitral valves.
The responses of the paced, isovolumic atria and ventricles to cervical vagosympathetic stimulation were examined in eight normal and seven sympathectomized dogs under chloralose anesthesia. Before atropine, stimulation usually caused decreases in both atrial and ventricular contractility but with significant quantitative and qualitative variation from animal to animal. The right atrium showed the greatest average decrease (>30%), followed by the left atrium (12%), right ventricle (4% to 12%), and the left ventricle (1% to 10%). After atropine, 0.5 mg/kg, all chambers responded positively to stimulation. The right ventricle was most responsive (about 30%), and the other chambers showed increases of 10% to 20%. These positive inotropic responses were eliminated by propranolol, 0.5 mg/kg, or by pentolinium tartrate, 0.5 mg/kg. In the sympathectomized animals, negative inotropic responses were usually greater and positive responses were reduced or eliminated. The data demonstrate that fibers exist in the cervical vagosympathetic trunks which have both negative and positive inotropic effects on all chambers of the heart. The net effect of vagosympathetic stimulation on a chamber's contractility reflects the relative numbers of the two fiber types which supply it. The fibers mediating the positive effects are probably preganglionic with significant postganglionic stations in the caudal cervical and stellate ganglia and perhaps in the heart itself.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.