title: Vagal control of left ventricular contractility is selectively mediated by a cranioventricular intracardiac ganglion in the cat.
abstract: Activation of the vagus nerve leads to decreases in sinoatrial (SA) rate, atrioventricular (AV) conduction, and myocardial contractility. Previous data are consistent with the hypothesis that vagal control of cardiac rate and AV conduction are mediated by two anatomically separated and physiologically independent parasympathetic intracardiac ganglia located in fat pads on the surface of the right and left atria, respectively. These data suggested that vagal control of ventricular contractility might be mediated through another intracardiac ganglion. We examined the ventricles of cat hearts histologically for the presence of ganglia. Multiple small basophilic ganglia composed of a few neurons, and an occasional larger ganglion were found embedded in the epicardial fat surrounding the cranial margin of the anterior surface of the left ventricle, near the juncture with the right ventricle, which we refer to as the CV ganglion. In anesthetized cats, right cervical vagal stimulation decreased SA rate by 44 +/- 5%, decreased the rate of AV conduction by 68 +/- 14%, and reduced ventricular contractility by 19.5 +/- 5.7%. Vagally induced negative inotropism was almost completely prevented by microinjection of a ganglionic blocking drug into the CV ganglion. However, these injections into the CV ganglion did not significantly effect vagally induced decreases in either SA rate or AV conduction. We conclude: (1) that ganglia are found in a fat pad on the surface of the left ventricle of the cat heart and (2) that the CV ganglion selectively mediates the negative inotropic effect of vagal stimulation on the left ventricle. Greater understanding of the physiological functions of intracardiac neuronal circuits may help in developing new strategies to treat disorders of cardiac contractility such as congestive heart failure.
authors.affiliation: Department of Pharmacology, Howard University College of Medicine, Washington, DC 20059, USA.
authors.forename: P J
authors.initials: PJ
authors.lastname: Gatti
authors.forename: T A
authors.initials: TA
authors.lastname: Johnson
authors.forename: J
authors.initials: J
authors.lastname: McKenzie
authors.forename: J M
authors.initials: JM
authors.lastname: Lauenstein
authors.forename: A
authors.initials: A
authors.lastname: Gray
authors.forename: V J
authors.initials: VJ
authors.lastname: Massari
mesh_terms: D000818:Animals; D002415:Cats; D018680:Cholinergic Antagonists / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D005726:Ganglia, Parasympathetic / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D006321:Heart / Q000033:anatomy & histology / Q000187:drug effects / Q000294:innervation*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D014294:Trimethaphan / Q000494:pharmacology; D014630:Vagus Nerve / Q000502:physiology*; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
chemical_list: D018680:Cholinergic Antagonists; D014294:Trimethaphan