‘Non-chronotropic’ mechanisms on withdrawal of efferent vagal stimulation in anesthetized dogs

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].…”