The left ventricular mechanoreceptor reflex: characterisation of the afferent pathway.

Abstract

To determine if the afferent, vagal pathway of the left ventricular (LV) mechanoreceptor reflex is bilaterally symmetrical, a working left ventricle was devised in pneumonectomised dogs on total cardiac by-pass in which the coronary and systemic circulations were isolated and perfused separately, the systemic being perfused at a constant rate so that changes in pressure reflected changes in resistance. The ventro-lateral cervical cardiac nerve (VLCCN), a sympathetic nerve to the heart, was stimulated electrically to increase myocardial contractility, changes in which initiate directionally opposite changes in the systemic resistance via the LV mechanoreceptor reflex. Increasing contractility by electrical stimulation of the VLCCN caused a 14 ± 1% decrease in the systemic arterial pressure or resistance. This decrease in resistance was attenuated or abolished by left or bilateral vagotomy but largely unaffected by right vagotomy, indicating that the afferent arm of the LV mechanoreceptor reflex is predominantly carried by the left vagus, under physiological conditions. However, the massive discharge initiated by the act of sectioning either vagus nerve, a near-maximal, unphysiological stimulus, elicited a 27 to 28% decrease in the systemic resistance, indicating that afferent fibres of either vagus central to the site of the section have equal access to inhibit the vasomotor centres and that the difference between the vagi when activated more physiologically lies in their connections to the LV mechanoreceptors. The absence of a biphasic response consisting of an increase followed by a decrease in contractility following electrical stimulation of the VLCCN, as well as the fact that the magnitude of the increase in contractility from such stimulation after bilateral vagotomy was similar to that prior to vagotomy, indicate that when the LV mechanoreceptor reflex, which plays an important permissive role in exercise, is initiated physiologically, negative feedback mechanisms decreasing myocardial contractility below control are not set up in our animal model. The absence of such negative feedback may make prolonged, vigorous exercise possible.