Vagus nerve stimulation decreases left ventricular contractility in vivo in the human and pig heart

Abstract

Studies of the effect of vagus nerve stimulation on ventricular myocardial function in mammals are limited, particularly in the human. The present study was designed to determine the effect of direct electrical stimulation of the left vagus nerve on left ventricular contractile state in hearts paced at 10 % above the natural rate, in anaesthetised pigs and anaesthetised human subjects undergoing open chest surgery for coronary artery bypass grafting. Contractility of the left ventricle was determined from a series of pressure‐volume loops obtained from a combined pressure and conductance (volume) catheter placed in the left ventricle. From the measurements a regression slope of the end‐systolic pressure‐volume relationship was determined to give end‐systolic elastance (Ees), a load‐independent measure of contractility. In six anaesthetised open chest pigs, stimulation of the peripheral cut end of the left cervical vagus nerve induced a significant decrease in Ees of 26 ± 14 %. In nine patients electrical stimulation of the left thoracic vagus nerve close to its cardiac branch resulted in a significant drop in Ees of 38 ± 16 %. The effects of vagal stimulation were blocked by the muscarinic antagonist glycopyrronium (5 mg kg−1). Administration of the β‐adrenoreceptor antagonist esmolol (1 mg kg−1) also attenuated the effect of vagal stimulation, indicating a degree of interaction of vagal and sympathetic influences on contractility. These studies show that in the human and pig heart the left vagus nerve can profoundly decrease the inotropic state of the left ventricular myocardium independent of its bradycardic effect.

Reduced N‐Type Ca 2+ Channels in Atrioventricular Ganglion Neurons Are Involved in Ventricular Arrhythmogenesis

“…The ventricular myocardium only receives the projection of nerve terminals from the AVG 25. In our present study we measured the left ventricular pressure and vagal efferent nerve stimulation‐induced negative inotropic response in the left ventricle; the latter serves as an index of ventricular vagal activity 37. In vivo transfection of Ca v 2.2‐α shRNA into AVG neurons increased basal LVSP with the absence of heart‐rate changes in anesthetized rats (Table 3).…”

“…Activation of the vagal efferent nerve results in a negative inotropic effect in the ventricle, which serves as an index of ventricular vagal function 37. Ca v 2.2‐α shRNA transfection into AVG neurons significantly blunted changes of the LVSP and maximum rate of left ventricular pressure rise in response to vagal efferent nerve stimulation, compared with sham rats (Figure 4).…”

Baroreflex mechanisms in major depression

“…In a physiologically normal condition, increase in baroreflex sensitivity is coupled with a reduction in stroke volume (Casadei, 2001) due to vagally mediated baroreflex control of left ventricular myocardial contractility (Casadei et al, 1992;Karlocai et al, 1998;Lewis et al, 2001). The current study supports the literature in showing that in healthy subjects the higher baroreflex sensitivity was determined by both a low gain of its afferent 'sympathetic' component restricted by stroke volume and a high gain of its efferent component, related to parasympathetic regulation of heart period (i.e., parasympatheticsympathetic reciprocity).…”

Ingestão De Água No Sistema Nervoso Autônomo: Uma Revisão Sistemática E Meta-Análise

“…Já foi demonstrado que a estimulação vagal em humanos e em animais causa efeitos inotrópicos negativos, capazes de gerar diminuição da frequência cardíaca 37 .…”