Vagus nerve stimulation protects against ventricular fibrillation independent of muscarinic receptor activation

Abstract

We show that the vagal anti-fibrillatory action in the rabbit ventricle occurs via post-ganglionic efferent nerve fibres, independent of muscarinic receptor activation, VIP, and the endothelium. Together with our previous publications, our data support the possibility of a novel ventricular nitrergic parasympathetic innervation and highlight potential for new therapeutic targets to treat ventricular dysrhythmias.

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

“…Based on the fact that the occurrence of fatal ventricular arrhythmias is accompanied by a marked decrease of parasympathetic activity in CHF, some studies demonstrate that decreased parasympathetic activity is correlated with malignant ventricular arrhythmogenesis in the CHF state 11, 46, 47, 48. Recent studies have also found that the parasympathetic activation induced by vagal nerve stimulation prevents fatal ventricular arrhythmias and improves survival rates in animal CHF models 17, 18, 19. However, there is no direct evidence to clarify the role of decreased parasympathetic activity in ventricular arrhythmogenesis and how decreased parasympathetic activity links to ventricular arrhythmogenesis in CHF due to the coexistence of multiple factors in the CHF state (such as sympathetic overactivation, ventricular morphological changes, and others).…”

“…However, such pharmacological treatment is not ideal because the ability of β‐adrenergic receptor blockers to affect cardiac vagal activity is limited,15 and survival rates even when β‐blockers are used are lower in CHF patients with depressed cardiac vagal activity than in CHF patients with normal cardiac vagal activity 16. Although modulation of cardiac vagal activation as a potential therapy has received only limited attention, direct cardiac vagal nerve stimulation has been found to suppress ventricular tachyarrhythmia and to improve survival rates in CHF 17, 18, 19. Therefore, exploring the mechanism(s) responsible for the impairment of cardiac vagal function can provide a new therapeutic strategy for eliminating ventricular tachyarrhythmia and reducing related mortality.…”

Systematic and comparative morphologies of the extrinsic cardiac nervous system in lemurs (Primates: Strepsirrhini: Infraorder Lemuriformes, Gray, 1821) with evolutionary morphological implications

“…Experimental and developmental studies of the autonomic cardiac nervous system have also been conducted in animals such as the mouse, rat, rabbit, chick, and dog (Armour et al, 1972;Benítez et al, 1959;Brack et al, 2011;Gomez, 1958;Haws and Burgess, 1978;Hildreth et al, 2008Hildreth et al, , 2009Kirby et al, 1980;Kuratani et al, 1991;Kuratani and Tanaka, 1990;Levy et al, 1966;Mabe and Hoover, 2011;Meyer et al, 2010;Mizeres, 1955Mizeres, , 1957Mizeres, , 1958Mizuno et al, 2010;Oliveira et al, 2010;Roberts, 1991;Schwartz, 2010;Scherlag et al, 2011;Shaner, 1930;Shoba and Tay, 2000;Uchida et al, 2010;Verberne et al, 1998). However, huge differences in the cardiac nervous system between humans and the experimental animals have been recognized (Batulevicius et al, 2003;Brugnaro et al, 2003;Kawashima, 2011;McKibben and Getty, 1968;Rysevaite et al, 2011;Pauza et al, 2002a,b).…”

Cholinergic stimulation with pyridostigmine protects myocardial infarcted rats against ischemic-induced arrhythmias and preserves connexin43 protein

“…There is evidence showing that vagal nerve stimulation reduced the incidence of ventricular fibrillation in conscious dogs subjected to cardiac ischemia (58) and that it increased the ventricular fibrillation threshold in hearts from rabbits subjected to coronary artery ligation (7). Furthermore, it has been argued that this antiarrhythmic effect of parasympathetic activity could occur because preventing Cx43 degradation in infarcted hearts, in turn, prevents the cell-to-cell electrical uncoupling of ventricular myocytes (4).…”