VENTRICULAR ARRHYTHMIAS INDUCED BY CHEMICALLY-MODIFIED INTRINSIC CARDIAC NEURONS

Objective: The aim was to investigate whether intrinsic cardiac neuron es can be involved in the genesis of ventricular arrhythmias. Methods: Nicotinic, muscarinic, beta adrenergic, peptidergic, and amino acider gic agonists, as well as purinergic compounds, were individually admin istered in mu 1 quantities adjacent to spontaneously active in situ ri ght atrial neurones in 57 anaesthetised dogs before and after acute de centralisation. Results: Ventricular arrhythmias were induced in one t hird of the dogs following neurochemical administration. Ventricular a rrhythmias are induced much less frequently when intrathoracic extraca rdiac neurones are modified chemically. Salvos of ventricular prematur e contractions or ventricular tachycardias were elicited when intrinsi c cardiac neurones were modified by locally applied nicotine, bethanec hol, isoprenaline, angiotensin II, bradykinin, substance P, vasoactive intestinal polypeptide, glutamate, or adenosine. In 60% of those inst ances in which intrinsic cardiac neuronal activity was modified by a n eurochemical, ventricular arrhythmias were elicited. When anhythmias w ere induced, activity generated by chemically modified intrinsic cardi ac neurones increased from 0.7(SD 0.2) to 2.2(0.4) impulses.s(-1) (p<0 .05). Following decentralisation of the intrinsic cardiac nervous syst em, repeat administration of the same neurochemicals into the same loc i elicited ventricular arrhythmias in 42% of those dogs in which ventr icular arrhythmias had been elicited previously. Neuronal activity inc reased [0.8(0.5) to 2.1(0.6) impulses.s(-1); p<0.05] in 86% of these i nstances. Conclusions: Intrinsic cardiac neurones can be involved in t he genesis of ventricular arrhythmias.