Effects of intravenous lidocaine on cardiac sympathetic nerve activity and A–V conduction in halothane–anesthetized cats

To study neural contributions to the alterations in intracardiac conduction induced by i.v. lidocaine, we measured cardiac sympathetic nerve activity (CSNA) simultaneously with sinus cycle length (SCL) and A-V cats. Sixteen cats were anesthetized with halothane in oxygen and mid-sternotomized. The His-bundle electrogram and CSNA were recorded from an electrode placed in the interatrial septum and from the left ventrolateral or ventromedial nerve, respectively. Atrium-His (A-H), His-Purkinje (H-V), and total intraventricular (H-S) conduction times were measured during atrial pacing conducted at a cycle length of 300 ms. In eight cats, 1 MAC, 2 MAC, and 3 MAC halothane were given during i.v. lidocaine (Groups H-1, H-2 and H-3). In the other eight cats, anesthesia was switched from halothane to i.v. alpha-chloralose (30-50 mg.kg BW-1; Group C). A significant decrease in CSNA with i.v. lidocaine, 2 mg.kg BW-1 was recognized in Groups C and H-1, but not in Groups H-2 and H-3. Prolongations of SCL during the spontaneous cycle, A-H and H-V in the paced mode following i.v. lidocaine were significant in Groups C, H-1 and H-2, but not significant in Group H-3. We conclude that i.v. lidocaine induces a significant decrease in CSNA during alpha-chloralose or 1 MAC halothane anesthesia which partly contributes to the control of intracardiac conduction.