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.