EFFECTS OF INTRAVENOUS LIDOCAINE ON CARDIAC SYMPATHETIC-NERVE ACTIVITY AND AV CONDUCTION IN HALOTHANE-ANESTHETIZED CATS

To study neural contributions to the alterations in intracardiac condu ction induced by IV lidocaine, we measured cardiac sympathetic nerve a ctivity (CSNA) simultaneously with sinus cycle length (SCL) and AV con duction time using His-bundle electrocardiography following IV lidocai ne in cats. Sixteen cats were anesthetized with halothane in oxygen an d 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), H is-Purkinje (H-V), and total intraventricular (H-S) conduction times w ere measured during atrial pacing conducted at a cycle length of 300 m s. In eight cats, 1 MAC, 2 MAC, and 3 MAC halothane were given during IV lidocaine (Groups H-1, H-2 and H-3). In the other eight cats, anest hesia was switched from halothane to IV alpha-chloralose (30-50 mg kg BW-1; Group C). A significant decrease in CSNA with IV 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 i n the paced mode following IV lidocaine were significant in Groups C, H-1 and H-2, but nor significant in Group H-3. We conclude that IV lid ocaine induces a significant decrease in CSNA during alpha-chloralose or I MAC halothane anesthesia which partly contributes to the control of intracardiac conduction.