Bupivacaine does not suppress cardiac sympathetic nerve activity during halothane anesthesia in the cat.

Abstract

The finding that i.v. lidocaine suppresses cardiac sympathetic nerve activity during 1 MAC halothane, but not during 2 MAC or 3 MAC halothane, suggests that the neurally mediated circulatory effects of i.v. local anesthetics may vary with background autonomic activity. This study aimed to compare the effects of i.v. lidocaine and bupivacaine on cardiac sympathetic nerve activity (CSNA) during normal and high levels of CSNA. Cats were anesthetized with halothane and allocated to three groups. In groups I-L and I-B, sympathetic hyperactivity was induced by electrical stimulation of the posterior hypothalamus. CSNA, heart rate and mean arterial pressure were then measured before and after administration of lidocaine 2 mg.kg BW-1 i.v. (Group I-L, n = 7) or bupivacaine 0.5 mg.kg BW-1 i.v. (Group I-B, n = 7) during 1% halothane anesthesia. In Group II (n = 7), following administration of bupivacaine 0.5 mg.kg BW-1 i.v., CSNA, sinus cycle length (SCL), and subintervals of atrioventricular conduction time (A-H, H-V, and H-S) at pacing were measured during 0.8%, 1.6% and 2.4% halothane anesthesia without sympathetic hyperactivity. Lidocaine suppressed CSNA hyperactivity and tachycardia significantly in Group I-L, but bupivacaine did not do so in Group I-B. In Group II, bupivacaine did not affect CSNA at any concentrations of halothane, but lengthened SCL, A-H, H-V and H-S intervals significantly at each concentration of halothane. We conclude that i.v. bupivacaine, unlike i.v. lidocaine, does not suppress CSNA during either normal or high CSNA under halothane anesthesia although i.v. bupivacaine has stronger depressive effects on cardiac conduction than does i.v. lidocaine during deep halothane anesthesia.