ATTENUATION OF ARTERIAL BAROREFLEX CONTROL OF RENAL SYMPATHETIC-NERVEACTIVITY DURING LIDOCAINE INFUSION IN ALPHA-CHLORALOSE-ANESTHETIZED DOGS

The purpose of this study was to identify the relationship between sen sitivity of arterial baroreflex and plasma concentrations lidocaine. U sing twelve mongrel dogs anesthetized with alpha-chloralose, the left kidney was exposed retroperitoneally, and renal sympathetic nerve acti vity was recorded continuously. Lidocaine was infused in four differen t doses: 2 mg.kg BW-1 bolus + 100 mu g.BW-1.min; 3 mg.kg BW-1 bolus 200 mu g.kg BW-1.min; 6 mg.kg BW-1 bolus + 400 mu g.kg BW-1.min; and 1 2 mg.kg BW-1 + 800 mu g.kg BW-1.min. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 mu g.kg(-1)) and phenylephrine (2-4 mu g.kg(-1)) were performed before and at 10 min after beginning lidocaine infusion. Plasma lidocaine concentrations determined by high performance liquid chromatography revealed that the steady-state leve ls were e maintained during the baroreflex tests. Baroreflex sensitivi ty was preserved at plasma concentrations of lidocaine below 5 mu g.ml (-1). However, cardiac and sympathetic baroreflex sensitivity were sig nificantly attenuated (P < 0.01) when plasma lidocaine concentrations were well above human convulsion levels (10 mu g.ml(-1)). The results indicate that hemodynamic derangement observed in the lidocaine-induce d central nervous system toxicity is, at least in part, due to the att enuated arterial baroreflex.