Effects of intravenous mepivacaine on renal sympathetic nerve activity in the cat during nitrous oxide and nitrous oxide-halothane anesthesia.

Abstract

Because hemodynamic responses to systemic mepivacaine may be influenced by sympathetic change and concurrent general anesthesia, the authors directly measured renal sympathetic nerve activity (RSNA) during intravenous administration of mepivacaine in subseizure through seizure doses under N2O-O2 and N2O-O2-halothane anesthesia. Thirty-four cats were randomly assigned to five groups. Groups I-A, I-B, and I-C received incremental subseizure doses of intravenous mepivacaine (2 mg/kg, 5 mg/kg, and 10 mg/kg). Groups II-A and II-B received intravenous infusion of mepivacaine (4 mg/kg/min). Anesthesia was maintained with N2O(70%)-O2 in groups I-A, I-C, and II-A, and with N2O(70%)-O2-halothane (1%) in groups I-B and II-B. Cats in group I-C had undergone total baroreceptor denervation. Heart rate (HR), mean arterial pressure (MAP), and RSNA were measured. In group I-A, MAP did not significantly change with intravenous mepivacaine, though RSNA and HR significantly decreased (P < .05) respectively with 5 mg/kg i.v. and 10 mg/kg i.v. mepivacaine. In group I-C, HR, MAP, and RSNA did not change significantly. In group I-B, HR and MAP decreased with bolus intravenous doses of mepivacaine in a dose-dependent fashion, but RSNA did not change significantly. All cats in group II-A developed seizure by mepivacaine infusion at mean total dose of 28.9 +/- 4.2 mg/kg without significant changes in HR, MAP, or RSNA. In group II-B, mepivacaine infusion resulted in circulatory collapse at mean total dose of 34.3 +/- 4.6 mg/kg without seizure or significant RSNA change. The authors conclude that intravenous mepivacaine induces occasional depression in HR and RSNA during N2O-O2 anesthesia, but in addition induces dose-related circulatory depression during N2O-O2-halothane anesthesia via nonsympathetic mechanism(s).