A double-blind comparison of 0.5% bupivacaine with 1:200,000 epinephrine and 0.5% levobupivacaine with 1:200,000 epinephrine for the inferior alveolar nerve block Filipe Polese Branco, MS, a Jose ´ Ranali, PhD, b Gla ´ucia M. B. Ambrosano, PhD, c and Maria Cristina Volpato, PhD, d Paricicaba, Brazil DENTISTRY SCHOOL OF PIRACICABA, STATE UNIVERSITY OF CAMPINAS This double-blind cross-over study compared the anesthetic success and onset and duration of lip and pulpal anesthesia of 0.5% bupivacaine and levobupivacaine solutions, both with 1:200,000 epinephrine, when administered for inferior alveolar nerve anesthesia. Thirty healthy volunteers were randomly anesthetized using one of the solutions. The inferior canine, second premolar, and molar were tested with electric stimulation. The pulpal anesthetic success rates for bupivacaine and levobupivacaine were 80% and 76.66%, respectively, for molars, 76.66% (both solutions) for premolars, and 70% (both solutions) for canines. At least 250 minutes of pulpal anesthesia was achieved. There were no significant differences between the solutions considering the measured parameters (P [ .05). Because of the similar anesthetic behavior of the 2 solutions in this study and the low toxicity related in the literature for levobupivacaine, there is justification for replacing bupivacaine with levobupivacaine for inferior alveolar nerve local anesthesia. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:442-7) In dentistry, the 2 most common long-acting anesthetics are bupivacaine and etidocaine. Bupivacaine, an amide- type local anesthetic, has been used in medicine and dentistry for sustained peripheral and central nerve blockade. 1 Bupivacaine with epinephrine is shown to produce longer-lasting pulpal and soft tissue anesthesia in the mandible when compared to lidocaine with epinephrine. 2-3 The success rate of anesthesia in the mandible is reported as being 80% for lidocaine and 86.7% for bupivacaine. 3 The onset of pulpal anesthesia in inferior alveolar nerve blocks is faster with lidocaine than with bupivacaine, 11 4-5 and 15 minutes, 6 respectively, for premolars as assessed through electrical stimulus. Bupivacaine has a good safety record overall, though the literature has reports of serious adverse central nervous system (CNS) and cardiovascular reactions, 7 as well as deaths, 8-9 caused by inadvertent intravascular injection or intravenous regional anesthesia. 10 Although the early toxicity signs of local anesthetics are usually seen in the CNS, bupivacaine overdose can cause cardio- vascular collapse and ventricular dysrrhythmia, which are often refractory to resuscitation. 1,7-11 As reported by de Jong et al., 12 dysrhythmia in cats may precede convulsions when bupivacaine is administered. The main cause of this toxicity is that bupivacaine blocks cardiac Na 1 channels preferentially in the inactivated channel state; lidocaine is bound preferentially in the open activated state. 13 Bupivacaine has a single chiral center and, like the majority of local anesthetics, is marketed as the racemate (R- and S-bupivacaine). Both enantiomers are active, but S-bupivacaine (levobupivacaine) is rep- resented as having a lower propensity towards CNS and cardiovascular toxicity, 10-11,14-17 with equivalent ef- ficacy in surgical anesthesia and pain management. 18-22 Levobupivacaine is also reported as being more potent than ropivacaine, a long-acting local anesthetic mar- keted as pure S-isomer, in labor analgesia 23-24 with no difference in the incidence of adverse effects such as hypotension, nausea and vomiting, motor block, and adverse cardiovascular effects to the fetus. 23 There have been no conclusive studies of levobupi- vacaine use in dentistry, with the exception of a study by Rood et al., 25 reporting less analgesia required 2 hours after extraction of impacted third molars, under general anesthesia, using 0.75% plain levobupivacaine com- pared to 2% lidocaine with 1:80,000 epinephrine for postoperative pain relief. Pulpal and soft tissue onset and duration of anesthesia were not recorded. a Graduate Student in Pharmacology, Anesthesiology and Therapeu- tics, Dentistry School of Piracicaba, State University of Campinas. b Chairman, Pharmacology, Anesthesiology and Therapeutics Area, Department of Physiological Sciences, Dentistry School of Piraci- caba, State University of Campinas. c Associate Professor, Biostatistics Area, Department of Social Dentistry, Dentistry School of Piracicaba, State University of Campinas. d Associate Professor, Pharmacology, Anesthesiology and Therapeu- tics Area, Department of Physiological Sciences, Dentistry School of Piracicaba, State University of Campinas. Received for publication Mar 14, 2005; returned for revision May 18, 2005; accepted for publication Jun 10, 2005. 1079-2104/$ - see front matter Ó 2006 Mosby, Inc. All rights reserved. doi:10.1016/j.tripleo.2005.06.005 442