BICARBONATE INCOMPLETELY REVERSES THE INHIBITORY EFFECT OF CHLORPROCAINE ON BUPIVACAINE IN A SCIATIC BLOCK IN SPRAGUE‐DAWLEY RATS

Abstract

Chloroprocaine (CP) and bupivacaine (BP) bind to the intracellular portion of Na‐channels and block Na influx into neurons, preventing depolarization. CP is a fast acting local anesthetic and BP is long acting. They have been coadministered to yield a block with rapid onset and long duration, with limited success. The lack of success was hypothesized to be due to the low pH of CP, or an inhibitory effect of CP or its metabolite on the action of BP at the Na‐channel. A recent unpublished study demonstrated the efficacy of a block with bicarbonated CP followed by BP administration. In order to understand the role bicarbonate (BC) plays in the success of the block, the sciatic nerve in 40 Sprague‐Dawley rats (250gm to 350gm) was blocked with CP and epinephrine (EPI), with or without BC, followed by BP and EPI. The time to onset and duration of analgesia were measured. The data show that addition of BC to CP and EPI, followed by BP and EPI, hastened the onset (1.38 ± 0.13 min vs. 2.73 ± 0.32 min; p < 0.001) and prolonged the duration (129.63 ± 5.24 min vs. 110.28 ± 5.56 min; p = 0.013) of the block. Controls show that adding BC to CP alone decreased the onset time and duration of block. BP alone had a longer duration than CP with BC followed by BP. These observations suggest that the apparent inhibitory effect of CP on BP‐induced block is a function of both the low pH of clinically available CP solutions and a direct effect of the CP molecule or its metabolite.