Anesthesiology
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Comparative Study
Differential peripheral nerve block by local anesthetics in the cat.
Controversy still surrounds the differential susceptibility of nerve fibers to local anesthetic conduction block. In order to help resolve this controversy, we developed an in vivo model of peripheral nerve blockade in the cat that closely reproduced the clinical state. Using this model, differential rate of nerve blockade of A-alpha, A-delta, and C fibers by 2-chloroprocaine, lidocaine, bupivacaine, and etidocaine was observed and quantitated. ⋯ Etidocaine blocked A-delta fibers first. A-alpha fibers always were blocked last. Of the four local anesthetics tested, 2-chloroprocaine produced the greatest differential rate of block of the nerve fibers, and etidocaine produced the least.
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Isolated rat sciatic nerves were used to study the interaction between 2-chloroprocaine (2-CP) and bupivacaine (BP). Five nerves studied as controls were treated with 5 X 10(-4) M BP and the amplitude of the compound action potential (CAP) evoked by suprathreshold stimulation was measured. This concentration of BP completely blocked nerve conduction; but, following washout with normal Krebs-Ringer solution, the CAP amplitude recovered to 50% of initial values in 50 (+/- 4) min with a rate of recovery of 1.7 (+/- 0.6) %/min. ⋯ When five nerves were exposed to a 5 X 10(-4) M solution of a 2-CP metabolite, 4-amino-2-chlorobenzoic acid, no nerve blockade was produced. When these nerves subsequently were blocked with BP, recovery to 50% of initial values occurred in 22 (+/- 5) min, with a rate of recovery of 2.0 (+/- 0.2) %/min. Although pretreatment with either 2-CP or 4-amino-2-chlorobenzoic acid significantly shortened the duration of BP-induced nerve blockade, neither drug had a significant effect on the rate of recovery once the CAP amplitude returned to measurable values.
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Controversy persists about the cardiac toxicity of bupivacaine if accidentally administered intravenously during regional anesthesia. Using awake, unanesthetized sheep, we evaluated the cardiac effects of low and high equivalent doses of lidocaine and bupivacaine given intravenously over 10 s. All animals convulsed within 30 s of injections. ⋯ Arterial blood gas and acid-base values stayed within the normal range during the studies, and serum potassium did not change significantly from control. In conclusion, in conscious adult sheep, equivalent doses of lidocaine or bupivacaine produced similar central nervous system (CNS) toxicity when rapidly injected intravenously. In the absence of marked hypoxia, respiratory or metabolic acidosis, hyperkalemia, or hypotension, serious cardiac arrhythmias occurred after bupivacaine but not lidocaine.