Letters to the Editor: Letters & Announcements
Bupivacaine and Ventricular Fibrillation
We thank Dr. Coleman for his thoughtful comments on our article (1) describing the ability of bupivacaine to retard myocardial acidosis during ventricular fibrillation. We agree that “inhibition of cellular metabolism” per se is an incomplete explanation, and identifying the precise molecular mechanisms of this phenomenon is a current focus of our laboratory. However, we question Dr. Coleman’s explanation that vasodilation and inhibition of capillary fibrin cuffs contribute significantly to the effect. If bupivacaine improved tissue perfusion and oxygen delivery, one would expect higher myocardial oxygen tension in those animals. We found the opposite: tissue PmO2, which is closely related to capillary perfusion, was depleted rapidly in all bupivacaine-treated animals. This observation is also consistent with the well-known uncoupling effect of bupivacaine that Dr. Coleman mentions (2,3). Uncoupling oxidative phosphorylation from mitochondrial respiration increases oxygen consumption but reduces ATP production, an effect consistent with a net inhibition of cellular metabolism.
Guy Weinberg, MD
William Hoffman, PhD
Douglas Feinstein, PhD
Chanannait Paisanthasan, MD
Department of Anesthesiology
University of Illinois at Chicago
1. Weinberg G, Paisanthasan C, Feinstein D, Hoffman W. The effect of bupivacaine on myocardial tissue hypoxia and acidosis during ventricular fibrillation. Anesth Analg 2004;98:790–5.
2. Sun X, Garlid KD. On the mechanism by which bupivacaine conducts protons across the membranes of mitochondria and liposomes. J Biol Chem 1992;267:19147–54.
© 2004 International Anesthesia Research Society
3. Dabadie P, Bendriss P, Erny P, Mazat JP. Uncoupling effects of local anesthetics on rat liver mitochondria. FEBS Lett 1987;226:77–82.