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Bakersfield, CA, lewiscoleman@bak.rr.com
To the Editor:
Weinberg et al. (1) have provided valuable information about the ability of bupivacaine to attenuate tissue acidosis and changes in PmO2 and PmCO2 in the myocardial tissue of dogs during ventricular fibrillation. I question their assumption that the explanation of these results was that bupivacaine inhibits cellular metabolism. As the authors noted, one of the known effects of bupivacaine is to uncouple oxidative phosphorylation, which would increase cellular metabolism, and would conflict with the observed results. I would suggest an alternative explanation: bupivacaine may preserve capillary bed perfusion in the presence of ventricular fibrillation. Like all amide local anesthetics, Marcaine exhibits both systemic anesthetic and anticoagulant properties (2). Lidocaine increases capillary blood flow when applied to capillary beds (3), and both lidocaine and bupivacaine attenuate bronchoconstriction (4), which may be due to improved capillary blood flow. Research literature is replete with reports of fibrin "cuffs" and deposits in capillaries of various models of stress and trauma (5). This may offer a simpler explanation than the hypothesis of decreased metabolism.
References
Department of Anesthesiology, University of Illinois at Chicago, Chicago, IL, guyw@uic.edu.
In Response:
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.
References
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