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.
Lewis S. Coleman, MD
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. Tobias MD, Pilla MA, Rogers C, Jobes DR. Lidocaine inhibits blood coagulation: implications for epidural blood patch. Anesth Analg 1996;82:766–9.
3. Luostarinen V, Evers H, Lyytikainen MT, et al. Antithrombotic effects of lidocaine and related compounds on laser-induced microvascular injury. Acta Anaesthesiol Scand 1981;25:9–11.
4. Groeben H, Schwalen A, Irsfeld S, et al. Intravenous lidocaine and bupivacaine dose-dependently attenuate bronchial hyperreactivity in awake volunteers. Anesthesiology 1996;84:533–9.
5. Zhang ZG, Chopp M, Goussev A, et al. Cerebral microvascular obstruction by fibrin is associated with upregulation of PAI-1 acutely after onset of focal embolic ischemia in rats. J Neurosci 1999;19:10898–907.