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Depression of Myocardial Contractility In Vitro by Bupivacaine, Etidocaine, and Lidocaine

Received from the Department of Anesthesiology, University of Virginia Medical Center, Charlottesville, Virginia.

Abstract

The effects of local anesthetics in depressing myocardial contractility were studied in isolated guinea pig right ventric ular papillary muscles. Bupivacaine and etidocaine, 4 and 10 µM, showed reverse frequency-dependent depression of contractility, that is, less significant depression of contractility at higher stimulation frequencies (2–3 Hz) than at lesser frequencies (<1 Hz). Lidocaine, 40 µM, demon strated a similar trend. In contrast, the normal action potential maximum rate of depolarization (_max), a measure of sodium channel conductance, was significantly more de pressed at 2–3 Hz by bupivacaine and etidocaine than by lidocaine. Consequently, contractile depression could be overcome only at higher stimulation frequencies, at which conduction was depressed. To explore the mechanism of the contractile depression, local anesthetic effects were studied on slow (calcium channel-mediated) action potentials in partially depolarized papillary muscles. Etidocaine and bupivacaine, 4 and 10 µM, and lidocaine, 40 and 100 µM, caused a marked depression of the late-peaking contractile responses, attributed to Ca²⁺ release from the sarcoplasmic reticulum. In contrast, only 10 µM bupivacaine caused any significant depression of the slow action potential rate of depolarization (to 89% of control), consistent with a possible small depression of Ca^{2 +} entry.

Key Words: ANESTHETICS, LOCAL—bupivacaine, etidocaine, lidocaine • HEART—action potential, contractility

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999