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British Journal of Anaesthesia, Vol 81, Issue 2 244-246, Copyright © 1998 by The Board of Management and Trustees of the British Journal of Anaesthesia

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Mechanical and electrophysiological effects of mepivacaine on direct myocardial depression in vitro

W. K. Park and C. K. Suh
Department of Anesthesiology, Yonsei University College of Medicine, CPO Box 8044, Seoul, Korea; Department of Physiology, Inha University College of Medicine, Incheon, Korea

The effects of various concentrations (20, 50, and 100 microgramsmol litre-1) of mepivacaine were studied in isolated guinea pig and rat right ventricular papillary muscles by measuring the effects on myocardial contractility and electrophysiological parameters. Mepivacaine produced dose-dependent depression of peak force during 0.5 to 3 Hz stimulation rates in guinea pig papillary muscles. Conduction block was frequently noted, especially at higher stimulation rates (2 and 3 Hz) with mepivacaine 50 and 100 microgramsmol litre-1. In rat papillary muscle experiments, about 20% depression of peak force was shown at rested state contraction. Shortening of action potential (AP) duration (APD50: about 10%, APD90: about 10%) and rate-dependent depression of dV/dt max was observed with mepivacaine 100 microgramsmol litre-1. In 26 mmol litre-1 K+ Tyrode's solution, mepivacaine 50 and 100 microgramsmol litre-1 produced a dose- dependent depression of early (50 microgramsmol litre-1: about 20%, 100 microgramsmol litre-1: about 30%) and late (50 microgramsmol litre-1: about 30%, 100 microgramsmol litre-1: about 50%) force development. In slow APs, neither shortening of AP duration nor changes of dV/dt max were shown by mepivacaine 100 microgramsmol litre-1. An approximate 30% depression of contracture induced by rapid cooling after 2 Hz stimulation rates was observed with mepivacaine 100 microgramsmol litre-1. It may be concluded that the direct myocardial depressant effect of mepivacaine is likely to be caused by inhibition of Ca2+ release from the sarcoplasmic reticulum. The Na+ channel blocking action may contribute indirectly to the depression of contractility.
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