• Anesthesiology · Sep 2009

    In vitro effects of propofol and volatile agents on pharmacologically induced chloride channel myotonia.

    • Oliver Bandschapp, Hans F Ginz, Charles L Soule, Thierry Girard, Albert Urwyler, and Paul A Iaizzo.
    • Department of Anesthesia, University of Basel Hospital, Spitalstrasse 21, 4031 Basel, Switzerland. bandschappo@uhbs
    • Anesthesiology. 2009 Sep 1; 111 (3): 584-90.

    BackgroundAnesthetic choice for patients with chloride channel myotonia remains under debate. The authors have, therefore, investigated the in vitro effects of various anesthetic agents on pharmacologically induced chloride channel myotonia.MethodsFunctionally viable (> 10 mN force generation) rectus abdominis muscle preparations obtained from normal swine were investigated using in vitro muscle contracture test baths. During continuous 0.1-Hz supramaximal electrical stimulation, the chloride channel blocker 9-anthracenecarboxylic acid (64 microM) was added before the addition of propofol or one of three volatile anesthetics. The concentration of propofol in either Intralipid (n = 11) or dimethyl sulfoxide (n = 10) was doubled every 10 min (from 4-512 microM). The concentration of halothane (n = 8), isoflurane (n = 8), and sevoflurane (n = 8) was doubled from 0.25 vol% up to the maximum dose according to calibrated vaporizers. Control muscle bundles were either untreated (n = 30) or exposed to 9-anthracenecarboxylic acid (n = 19).ResultsThe myotonic reactions induced by 9-anthracenecarboxylic acid were reversed by high-dose (> 64 microM) propofol (P < 0.01). Halothane, isoflurane, or sevoflurane each enhanced the myotonic reactions at 5.4 (P < 0.001), 0.21 (P < 0.01), and 0.5 minimum alveolar concentrations (P < 0.05), respectively.ConclusionsThe authors' in vitro data imply that propofol administration for general anesthesia may be better suited for patients with chloride channel myotonia versus volatile anesthetics. In isolated swine skeletal muscle bundles, propofol elicited a reversal of 9-anthracenecarboxylic acid-induced chloride channel myotonia, whereas volatile anesthetics further increased the associated myotonic reactions.

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