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ANESTHETIC PHARMACOLOGY

Intrathecal Veratridine Administration Increases Minimum Alveolar Concentration in Rats

Yi Zhang, MD^*, Manohar Sharma, PhD, Edmond I. Eger, II, MD, Michael J. Laster, DVM, Hugh C. Hemmings, Jr, MD, PhD, and R. Adron Harris, PhD

From the *Department of Anesthesiology, Fuwai Hospital and Cardiovascular Institute, Beijing, China; Department of Anesthesia and Perioperative Care, University of California, San Francisco, California; Department of Anesthesiology and Pharmacology, Weill Cornell Medical College of Cornell University, New York, New York; and Waggoner Center for Alcohol and Addiction Research, The University of Texas, Austin, Texas.

Address correspondence and reprint requests to Dr. Eger, Department of Anesthesia, S-455, University of California, San Francisco, CA 94143-0464. Address e-mail to egere{at}anesthesia.ucsf.edu.

BACKGROUND: Results from several studies point to sodium channels as potential mediators of the immobility produced by inhaled anesthetics. We hypothesized that the intrathecal administration of veratridine, a drug that enhances the activity or effect of sodium channels, should increase MAC.

METHODS: We measured the change in isoflurane MAC caused by intrathecal infusion of various concentrations of veratridine into the lumbothoracic subarachnoid space of rats. We compared these result with those obtained from intracerebroventricular infusion.

RESULTS: As predicted, intrathecal infusion of veratridine increased MAC. The greatest infused concentration (25 µM) also produced neuronal injury in the hindlimbs of two rats and decreased the peak effect on MAC. A concentration of 1.6 µM produced the largest (21%) increase in MAC. Intraventricular infusion of 1.6 and 6.4 µM veratridine did not alter MAC. Rats given 25 µM died.

CONCLUSIONS: Intrathecal administration of veratradine increases MAC of isoflurane, a finding consistent with a role for sodium channels as potential mediators of the immobility produced by inhaled anesthetics.

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