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ANESTHETIC PHARMACOLOGY

Increases in Spinal Cerebrospinal Fluid Potassium Concentration Do Not Increase Isoflurane Minimum Alveolar Concentration in Rats

Dimitry Shnayderman, BS^*, Michael J. Laster, DVM^*, Edmond I. Eger, II, MD^*, Irene Oh, BS^*, Yi Zhang, MD^*, Steven L. Jinks, PhD, Joseph F. Antognini, MD, and Douglas E. Raines, MD

From the *Department of Anesthesia and Perioperative Care, University of California, San Francisco, California; Department of Anesthesiology and Pain Medicine, University of California, Davis, California; and Department of Anesthesia and Critical Care, The Massachusetts General Hospital, Boston, Massachusetts.

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: Previous studies demonstrated that MAC for isoflurane directly correlates with the concentration of Na⁺ in cerebrospinal fluid surrounding the spinal cord, the primary site for mediation of the immobility produced by inhaled anesthetics. If this correlation resulted from increased irritability of the cord, then infusion of increased concentrations of potassium (K⁺) might be predicted to act similarly. However, an absence of effect of K⁺ might be interpreted to indicate that K⁺ channels do not mediate the immobility produced by inhaled anesthetics whereas Na⁺ channels remain as potential mediators. Accordingly, in the present study, we examined the effect of altering intrathecal concentrations of K⁺ on MAC.

METHODS: In rats prepared with chronic indwelling intrathecal catheters, we infused solutions deficient in K⁺ and with an excess of K⁺ into the lumbar space and measured MAC for isoflurane 24 h before, during, and 24 h after infusion. Rats similarly prepared were tested for the effect of altered osmolarity on MAC (accomplished by infusion of mannitol) and for the penetration of Na⁺ into the cord.

RESULTS: MAC of isoflurane never significantly increased with increasing concentrations of K⁺ infused intrathecally. At infused concentrations exceeding 12 times the normal concentration of KCl, i.e., 29 mEq/L, rats moved spontaneously at isoflurane concentrations just below, and sometimes at MAC, but the average MAC in these rats did not exceed their control MAC. At the largest infused concentration (58.1 mEq/L), MAC significantly decreased and did not subsequently return to normal (i.e., such large concentrations produced injury). Infusions of lower concentrations of K⁺ had no effect on MAC. Infusion of osmotically equivalent solutions of mannitol did not affect MAC. Na⁺ infused intrathecally measurably penetrated the spinal cord.

CONCLUSIONS: The results do not support a mediation or modulation of MAC by K⁺ channels.

This article has been cited by other articles:

				E. I. Eger II, D. E. Raines, S. L. Shafer, H. C. Hemmings Jr, and J. M. Sonner Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility? Anesth. Analg., September 1, 2008; 107(3): 832 - 848. [Abstract] [Full Text] [PDF]

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