JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Wong, S. M.E. Articles by Kendig, J. J. Search for Related Content PubMed PubMed Citation Articles by Wong, S. M.E. Articles by Kendig, J. J.

---

ANESTHETIC PHARMACOLOGY

Hyperresponsiveness on Washout of Volatile Anesthetics from Isolated Spinal Cord Compared to Withdrawal from Ethanol

Shirley M.E. Wong, MSc, Sarah M. Sweitzer, PhD, Michael C. Peters, BS, and Joan J. Kendig, PhD

Department of Anesthesia, Stanford University School of Medicine, Stanford, California.

We performed experiments in spinal cords isolated from neonatal rats to probe the mechanisms responsible for hyperresponsiveness of the population excitatory evoked potential (pEPSP) observed on washout of the volatile anesthetics halothane and isoflurane (1 minimal alveolar anesthetic concentration equivalent, MAC) compared with that observed after an anesthetic concentration of ethanol. After 30 min exposure to each anesthetic and washout, pEPSP area increased to levels significantly more than control (P < 0.01–0.001). Exposure to a very small (0.025 MAC) concentration of isoflurane over the same period itself produced a similarly exaggerated pEPSP (P < 0.05) in the continued presence of the drug, suggesting that the phenomenon is a direct excitatory effect of the small concentrations of anesthetic on washout, unlike the true withdrawal observed with ethanol. Isoflurane, but not halothane, significantly increased the amount of potassium-stimulated release of the excitatory neurotransmitters glutamate, aspartate, and substance P, suggesting the hyperresponsiveness for that drug is the result of a presynaptically mediated increase in transmitter release. A broad spectrum specific protein kinase C inhibitor, GF109203X, blocked ethanol withdrawal hyperresponsiveness but not hyperresponsiveness after halothane. If the behavioral symptoms of emergence from anesthesia are based on excitatory actions similar to those observed in the spinal cord, the results show that they represent direct excitatory actions rather than withdrawal and are attributable to direct actions on ion channels or receptors, rather than indirect effects mediated by protein kinase C.

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