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Anesth Analg 2008; 106:347-
© 2008 International Anesthesia Research Society
doi: 10.1213/01.ane.0000297279.12358.29
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LETTER TO THE EDITOR

Section Editor:
Lawrence Saidman

Remifentanil-Induced Cerebral Blood Flow Effects in Normal Humans: Dose and ApoE Genotype

Kyle T. S. Pattinson, BM, FRCA, Richard Rogers, MB, BS, FRCA, Stephen D. Mayhew, MPhys, Bradley J. MacIntosh, MSc, PhD, Michael C. Lee, MB, BS, FRCA, and Richard G. Wise, PhD

Nuffield Department of Anaesthetics; University of Oxford; Oxford, UK; kyle.pattinson{at}nda.ox.ac.uk (Pattinson, Rogers) Oxford Centre for Functional MRI of the Brain; University of Oxford, UK (Mayhew, MacIntosh) Division of Anaesthesia; University of Cambridge, UK (Lee) CUBRIC, School of Psychology; Cardiff University, UK (Wise)

To the Editor:

A recent study by Kofke et al.1 assessing the effect of remifentanil on magnetic resonance imaging-measured cerebral blood flow (CBF) highlights the importance of determining whether CBF changes observed are due to opioid agonism or hypercapnic cerebral vasodilatation. In this study, normalization was used to account for the additional effect that hypercapnia has on CBF in an attempt to isolate the effects of opioid agonism. This assumption is reasonable providing the normalization factor takes into account regional heterogeneity of the CBF response to hypercapnia. Unfortunately, only a global estimate of CBF was possible in this study. Even if accurate normalization allowed an estimate of the effects of opioid agonism on CBF, further investigation would be required to determine if such agonism occurs within neural or vascular structures.2 Only then can we be certain that remifentanil truly produces "limbic system activation." We suggest that an alternative approach to dissociate the hypercapnia from the opioid agonist effects would be to perform studies over an equivalent CO2 range,3,4 or based on region of interest derived CO2 reactivity maps5,6 obtained in the same subjects.

REFERENCES

  1. Kofke WA, Blissitt PA, Rao H, Wang J, Addya K, Detre J. Remifentanil-induced cerebral blood flow effects in normal humans: dose and ApoE genotype. Anesth Analg 2007;105:167–75[Abstract/Free Full Text]
  2. Wise R, Tracey I. The role of FMRI in drug discovery. J Magn Reson Imag 2006;23: 862–76[Web of Science][Medline]
  3. McKay LC, Evans KC, Frackowiak RS, Corfield DR. Neural correlates of voluntary breathing in humans. J Appl Physiol 2003;95:1170–8[Abstract/Free Full Text]
  4. Pattinson KT, Rogers R, Mayhew SD, Tracey I, Wise RG. Pharmacological FMRI: measuring opioid effects on the BOLD response to hypercapnia. J Cereb Blood Flow Metab 2007;27:414–23[Web of Science][Medline]
  5. Wise RG, Ide K, Poulin MJ, Tracey I. Resting fluctuations in arterial carbon dioxide induce significant low frequency variations in BOLD signal. Neuroimage 2004;21:1652–64[Web of Science][Medline]
  6. Rostrup E, Law I, Blinkenberg M, Larsson HB, Born AP, Holm S, Paulson OB. Regional differences in the CBF and BOLD responses to hypercapnia: a combined PET and fMRI study. Neuroimage 2000;11:87–97[Web of Science][Medline]



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W. A. Kofke, J. A. Detre, J. Wang, and P. A. Blissitt
Remifentanil-Induced Cerebral Blood Flow Effects
Anesth. Analg., January 1, 2008; 106(1): 347 - 348.
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2008 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press