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BJA Advance Access originally published online on June 13, 2007
British Journal of Anaesthesia 2007 99(2):245-251; doi:10.1093/bja/aem123
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Effects of sevoflurane on the cAMP-induced short-circuit current in mouse tracheal epithelium and recombinant Cl– (CFTR) and K+ (KCNQ1) channels{dagger}

J. K. Kim1,{ddagger}, H. Y. Yoo2,{ddagger}, S. J. Kim2, Y.-S. Hwang3, J. Han4, J. A. Kim1, C. S. Kim1 and H. S. Cho1,*

1 Department of Anesthesiology and Pain Medicine, Samsung Medical Center, Sung Kyun Kwan University School of Medicine, Seoul 135-710, Republic of Korea
2 Department of Physiology and Biophysics, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea
3 Institute of Industrial Medicine and Department of Environmental Occupational Medicine, Busan Paik Hospital
4 Department of Physiology and Biophysics, College of Medicine, Inje University, Busan 633-165, Republic of Korea

* Corresponding author: Department of Anesthesiology and Pain Medicine, Samsung Medical Center, Sung Kyun Kwan University School of Medicine, 50 Ilwon-dong, Kangnam-Ku, Seoul 135-710, Republic of Korea. E-mail: chohs.cho{at}samsung.com

Background: An optimal level of airway surface liquid is essential for mucociliary clearance in lungs. The cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR) and KCNQ1 channels in tracheal epithelium play key roles in luminal and basolateral membranes, respectively. The aim of this study was to examine the effects of sevoflurane on cAMP-induced chloride secretion by the mouse tracheal epithelium and the modulation of recombinant CFTR and KCNQ1 channels.

Methods: The equivalent short-circuit current (Isc) of the mouse tracheal epithelium was measured using a flow-type Ussing chamber technique. Inhibition of Na+ absorption was achieved through the luminal application of amiloride. cAMP-dependent Cl– secretion was evoked by forskolin and isobutylmethylxanthine (Fsk/IBMX) applied to the basolateral side. The effect of sevoflurane on CFTR and KCNQ1 channels was assessed using a whole-cell patch clamp in human embryonic kidney 293T cells expressing CFTR and KCNQ1 channels.

Results: Fsk/IBMX induced a sustained Isc that was suppressed by the application of sevoflurane [decreased by 49 (4.5)% at 190 µM]. The Fsk/IBMX-induced Isc was also blocked by basolateral application of chromanol 293B, a blocker of the KCNQ1 K+ channel. In KCNQ1-expressing cells, sevoflurane 190 µM reduced the outward currents to 59 (4.9)% at 80 mV. The CFTR current was not affected by sevoflurane (~360 µM).

Conclusions: These results suggest that the inhibition of KCNQ1 underlies sevoflurane-induced decrease in airway secretion.

Keywords: anaesthetic volatile, sevoflurane; ions, ion channels; lung, trachea

{dagger} This work has been presented to the Sixth Congress of FAOPS (Federation of Asian Oceanian Physiological Societies), October 16, 2006, Seoul, Republic of Korea.

{ddagger} J. K. Kim and H. Y. Yoo have contributed equally to this study.


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