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BJA Advance Access originally published online on July 18, 2006
British Journal of Anaesthesia 2006 97(3):307-314; doi:10.1093/bja/ael174
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

The mechanism of sevoflurane-induced cardioprotection is independent of the applied ischaemic stimulus in rat trabeculae

R. A. Bouwman1,*, F. N. G. van't Hof2, W. de Ruijter1, B. J. van Beek-Harmsen2, R. J. P. Musters2, J. J. de Lange1 and C. Boer3,{dagger}

1 Department of Anesthesiology, VU University Medical Center (VUmc)-Institute for Cardiovascular Research Vrije Universiteit (ICaR-VU) De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands
2 Laboratory for Physiology, VU University Medical Center (VUmc)-Institute for Cardiovascular Research Vrije Universiteit (ICaR-VU) van der Boechorststraat 7, 1081 BT Amsterdam, The Netherlands
3 Abbott B.V. Siriusdreef 51, NL-2131 WT Hoofddorp The Netherlands

*Corresponding author: Department of Anesthesiology, De Boelelaan 1117, 1081 HV Amsterdam, The Netherlands. E-mail: a.bouwman{at}vumc.nl

Background. Sevoflurane protects the myocardium against ischaemic injury through protein kinase C (PKC) activation, mitochondrial Formula -channel (Formula) opening and production of reactive oxygen species (ROS). However, it is unclear whether the type of ischaemia determines the involvement of these signalling molecules. We therefore investigated whether hypoxia (HYP) or metabolic inhibition (MI), which differentially inhibit the mitochondrial electron transport chain (ETC), are comparable concerning the relative contribution of PKC, Formula and ROS in sevoflurane-induced cardioprotection.

Methods. Rat right ventricular trabeculae were isolated and isometric contractile force (Fdev) was measured. Trabeculae were subjected to HYP (hypoxic glucose-free buffer; 40 min) or MI (glucose-free buffer, 2 mM cyanide; 30 min), followed by 60 min recovery (60 min). Contractile recovery (Fdev,rec) was determined at the end of the recovery period and expressed as a percentage of Fdev before hypoxia or MI, respectively. Chelerythrine (CHEL; 6 µM), 5-hydroxydecanoic acid sodium (100 µM) and n-(2-mercaptopropionyl)-glycine (MGP; 300 µM) were used to inhibit PKC, Formula and ROS, respectively.

Results. Fdev,rec after HYP was reduced to 47 (3)% (P<0.001 vs control; n=5) whereas MI reduced Fdev,rec to 28 (5)% (P<0.001 vs control; n=5). A 15 min period of preconditioning with sevoflurane (3.8%) equally increased contractile recovery after HYP [76 (9)%; P<0.05 vs HYP] and MI [67 (8)%; P<0.01 vs MI]. Chelerythrine, 5-hydroxydecanoate and n-(2-mercaptopropionyl)-glycine abolished the protective effect of sevoflurane in both ischaemic models. Trabeculae subjected to HYP or MI did not demonstrate any increased apoptotic or necrotic markers.

Conclusions. PKC, Formula and ROS are involved in sevoflurane-induced cardioprotection after HYP or MI, suggesting that the means of mitochondrial ETC inhibition does not determine the signal transduction pathway for cardioprotection by anaesthetics.

{dagger}Declaration of Interest. Christa Boer is currently working for Abbott B.V., Hoofddorp, The Netherlands; this laboratory study and paper were finalized at the Laboratory for Physiology (VU University Medical Center, Amsterdam, The Netherlands) before she accepted the job offer from Abbott.


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R. A. Bouwman, R. J. P. Musters, B. J. van Beek-Harmsen, J. J. de Lange, R. R. Lamberts, S. A. Loer, and C. Boer
Sevoflurane-induced cardioprotection depends on PKC-{alpha} activation via production of reactive oxygen species
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