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BJA Advance Access originally published online on February 27, 2008
British Journal of Anaesthesia 2008 100(4):465-471; doi:10.1093/bja/aen022
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2008. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Hyperglycaemia blocks sevoflurane-induced postconditioning in the rat heart in vivo: cardioprotection can be restored by blocking the mitochondrial permeability transition pore

R. Huhn, A. Heinen, N. C. Weber*, M. W. Hollmann, W. Schlack and B. Preckel

Laboratory of Experimental Intensive Care and Anaesthesiology, Academic Medical Center, Department of Anaesthesiology, University of Amsterdam, Meibergdreef 9, 1100 DD Amsterdam, The Netherlands

* Corresponding author. E-mail: n.c.hauck{at}amc.uva.nl

Background: Recent studies showed that hyperglycaemia (HG) blocks anaesthetic-induced preconditioning. The influence of HG on anaesthetic-induced postconditioning (post) has not yet been determined. We investigated whether sevoflurane (Sevo)-induced postconditioning is blocked by HG and whether the blockade could be reversed by inhibiting the mitochondrial permeability transition pore (mPTP) with cyclosporine A (CsA).

Methods: Chloralose-anaesthetized rats (n=7–11 per group) were subjected to 25 min coronary artery occlusion followed by 120 min reperfusion. Postconditioning was achieved by administration of 1 or 2 MAC sevoflurane for the first 5 min of early reperfusion. HG was induced by infusion of glucose 50% (G 50) for 35 min, starting 5 min before ischaemia up to 5 min of reperfusion. CsA (5 or 10 mg kg–1) was administered i.v. 5 min before the onset of reperfusion. At the end of the experiments, hearts were excised for infarct size measurements.

Results: Infarct size (% of area at risk) was reduced from 51.4 (5.0)% [mean (SD)] in controls to 32.7 (12.8)% after sevoflurane postconditioning (Sevo-post) (P<0.05). This infarct size reduction was completely abolished by HG [51.1 (13.2)%, P<0.05 vs Sevo-post], but was restored by administration of sevoflurane with CsA [35.2 (5.2)%, P<0.05 vs HG+Sevo-post]. Increased concentrations of sevoflurane or CsA alone could not restore cardioprotection in a state of HG [Sevo-post2, 54.1 (12.6)%, P>0.05 vs HG+Sevo-post; CsA10, 58.8 (11.3)%, P>0.05 vs HG+CsA].

Conclusions: Sevoflurane-induced postconditioning is blocked by HG. Inhibition of the mPTP with CsA is able to reverse this loss of cardioprotection.

Keywords: anaesthetics volatile, sevoflurane; cyclosporine A; heart, infarct; heart, postconditioning; hyperglycaemia


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