Sevofluraneinduced preconditioning in the isolated heart is abolished in Ecto5'nucleotidase and A2Badenosine receptor knockout mice: BAPCAP26

Damm, M.; Stehr, S. N.; Huebler, A.; Panousis, P.; Koch, T.; Deussen, A.

European Journal of Anaesthesiology: June 2011 - Volume 28 - Issue - p 6
Abstracts and Programme: EUROANAESTHESIA 2011: The European Anaesthesiology Congress: Best Abstracts - Runner-up Session 2

University Hospital Carl Gustav Carus, Department of Anaesthesiology and Intensive Care, Dresden, Germany

Article Outline

Background and Goal of Study: Ecto‐5'‐nucleotidase (CD73) and A2B‐adenosine receptors (A2B‐AR) are involved in both ischemic preconditioning and anaesthetic‐induced preconditioning [1; 2]. This study focused on sevoflurane (sevo) ‐induced preconditioning in CD73 (CD73‐KO) and A2B‐AR (A2BAR‐KO) knockout mice.

Materials and Methods: Experiments were performed with isolated hearts from 12 (6‐wk‐old) male C57BL/6 (wild type = WT), 12 (6‐wk‐old) male CD73‐KO and 12 (6‐wk‐old) male A2BAR‐KO mice. In all three groups six control hearts were matched to six hearts subjected to 15 min of 2.8 vol. % sevo. Infarction was induced by 60 min of left coronary artery occlusion followed by 30 min reperfusion. Ventricular pressure, +dP/dtmax, heart rate, coronary flow and coronary perfusion pressure were continuously measured. Arterial and venous perfusate samples were collected. The area at risk (AAR) and the infarct size were determined by microspheres and propidium iodide staining. Data analysis was performed using Two‐Way‐ANOVA and post‐hoc analysis by Bonferroni.

Results and Discussion: Infarct size in the WT‐control group was 67.3 ± 2.3 % of AAR. Control hearts from CD73‐KO (55.3 ± 2.3 % of AAR) and A2BAR‐KO (66.2 ± 1.8 % of AAR) showed similar infarct sizes. Application of sevo in WT reduced infarction significantly (33.6 ± 2.1 % vs. 67.3 ± 2.3 % of AAR; with sevo vs. without sevo; n=6 each; p ≤ 0.01). Sevo‐induced preconditioning failed in CD73‐KO (52.3 ± 3.6 % vs. 55.3 ± 2.3 % of AAR; CD73‐KO with sevo vs. CD73‐KO without sevo; n=6 each) and in A2BAR‐KO (70.3 ± 1.7 % vs. 66.2 ± 1.8 % of AAR; A2BAR‐KO with sevo vs. A2BAR‐KO without sevo; n=6 each).

Conclusion(s): These data underlines the major role of CD73 and A2B‐AR in sevo‐induced preconditioning in the isolated mouse heart.

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(1) Eckle T et al. Cardioprotection by ecto-5'-nucleotidase (CD73) and A2B adenosine receptors. Circulation 2007; 115:1581-90.
(2) M. Damm, et al. Sevoflurane-induced preconditioning in the isolated mouse heart: role of the adenosine pathway. Eur J Anaesth. 2009;26: suppl. 45; 4AP 4-8.

Acknowledgements: CD73‐KO and A2BAR‐KO were kindly provided by Prof. Triantafyllos Chavakis and Dr. David Köhler. This study was supported by the ESA research grant.

© 2011 European Society of Anaesthesiology