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British Journal of Anaesthesia, 2002, Vol. 88, No. 6 828-835
© 2002 The Board of Management and Trustees of the British Journal of Anaesthesia

Laboratory Investigations

Cardioprotection by sevoflurane against reperfusion injury after cardioplegic arrest in the rat is independent of three types of cardioplegia

D. Ebel*,1, B. Preckel1, A. You2, J. Müllenheim1, W. Schlack1 and V. Thämer2

1Klinik für Anaesthesiologie and 2Physiologisches Institut I, Abteilung für Herz- und Kreislaufphysiologie, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany*Corresponding author: Klinik für Anaesthesiologie, Heinrich-Heine-Universität Düsseldorf,Postfach 10 10 07, D-40001 Düsseldorf, Germany

Background. Sevoflurane protects the heart against reperfusion injury even after cardioplegic arrest. This protection may depend on the cardioplegic solution. Therefore, we investigated the effect of sevoflurane on myocardial reperfusion injury after cardioplegic arrest with University of Wisconsin solution (UW), Bretschneider’s cardioplegia (HTK), and St Thomas’ Hospital solution (STH).

Methods. We used an isolated rat heart model where heart rate, ventricular volume, and perfusion pressure were constant. The hearts underwent 30 min of normothermic ischaemia followed by 60 min of reperfusion. Seven groups were studied (n=9 each). Three groups received 7°C cold cardioplegic solutions (UW, HTK, STH) during the first 2 min of ischaemia at a flow of 2 ml min–1. In three groups (UW+Sevo, HTK+Sevo, STH+Sevo), sevoflurane was additionally added to the perfusion medium (membrane oxygenator) at 3.8% (1.5 MAC) during the first 15 min of reperfusion after cardioplegic arrest. Nine hearts served as untreated control group (control). We measured left ventricular developed pressure (LVDP) and infarct size.

Results. LVDP was similar in all groups during baseline (130 (SEM 2) mm Hg). HTK and STH improved recovery of LVDP during reperfusion from 5 (1) (control) to 67 (7) (HTK) and 52 (8) mm Hg (STH, both P<0.05), while UW had no effect on myocardial function (7 (2) mm Hg). In the sevoflurane-treated groups, LVDP at the end of the experiments was not significantly different from the respective group without anaesthetic treatment (UW+Sevo 11 (2); HTK+Sevo 83 (8); STH+Sevo 64 (8) mm Hg; P=ns). Infarct size was reduced in the HTK and STH groups (HTK 20 (4); STH 17 (3)%; P<0.05) compared with controls (39 (5)%; P<0.05), but not in the UW group (52 (4)%). Compared with cardioplegia alone, sevoflurane treatment during reperfusion reduced infarct size (UW+Sevo 31 (4); HTK+Sevo 8 (1); STH+Sevo 4 (1)%; P<0.05).

Conclusion. We conclude, that the protection against reperfusion injury offered by sevoflurane is independent of the three cardioplegic solutions used.

Br J Anaesth 2002; 88: 828–35


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