Recent work using isolated perfused heart models have shown that propofol may protect hearts against reperfusion injury by inhibiting the mitochondrial permeability transition pore (Javadov et al. 2000). This study investigates the protective effects of propofol using a pig model of cardiopulmonary bypass (CPB) and cardioplegic arrest. This study was conducted under the authority of the Animals (Scientific Procedures) Act 1986, UK. Large White Landrace cross-breed pigs, weighing between 43 and 78 kg were anaesthetised using a standardised intravenous regime of diazepam (1 mg kg^-1), thiopentone sodium (20 mg kg^-1) and fentanyl (50 µg kg^-1 h^-1). Through median sternotomy access, CPB was established, the aorta cross-clamped and the heart arrested for 60 min using intermittent (every 15 min) antegrade hyperkalaemic warm blood cardioplegia. Following clamp release, CPB was discontinued and the anaesthetised animal monitored for 2 h. When used, propofol (I.V. 6 mg kg^-1 h^-1) was administered systemically during CPB. Myocardial biopsies and blood samples were collected before CPB (baseline), end of cardioplegic arrest, and 5, 20, 60 and 120 min following clamp release. At the end of the experiments the animals were humanely killed. Baseline data were similar between control (n = 8) and propofol (n = 6) groups. Pigs in the control group showed greater evidence of ischaemic stress: tissue ATP (nmol (mg protein)^-1) fell from baseline 37.2 ± 8.0 (mean ± S.D.) to end of arrest 21.2 ± 11.1 (t test, P < 0.05) and 35.5 ± 10.5 to 29.0 ± 8.8 in control and propofol groups, respectively. On reperfusion (20 min after clamp release), ATP was lower in control (19.3 ± 8.6) than in propofol hearts (32.9 ± 9.5) (t test, P < 0.05). Serum Troponin-I levels and tissue alanine-glutamate ratio were 4.9 ± 2.1 ng ml^-1 and 1.2 ± 0.5, respectively, in controls, and 1.7 ± 0.7 ng ml^-1 and 0.6 ± 0.2 in propofol group (t test, both P < 0.05). In this pig experimental model, propofol protects the heart against ischaemia-reperfusion injury associated with cardioplegic arrest.We wish to thank the British Heart Foundation, The Royal College of Surgeons of Edinburgh and The Jules Thorn Trust for their support in this study.

Javadov, S.A., Lim, K.H.H., Kerr, P.M., Suleiman, M.-S., Angelini, G.D. & Halestrap, A.P. (2000). Cardiovasc. Res. 45, 360-369.