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Propofol neuroprotection in a rat model of ischaemia reperfusion injury

Published online by Cambridge University Press:  16 August 2006

Y. Young ,
D. K. Menon ,
N. Tisavipat ,
B. F. Matta  and
J. G. Jones
Y. Young
Affiliation:
Department of Anaesthesia, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
D. K. Menon
Affiliation:
Department of Anaesthesia, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK MRC Centre for Brain Repair, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
N. Tisavipat
Affiliation:
Department of Neurosurgery, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
B. F. Matta
Affiliation:
Department of Anaesthesia, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
J. G. Jones
Affiliation:
Department of Anaesthesia, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, Hills Road, Cambridge CB2 2QQ, UK
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Abstract

This study was designed to test the hypothesis that propofol, which possesses antioxidant properties, would produce greater protection than isoflurane incerebral ischaemia reperfusion injury, at dose levels that produced similar effects on brain electrical activity. Twenty Sprague-Dawley rats were anaesthetized using isoflurane 1.5% in air/oxygen, and mechanically ventilated to a PaCO2 of 4.5 kPa. Following 90 min of middle cerebral artery occlusion using an intraluminal filament, rats were given, in random order, either propofol 1mg kg−1 min−1 or isoflurane 3% (both of which have been shown to reliably produce EEG burst suppression). After a further 30 min, reperfusion was induced by withdrawing the filament. Animals were killed following 240 min of reperfusion. Rats in the propofol group showed a 21% reduction in mean hemispheric infarct volume when compared with the isoflurane group (P < 0.0001). These data suggest that propofol may act by mechanisms in addition to CMRO2 depression, and provide a basis for further studies of propofol neuroprotection.

Keywords

anaestheticsbrain ischaemia reperfusion injuryfree radicalspropofol
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 14 , Issue 3 , May 1997 , pp. 320 - 326
Copyright
1997 European Society of Anaesthesiology

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