British Journal of Anaesthesia, 2002, Vol. 88, No. 3 412-417
© 2002 The Board of Management and Trustees of the British Journal of Anaesthesia
Laboratory Investigations |
Effects of propofol on lactate accumulation and oedema formation in focal cerebral ischaemia in hyperglycaemic rats
1Department of Anesthesia, Kyoto University Hospital, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8507, Japan. 2Molecular Neuroscience Research Center, Shiga University of Medical Science, Shiga 520-2192, Japan*Corresponding author
Background. In cerebral ischaemia, hyperglycaemia brings about severe lactate accumulation and neuronal damage when compared with normoglycaemia. Propofol has been known to suppress glucose metabolism in the brain and possess neuroprotective properties in cerebral ischaemia. Therefore, in this study we examined if propofol could attenuate lactate accumulation and neuronal damage in cerebral ischaemia under hyperglycaemic conditions.
Methods. Ten male wistar rats were divided into two experimental groups: low-dose (
12 mg kg1 h1) and high-dose (
60 mg kg1 h1) propofol groups (n=5 for each). Following injection of 2 g kg1 glucose intraperitoneally, the middle cerebral artery was occluded for 1 h, and then reperfused for the following 2 h. Lactate accumulation and oedema formation were estimated consecutively using nuclear magnetic resonance (NMR) techniques.
Results. Lactate accumulation and oedema formation increased continuously during ischaemia and reperfusion in the low-dose propofol group, which was attenuated in the high-dose propofol group. Lactate/NAA (N-acetylaspartate) ratio (as an index of lactate accumulation) 60 and 120 min after reperfusion were 2.67 and 3.26 in low-dose group and 0.30 and 0.10 in high-dose group. For NMR images the number of pixels with a low average diffusion coefficient (an index of the oedema formation), 60 and 120 min after reperfusion were 250.0 and 317.8 in low-dose group, and 16.0 and 12.4 in high-dose group.
Conclusion. High-dose propofol attenuated lactate accumulation and oedema formation in cerebral ischaemia in hyperglycaemic rats.
Br J Anaesth 2002; 88: 41217
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