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Effects of graded suppression of the EEG with propofol on the neurological outcome following incomplete cerebral ischaemia in rats

Published online by Cambridge University Press:  16 August 2006

T. Yamasaki
Affiliation:
Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, Japan
K. Nakakimura
Affiliation:
Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, Japan
M. Matsumoto
Affiliation:
Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, Japan
L. Xiong
Affiliation:
Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, Japan
T. Ishikawa
Affiliation:
Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, Japan
T. Sakabe
Affiliation:
Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1144 Kogushi, Ube, Yamaguchi, Japan
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Abstract

We evaluated the relation between dose and response for the neuroprotective effect of propofol in a rat model with incomplete cerebral ischaemia. For clarification of the mechanism of neuroprotection, plasma catecholamines and tumour necrosis factor-α levels were measured. Three doses (low, moderate and high-dose) of propofol were tested. These produced, respectively, a low amplitude, slowing and a burst-suppression pattern of electroencephalographic activity. Incomplete cerebral ischaemia was produced by right carotid artery occlusion combined with haemorrhagic hypotension (35 mmHg) for 30 min. Neurological outcome at 72 h post-ischaemia in the high-dose group was significantly better than that in both low-dose and moderate-dose groups. Propofol exhibited a trend in the dose-related attenuation of the increases in plasma adrenaline and noradrenaline during ischaemia. Tumour necrosis factor-α increased during and after ischaemia in all groups with no intergroup differences. The results indicate that a burst-suppression dose of propofol provides neuroprotection. The protective effect can not be completely explained by the attenuating effect on circulating catecholamines.

Type
Original Article
Copyright
1999 European Society of Anaesthesiology

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