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Effects of propofol and halothane on long-term potentiation in the rat hippocampus after transient cerebral ischaemia

Published online by Cambridge University Press:  01 December 2007

J. Kakehata ,
H. Togashi ,
T. Yamaguchi ,
Y. Morimoto  and
M. Yoshioka
J. Kakehata*
Affiliation:
Tonan Hospital, Department of Anesthesia, Sapporo, Japan Department of Anesthesiology and Critical Care Medicine, Sapporo, Japan
H. Togashi
Affiliation:
Hokkaido University Graduate School of Medicine, Department of Neuropharmacology, Sapporo, Japan Health Sciences University of Hokkaido, School of Pharmaceutical Sciences, Department of Pharmacology, Tobetsu-cho, Japan
T. Yamaguchi
Affiliation:
Hokkaido University Graduate School of Medicine, Department of Neuropharmacology, Sapporo, Japan
Y. Morimoto
Affiliation:
Department of Anesthesiology and Critical Care Medicine, Sapporo, Japan
M. Yoshioka
Affiliation:
Hokkaido University Graduate School of Medicine, Department of Neuropharmacology, Sapporo, Japan
*
Correspondence to: Jin Kakehata, Department of Anesthesia, Tonan Hospital, Kita-1 Nishi- 6, Cyuo-ku, Sapporo 060-0001, Japan. E-mail: [email protected]; Tel: +81 11 231 2121; Fax: +81 11 231 2630
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Summary

Background

Propofol is reported to have protective effects on cerebral ischaemia-induced neuronal death. The aim of this study was to explore whether propofol and halothane can protect hippocampal neuronal function from ischaemic injury during general anaesthesia in rats.

Methods

Rats were divided into 2-vessel occlusion (incomplete cerebral ischaemia) and 4-vessel occlusion (complete cerebral ischaemia) groups consisting of three subgroups each (sham-operated, propofol and halothane groups). One hour after starting propofol 1 mg kg−1 min−1 with 30% O2 and N2 or halothane 0.8% in 30% O2 and N2 rats with or without bilateral vertebral artery occlusion had bilateral common carotid arteries occluded by vessel clips for 10 min. Anaesthesia was maintained for another 1 h. Seven days after ischaemia–reperfusion, hippocampal long-term potentiation in the perforant path–dentate gyrus synapse was determined as an index of cerebral outcome.

Results

In the propofol groups, the formation of long-term potentiation was significantly impaired in the 2-vessel and 4-vessel occlusion groups compared to the respective sham-operated groups (P < 0.01 and P < 0.05, respectively). Impaired formation of long-term potentiation in propofol groups was comparable to that in halothane groups. The formation of long-team potentiation in the propofol and halothane 2-vessel group was not significantly different from that in the awake 2-vessel group.

Conclusions

Propofol and halothane administered during ischaemia do not possess protective effects against hippocampal neuronal dysfunction induced by cerebral ischaemia–reperfusion as evaluated by our transient ischaemic rat models.

Keywords

ANESTHESIA INTRAVENOUSPROPOFOLHIPPOCAMPUSLONG-TERM POTENTIATIONINTRAOPERATIVE PERIOD
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 24 , Issue 12 , December 2007 , pp. 1021 - 1027
Copyright
Copyright © European Society of Anaesthesiology 2007

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