*Presented in part at the Annual Meeting of the Japanese Society of Anesthesiologists, Nagoya, Japan, 26 May 2004, and the China–Japan–Korea Joint symposium for Neuroanesthesia, Jeju, Korea, 28 August 2004.
Effect of mivazerol, a α2-agonist, on striatal norepinephrine concentration during transient forebrain ischemia in rats*
Article first published online: 20 MAY 2008
© 2008 The Authors. Journal compilation © 2008 The Acta Anaesthesiologica Scandinavica Foundation
Acta Anaesthesiologica Scandinavica
Volume 52, Issue 7, pages 997–1002, August 2008
How to Cite
KIMURA, T., SATO, K., NISHIKAWA, T., TOBE, Y. and MASAKI, Y. (2008), Effect of mivazerol, a α2-agonist, on striatal norepinephrine concentration during transient forebrain ischemia in rats. Acta Anaesthesiologica Scandinavica, 52: 997–1002. doi: 10.1111/j.1399-6576.2008.01683.x
- Issue published online: 9 JUL 2008
- Article first published online: 20 MAY 2008
- Accepted for publication 13 March 2008
- forebrain ischemia;
Background: We have previously reported that mivazerol, a α2-agonist, possibly provides neuroprotection against transient forebrain ischemia in rats. This study was designed to investigate the ability of mivazerol to attenuate ischemia-induced increase in striatal norepinephrine concentration after transient forebrain ischemia in rats.
Methods: Male Sprague–Dawley rats, anesthetized with halothane, were assigned to one of three groups (n=10 each); control (C, normal saline 1 ml/kg), mivazerol 20 μg/kg (M20), and 40 μg/kg (M40) groups. Monitored variables included temporal muscle temperature (maintained at 37.5±0.1 °C), electroencephalogram, systolic/diastolic blood pressure, heart rate, arterial blood gases, and blood glucose concentrations. Thirty minutes after subcutaneous drug administration, forebrain ischemia was induced with hemorrhagic hypotension (systolic arterial pressure: 40–50 mmHg) and bilateral carotid artery occlusion for 10 min, and then the brain was reperfused. Norepinephrine concentration in the interstitial fluids in the striatum was analyzed using in vivo microdialysis in combination with high-performance liquid chromatography.
Results: Ischemia resulted in a prompt increase in norepinephrine concentrations in the striatum in all groups. However, there were no significant differences in norepinephrine concentrations in the striatum between the three groups at any period.
Conclusions: Our results indicate that mivazerol did not attenuate ischemia-induced increase in striatal norepinephrine concentration. This suggests that the possible neuroprotective property of mivazerol is not related to inhibition of norepinephrine release in the brain.