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NEUROSURGICAL ANESTHESIA

The Effect of Sevoflurane and Propofol on Cerebral Neurotransmitter Concentrations During Cerebral Ischemia in Rats

Kristin Engelhard, MD^*, Christian Werner, MD^*, William E. Hoffman, PhD, Bianca Matthes, BS, Manfred Blobner, MD^*, and Eberhard Kochs, MD^*

*Klinik für Anaesthesiologie and Institut für klinische Chemie und Pathobiochemie, Technische Universität München, Klinikum rechts der Isar, Munich, Germany; and Department of Anesthesiology, University of Illinois at Chicago

Address correspondence and reprint requests to Kristin Engelhard, MD, Klinik für Anaesthesiologie, Technische Universität München, Klinikum rechts der Isar, Ismaninger Straße 22, 81675 MÜNCHEN, Germany. Address e-mail to k.engelhard{at}lrz.tu-muenchen.de

Sevoflurane and propofol are neuroprotective possibly by attenuating central or peripheral catecholamines. We evaluated the effect of these anesthetics on circulating catecholamines and brain neurotransmitters during ischemia in rats. Forty male Sprague-Dawley rats were randomly assigned to one of the following treatment groups: fentanyl and N₂O/O₂ (control), 2.0% sevoflurane, 0.8–1.2 mg · kg^-1 · min^-1 of propofol, and sham-operated rats with fentanyl and N₂O/O₂. Ischemia (30 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension to a mean arterial blood pressure of 32 ± 2 mm Hg. Pericranial temperature, arterial blood gases, and pH value were maintained constant. Cerebral catecholamine and glutamate concentrations, sampled by microdialysis, and plasma catecholamine concentrations were analyzed using high-pressure liquid chromatography. During ischemia, circulating catecholamines were almost completely suppressed by propofol but only modestly decreased with sevoflurane. Sevoflurane and propofol suppressed brain norepinephrine concentration increases by 75% and 58%, respectively, compared with controls. Intra-ischemia cerebral glutamate concentration was decreased by 60% with both sevoflurane and propofol. These results question a role of circulating catecholamines as a common mechanism for cerebral protection during sevoflurane and propofol. A role of brain tissue catecholamines in mediating ischemic injury is consistent with our results.

IMPLICATIONS: During incomplete cerebral ischemia, the neuroprotective anesthetics sevoflurane and propofol suppressed cerebral increases in norepinephrine and glutamate concentrations. In contrast, propofol, but not sevoflurane, suppressed the ischemia-induced increase in circulating catecholamines to baseline levels. The results question a role for plasma catecholamines in cerebral ischemic injury.

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