Introduction
The volatile anesthetic agent isoflurane was though to provide neuroprotection against ischemic damage, howerer, this effect remains controversial.
Material and Methods
In this study, we compared the efflux of several excitatory amino acids such as glutamate and taurine, brain tissue injury and brain swelling in male rats subjected to 90 minutes ischemia followed by 24 hours of reperfusion. These rats were anesthetized either with pentobarbital (50 mg/kg, ip), or with isoflurane (1.5% in a mixture of 70% N2 - 30% O2 via a nose mask). Using the middle cerebral artery transient occlusion (MCAO) model, combined with intracerebral microdialysis, we monitored the variations of glutamate and taurine concentrations in the extracellular space before occluding the MCA, during the occlusion period and during the first 3 hours of reperfusion. At the end of the reperfusion period, the ischemic damage and brain water content were evaluated by immunohistological staining of the brains using anti-MAP-2 antibodies.
Results
Isoflurane completely prevented the dramatic efflux of glutamate observed during occlusion in rats anesthetized with pentobarbital, and slightly reduced the ischemia-induced release of taurine. However, no difference in the size of the brain lesion was observed between both anesthetics, but isoflurane induced the formation of a bigger brain edema.
Conclusions
These results suggest that, although isoflurane inhibits the release of the majorexcitotoxic neurotransmitter glutamate during ischemia, this agent does not efficiently protect the brain against ischemic damage. Moreover, it may exaggerate ischemia-induced brain swelling, by decreasing taurine release during ischemia. Blocking the excitotoxic pathway during ischemia may be necessary but does not seem to be sufficient to efficiently improve brain outcome after ischemia-reperfusion. (See Figure 1).
