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Halothane anesthesia (2%) given continuously during the ischemic and post-ischemic period in gerbils does not protect against cytotoxic edema but counteracts superimposed vasogenic edema due to the first BBB opening to serum protein during the reflow period, thus allowing specific gravity values at 1-hour reflow to return to initial levels. It seems likely that this effect of halothane is due to a reduction of the hyperemia by halothane, which reduces both blood pressure and brain metabolism. CBF measurements in halothane-treated animals also indicated that intense early postischemic hypoperfusion may well exist in the absence of brain edema.
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