Isoflurane preconditioning improved short-term neurological outcome after focal
brain ischemia in adult rats. It is not known whether
desflurane induces a delayed phase of preconditioning in the brain and whether
isoflurane preconditioning-induced neuroprotection is long-lasting. Two months-old Sprague-Dawley male rats were exposed to or were not exposed to
isoflurane or
desflurane for 30 min and then subjected to a 90 min middle cerebral
arterial occlusion (MCAO) at 24 h after the
anesthetic exposure. Neurological outcome was evaluated at 24 h or 4 weeks after the MCAO. The density of the
terminal deoxynucleotidyl transferase biotinylated
UTP nick end labeling (TUNEL) positive cells in the penumbral cerebral cortex were assessed 4 weeks after the MCAO. Also, rats were pretreated with
isoflurane or
desflurane for 30 min. Their cerebral cortices were harvested for quantifying B-cell lymphoma-2 (Bcl-2) expression 24 h later. Here, we showed that pretreatment with 1.1% or 2.2%
isoflurane, but not with 6% or 12%
desflurane, increased Bcl-2 expression in the cerebral cortex, improved neurological functions and reduced
infarct volumes evaluated at 24 h after the MCAO.
Isoflurane preconditioning also improved neurological functions and reduced
brain infarct volumes in rats evaluated 4 weeks after the MCAO.
Isoflurane preconditioning also decreased the density of TUNEL-positive cells in the penumbral cerebral cortex. We conclude that
isoflurane preconditioning improves short-term and long-term neurological outcome and reduces delayed cell death after transient focal
brain ischemia in adult rats. Bcl-2 may be involved in the
isoflurane preconditioning effect.
Desflurane pretreatment did not induce a delayed phase of neuroprotection.