BACKGROUND: Volatile anesthetics have been shown protective against focal or global cerebral ischemia in animal models. However isoflurane failed to provide persistent protection because of late onset of apoptosis after ischemia. The aim of this study was to elucidate the effects of desflurane on delayed neuronal damage after forebrain ischemia. METHODS: Rats were divided into 2 groups and anesthetized with desflurane or isoflurane. Forebrain ischemia was produced by both induced hypotension and 10 minutes of common carotid artery clamping. After 2 days and 2 weeks, rats were killed under anesthesia and brains were removed for Western blot analysis of Bcl-2, Bax, and caspase 3 expression and histopathologic study. RESULTS: The apoptotic cell numbers in hippocampal CA1 area were increased after 2 weeks, and there was no significant difference between groups. There was no significant difference in caspase 3 expression between groups. The Bax/Bcl-2 ratio was increased at 2 weeks after ischemia, and there was no significant difference between group. CONCLUSIONS: The data indicate that desflurane also delays but does not prevent the neuronal injury caused by ischemia. Desflurane reduced the development of apoptosis early after ischemia but did not prevent it at later stages of post-ischemic recovery.
Anesthesia ; Anesthetics ; Animals ; Apoptosis ; Blotting, Western ; Brain ; Brain Injuries ; Brain Ischemia ; Carotid Artery, Common ; Caspase 3 ; Cell Count ; Constriction ; Hypotension ; Ischemia ; Isoflurane ; Models, Animal ; Neurons ; Prosencephalon ; Rats