Background: At present, the proof of the cerebral protective effects of desflurane on morphology is insufficient and the mechanism is unclear. Objective: To investigate the cerebral protective effects of desflurane on complete cerebral ischemia-reperfusion injury and its impacts on gene expression related with apoptosis and stress response. Design: A randomized controlled trial based on the experimental animals. Setting: Departments of anesthesiology and neurosurgery in a university hospital. Materials: The study was conducted in Beijing Neurosurgery Institute Affiliated with Capital University of Medical Sciences between February 2003 and February 2004. Seventeen adult male Wister rats were randomly divided into ischemia group(n = 7), desflurane group (n = 7) and sham-operation group(n = 3). Interventions: Rat complete cerebral ischemia-reperfusion model was established. Desflurane was immediately inhaled for 1 hour after the beginning of reperfusion in rats of desflurane group. Brains of were harvested from 3 rats of either ischemia group or desflurane group after 1 hour of reperfusion (after 1 hour of operation in sham-operation group) and the cortical ultrastructural changes were observed under electron microscope. The rest 4 rats of either ischemia group or desflurane group were used for the analysis of the variable expression of genes related with apoptosis and stress response by gene chip combined image analysis technique. Main outcome measures: 1 cortical ultrastructural changes; 2 variable expression of genes related with apoptosis and stress response analyzed by gene chip. Results: Compared with ischemia group, desflurane group had less neuronal pyknosis with almost normal cell organs and ultrastructure in neurons. Compared with ischemia group, the apoptotic protease activating factor 1(APAF1) of desflurane group down-regulated. Conclusion: Desflurane might have protective effects on neurons and cell skeleton and its mechanism might be related with APAF1 down-regulation.