Objective   To assess changes in the cognitive function and hippocampal ultrastructure of elderly rats exposed to sevoflurane. Methods Ault male Sprague-Dawley rats were given subcutaneous injection of D-galactose on the neck for 40 d to establish elderly models, after 9-day behavioral training. The model rats were divided into 3 groups randomly: control group with natural air, A/O group with 6 h exposure to carrier gas (2 L/min Air+2 L/min O₂), and Sev group with 6 h exposure to 3.2% sevoflurane through carrier gas.

  Morris   Water Maze and balance beam experiment were conducted on 6 rats in each group 2 h, 1 week and 4 weeks after treatments, respectively. The hippocampal tissues of the rats were rapidly dissected and prepared by glutaraldehyde fixation, ethanol dehydration, infiltration, embedding polymerization, semimembrane section localization and staining for examinations under transmission electron microscopy. The hippocampal ultrastructure such as nucleus, cytoplasm, mitochondria, endoplasmic reticulum, medullary nerve fiber, synapse and apoptotic corpuscle were observed.

  Results   Ethology: compared with the control and A/O groups, significant reductions in the probe trial capability were found in the rats after 2 h exposure to sevoflurane, which recovered at 1 week and 4 weeks. Sevoflurane also increased the working memory escape latency 2 h and 1 week after exposure. The balance beam experiment showed that sevoflurane prolonged the staring time of rats after 2 h exposure, which recovered at 1 week and 4 weeks. Prolonged length for going through the balance beam was found consistently in the rats exposed to sevoflurane. Transmission electron microscopy: rats in the control group were found to have clear hippocampal ultrastructure, intact nuclear membrane, no edema fluid in the cytoplasm, intact mitochondria and endoplasmic reticulum, normal medullary nerve fibers, intact synaptic structure, and no apoptotic bodies in the cells. But a small amount of edema were observed in the cytoplasm of hippocampal cells in the rats exposed to sevoflurane and A/O at 2 h, which increased at 1 week. The cytoplasmic morphology of rats in the A/O group returned to normal at 4 weeks. But further increase of edema was observed in the rats 4 weeks after exposure to sevoflurane. No abnormal morphological structures or apoptotic bodies in other organelles were found.

  Conclusion   Sevoflurane can induce early neurocognitive impairments in elderly rats, which may be related with changes in the hippocampus ultrastructure.