Objective To investigate the protective effects of dexmedetomidine on bupivacaine-induced neurotoxicity. Methods Mouse neuroblastoma cell line N2a cells were divided into four groups. The cells in the control group were incu?bated with no drug adding while the cells in bupivacaine group were treated with 1 000 μmol/L bupivacaine for 24 h. The cells in the group Dex1 and Dex2 were incubated with 1 000 μmol/L bupivacaine and 50 μmol/L, 200 μmol/L dexmedetomi?dine for 24 h respectively. MTT assay was used to evaluate the cell viability. The reactive oxygen species (ROS) activity, mito?chondrial membrane potential (MMP), the expression of Caspase-3 and apoptotic rate of N2a cells were detected by flow cy?tometry. Results The cell viabilities were significantly decreased after being treated with 1 000 μmol/L bupivacaine, MMP was also significantly decreased, and apoptotic rates, levels of ROS and Caspase-3 were significantly increased. The bupiva?caine-induced cytotoxicity was inhibited by dexmedetomidine (50 and 200 μmol/L), which resulted in the increase in the cell viability and MMP, but decrease in apoptotic rate and levels of ROS and Caspase-3. These effects were more significant in 200 μmol/L dexmedetomidine group than those of 50 μmol/L dexmedetomidine group. Conclusion Dexmedetomidine at?tenuates bupivacaine-induced cytotoxicity of N2a cells, which may be related with the inhibition of ROS, the decrease in MMP and Caspase-3, and inhibiting appotosis in N2a cells.

Objective To evaluate the neurotoxic effects of intrathecal (IT) chloroprocaine on the spinal cord in rats. Methods Forty male SD rats weighted 180 ～250g, which IT catheters were successfully placed, were randomly divided into 4 groups( n = 10 each). Group NS received normal saline 40 μl IT, group CP_1 received 2% chloroprocaine 40 μl IT, group CP_2 received 3% chloroprocaine 26.7 μl IT, and group CP_3 received 3% chloroprocaine 40 μl IT. The onset time of bilateral hindlimb paralysis were recorded. Degree of motor block was assessed and scored before (T_1, baseline) and at 10, 30, 60, 120, and 150 min (T_(1-6)) after IT injection. On the 3rd day after IT injection , specimens were obtained from lumbar spinal cord for mincroscopic examination. Results The onset time of bilateral hindlimb paralysis in group CP, and CP_3 was shorter than that in group CP_1. The onset time of bilateral hindlimb paralysis in group CP, was shorter than that in group CP_2. The motor block scores in group CP_1 and CP_2(T_(2-4))and group CP_3(T_(2_5)) were higher than that in group NS. The motor block scores in both group CP_1 and CP_2 at T_(4-5) was lower than group CP_3. The tissue damage in group CP_3 was severer, compared with group CP_1 and CP_2. Conclusion Large dose of 3% chloroprocaine may produce neurotoxicity to the spinal cord.

We report in detail ultrastructural changes and freezing damage mechanism about heart muscle and some organelles after rapid freezing. The ventricles of rat heart were cut pieces about 100-150/?m by microsiicer. The pieces were quickly injected liquid cryogen Freon 22 by Reichert-Jung spring-assistant mechanism (KF-80). The specimens frozen were rapidly transferred into substitution medium aceton and kept at -80℃(28h), then -60℃ (48h),-20℃(12h)and 4℃ (1 h). The structures of specimens frozen were well and there were no ice crystals in the area of the tissue frozen surface to 20?m depth. However, there were freezing damages in mitochondrial crista, intercellular substance and muscular fibre in the tissue surface to 30?m depth. The structure of tissue was destroyed by ice crystal over 50?m depth in the tissue. The results suggest that intercellular substance and mitochondrial crista are the most sensitive to ice crystal damage after rapid freezing of heart tissue, then the less sensitive are muscular fibre and nucleus. The unit membrane is not easy to be damaged by ice crystal.