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Objective To investigate the effects of different degrees of autophagy on the apop-tosis of GABAergic neurons in spinal dorsal horn of postherpetic neuralgia model mice. Methods Forty-eight Kunming mice,approximately 6-8 weeks of age and weighing 18-22 g,were randomly divided into four groups by a random digital generator of SPSS 19.0:resinotoxin+autoph-agy induction group (group PHN+Rapa),resinotoxin group (group PHN),resinotoxin+autophagy inhibitor group (group PHN+3-MA)and blank control group (group C),12 mice in each group. Group C was given no treatment,and the other groups were given intraperitoneal injection of 0.2 μg/g resiniferatoxin (RTX)to prepare PHN model.After successful model establishment,group PHN+Rapa was given Rapamycin (1 μg·kg-1·d-1),physiological saline was given to group PHN, group PHN+3-MA was given 2 μg·kg-1·d-1autophagy inhibitor 3-MA.The intraperitoneal injection was continued for 14 day.The mechanical withdrawal threshold (MWT)and the latent period of thermal withdrawal latency (TWL)were detected and the mice were killed after stability. The segments of L4-6spinal cord were extracted and the relative expressions of bcl-2,Bax and autoph-agy-associated protein LC3 were detected by western blot.Detection of the number of apoptotic cells in the spinal cord by fluorescence Tunel.The number of GABA intermediate neurons in the dorsal horn of the spinal cord was labeled by immunofluorescence.Results Compared with group C,the rel-ative expression level of Bax protein increased significantly,the LC3-II/I ratio and the number of ap-optotic cells increased significantly,the relative expression level of Bcl-2 protein and the number of GABA neurons in spinal dorsal horn were significantly reduced in other groups (P<0.05).Compared with group PHN,the LC3-II/I ratio and the relative expression level of Bax protein,the number of apoptotic cells increased significantly,the relative expression level of Bcl-2 protein and the number of GABA neurons in the spinal dorsal horn were significantly decreased of group PHN+Rapa (P<0.05).Compared with group PHN,the relative expression level of LC3-II/I ratio and Bax protein, the number of apoptotic cells decreased significantly,the relative expression level of Bcl-2 protein and the number of GABA neurons in spinal dorsal horn increased significantly of group PHN+3-MA,(P<0.05).Conclusion Over activation of autophagy may be one of the mechanisms leading to the ap-optosis of GABA neurons in the dorsal horn of the spinal cord in postherpetic neuralgia.
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Objective To investigate the effect of dexmedetomidine on cognitive dysfunction after offpump coronary artery bypass grafting in patients.Methods Fifty-eight ASA physical status Ⅱt or Ⅲ patients,aged 51-63 yr,weighing 52-83 kg,undergoing off-pump coronary artery bypass grafting,were randomly divided into 2 groups (n =29 each):control group (group C) and dexmedetomidine group (group D).Anesthesia was induced with midazolam,etomidate,sufentanil and pipecuronium.The patients were thracheal intubated and mechanically ventilated.Anesthesia was maintained with propofol,sufentanil,isoflurane and pipecuronium.A loading dose of dexmedetomidine 1 μg/kg was infused over 15 min after tracheal intubation,followed by dexmedetomidine infusion at 0.5 μg· kg-1 · h-1 until the end of operation in group D,while the equal volume of normal saline was infused in group C.Cognitive function was assessed by Mini-Mental State Examination (MMSE) at 24 h before operation and 24,48 and 72 h after operation.The development of postoperative cognitive dysfunction was recorded within 72 h after operation.The consumption of sufentanil and extubation time after extubation was recorded.Results Compared with group C,MMSE scores at 24 and 48 h after operation were significantly increased and the incidence of postoperative cognitive dysfunction within 72 h after operation was decreased (P ＜ 0.05),and no significant change was found in the consumption of sufentanil and extubation time in group C (P ＞ 0.05).Conclusion Dexmedetomidine can decrease the development of postoperative cognitive dysfunction after off-pump coronary artery bypass grafting in patients.