Dexmedetomidine( DEX) is a pure potent, highly se-lective and highly specific agonist ofα2-adrenergic receptors with sedative, analgesic and sympatholytic properties. The sedative effect mimics natural sleep of“arousable” and“cooperative” se-dation without respiratory depression. Due to the above properties and advantages, DEX has received adequate attention in clinical practice and its spectrum of application is also expanding. In re-cent years, it is proved that DEX is neuroprotective not only in animal researches but also in clinical studies. The neuroprotec-tion of DEX and its related mechanism will be briefly reviewed in this paper.

Objective To investigate the effects of propefol on β-amyloid protein(β-AP)-induced injury to cultured rat cortical neurons.Methods Eighteen days pregnant SD rats were anesthetized with ether.The fetal rats were obtained under sterile condition and decapitated. Cortices were then dissected under dissecting microscope.Cortical neurons were isolated according to the method described by Velly LJ et al and cultured for 7 days.There were 5×104 neurons in each well (200 μl).The experiment included 2 parts.In part T 15 wells of neurons were randomly divided into 5 groups(n=3 each ) : group I control(C);group II β-AP 25 μmol/L; group III and IV 2 propofol pretreatment groups (PP1,PP2) and greup V propofol treatment (PT).In group PPt propofol 50 μmol/L was added to the culture medium 24 h before the addition of β-AP 25 μmol/L and the neurons were incubated for another 24 h.In group PP2 propofol 50 μmol/L and μ-AP 25 μmol/L were added to the culture medium simultaneously and the neurons were then incubated for 24 h.In group PT propefol 50 μmol/L was added to the culture medium at 6 h after the addition of β-AP 25 μmol/L and the neurons were incubated for another 18 h.In part Ⅱ 18 wells of neurons were randomly divided into 6 groups(n=3 each):group I control (C) ; group IIβ-AP 25 μmol/L; group III intralipid; group IV,V,and VI 3 prepofol treatment groups (P1,P10,P50).In intralipid group equal volume of 10% intralipid was added to the culture medium at 6 h after β-AP 25 μmol/L and the neurons were then incubated for another 18 h.In group IV- VI propofol 1,10 and 50 μmol/L were added at 6 h alter β-AP 25 μmol/L respectively and the neurons were incubated for another 18 h.The amount of lactic dehydrogenase (LDH) released was measured.Neuronal viability was assessed by MTT assay.The neuronal apoptosis was detected using Hoechst33342 staining and TUNEL technique,and the.apoptosis rate was calculated.Results In part Ⅰ there was no significant difference in the amount of LDH released between group Ⅱ(β-AP) and the 2 propofol pretreatment groups(Ⅲ,Ⅳ).The amount of LDH released was significantly lower in group Ⅴ (propofol treatment) than in group β-AP(Ⅱ).In part Ⅱ the amount of LDH released was significantly lower,neuronal viability higher and the apoptosis rate was lower in group P50 than in group Ⅱ(β-AP).Conclusion Propofol 50 μmol/L given after β-AP can attenuate β-AP induced injury to cultured rat cortical neurons while prophylactic administration of propofol can't.

Objective To investigate the effectiveness of entropy in measuring the level of sedation during target controlled infusion (TCI) of propofol in patients of different ages. Methods Twenty-nine ASA Ⅰ-Ⅱ patients undergoing elective surgery under general anesthesia were divided into two age groups: Ⅰ adult group (20-64 yr) (n = 16) and Ⅱ the aged group (65-85 yr) ( n = 13). The patients were unpremedicated. The level of sedation was assessed using OAA/S scale. Propofol was given by TCI. The effect-site concentration (Ce) of propofol was set first at 1 ?g?ml-1 and then increased step by step by 0.5 ?g?ml-1 every 60 seconds until Ce reached 6 ?g?ml-1. Response entropy ( RE), state entropy ( SE), BP, HR, SpO2 were monitored and recorded at each Ce, before intubation, and immediately and 1, 2, 3, 4, 5, 10 min after intubation. The predictive performance of entropy was evaluated by prediction probability (Pk) .Results The two groups were comparable with respect to sex (M/F ratio), body weight and body weight index (kg?m-2). The RE and SE values decreased as Ce increased. The difference between RE and SE was also reduced. In adult group when Ce reached 2.0 ?g?ml-1, the RE and SE values were lower than the baseline values ( P

Objective To investigate the protective effects of etomidate on the cortex and hippocampus against anoxia-reoxygenation (A/R) injury.Methods Male adult SD rats weighing 90-100 g were anesthetized with ether and decapitated. Their brains were immediately removed. Cortical and hippocampal slices were prepared and were randomly divided into 6 groups: group Ⅰ control; groupⅡ A/R; in group Ⅲ - Ⅵ the brain slices were first incubated in the presence of etomidate 3, 6, 15 ?mol?L-1 or etomidate 6 ?mol?L-1 + picrotoxin 50 ?mol?L-1 (GABA receptor antogonist) for 30 min. Then the slices were subjected to 10 min anoxia (95% N2 +5% CO2) followed by 120 min reoxygenation. The absorbance value (A490) of TTC staining (2. 3. 5-triphenyl tetrazolum chloride) and intracellular free Ca2+ ([Ca2+]i) accumulation were determined. Results The A490 in cortical and hippocampal slices were significantly decreased while [Ca2+] i significantly increased in A/R group as compared with control group. Different concentrations of etonlidate attenuated the changes induced by A/R especially 6 ?mol?L-1. The protective effects of etomidate could be antagonized by GABAA antagonist. Conclusion Etomidate can protect the cortex and hippocampus against A/R injury to some extent by acting on GABAA recoptor and decreasing intracellular Ca2+ overloading.

Aim To investigate the effects of propofol on focal cerebral ischemia and the changes of protein kinase C isoform ?(PKC?) expression in rats brain. Methods Male SD rats were randomly allocated into five groups: Ⅰ: sham group, Ⅱ: injury group, Ⅲ: propofol (25 mg?kg-1) plus injury group, Ⅳ: propofol (50 mg?kg-1) plus injury group, Ⅴ: intralipid plus injury group. The focal cerebral ischemia was induced by 3 h of middle cerebral artery occlusion (MCAO) and 24 h of reperfusion. 30 min before reperfusion, propofol and intralipid were infused intraperitoneal of the rats in groups Ⅲ, Ⅳ, Ⅴ, respectively. After 24 h of reperfusion, rats were weighted and the neurological deficit was assessed by 5-point scale. Brain pathologic changes were observed by HE staining, the method of terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) was carried out for the assessment of neural apoptosis, and immunocytochemistry was used to investigate the changes of PKC?.Results After 3 h of MCAO and 24 h of reperfusion, the weight of rats in group Ⅱ, Ⅲ, Ⅳ, Ⅴ decreased and their neurological deficits scores increased. Compared to the rats of sham group, the numbers of apoptosis neurons in striatum were marked-ly increased, and the expression of PKC? were significantly decreased in rats of injury group (P

Objective To evaluate the desflurane-induced sympathetic activation with finger tip perfusion index (FTPl). Methods Forty-eight ASA ⅠorⅡ patients aged 25-60 yr undergoing elective surgery under general anesthesia were randomly divided into 3 groups (n=16 each): groupⅠsevoflurane; group Ⅱ desflurane and groupⅢ desthrane + propofol. Anesthesia was induced with midazolam 0.03 mg/kg, propofol 2 mg/kg and fentanyl 2 μg/kg. Tracheal intubatian was facilitated with vecuronium 0.1 mg/kg. The patients were mechanically ventilated (VT 8-10 ml/kg, RR 12 bpm). PETCO2 was maintained at 35-40 mm Hg. In group ⅠandⅡanesthesia was maintained with sevoflurane and desflurane respectively. The end-tidal concentration of sevoflurane and desflurane were rapidly increased to 0.5 MAC, 1.0 MAC and 1.5 MAC and maintained at each level for 5 rain. In group Ⅲanesthesia was maintained with TCI of propofol and destlurane. The target plasma prepofol concentration was set at 1 μg/ml and the end-tidal concentration was rapidly increased to 0.5 MAC and 1.0 MAC and maintained at each level for 5 mitt. MAP, HR, FTPI and BIS were continuously monitored and recorded at 5 rain after midazolam (T0), 3 rain after induction of anesthesia (T1), immediately after tracheal intubation (T2), as soon as the end-tidal concentration of sevoflurane and desflurane reached 0.5 MAC(T3), 1.0 MAC(T5) and 1.5 MAC(T7) and after being maintained at 0.5 MAC (T4), 1.0 MAC (T6) and 1.5 MAC (T8) for5 rain. The plasma renin activity and the levels of angintonin Ⅱwere determined at T0, T1, T2, T5 and T7 by using radioimmuno-ssay. Results FTPI was significantly lower at T5 than at T4 in group Ⅱ HR and MAP were significantly lower at T4-6 and T8 and FTPI were significantly lower at T3～6 and T0 than at T7 in group Ⅱ. HR and MAP were significantlyhigher while FTPI was lower at T7 in groupⅡthan in group Ⅰ The changes in MAP and FTPI between T4 and T5 were significantly less in group Ⅲthan in group Ⅱ. The time when the highest value of FTPI was maintain was significantly shorter than the time when the highest values of HR and MAP were maintained at T5 and T7 in group ⅡΔFTPI was negatively correlated with ΔHR and ΔMAP (r=-0.593, P<0.05;r=-0.591, P<0.05). Conclusion FTPI can reflect the desflurane-induced sympathetic activation promptly and sensitively.

Objective To evaluate the efficacy and safety of bilateral transversus abdominis plane block (TAPB)combined with bilateral rectus sheath block (RSB)in abdominal surgery. Methods Ninety ASA Ⅰ or Ⅱ patients,35 males,55 females,aged 19-79 years,with body mass index 18-30 kg/m2 ,scheduled for elective laparoscopic cholecystectomy were randomly divided into three groups(n=30):ultrasound-guided bilateral TAPB combined with bilateral RSB group (group TR),ultrasound-guided bilateral TAPB group (group T),patient-controlled intravenous analgesia (PCIA)group (group P).In group TR,ultrasound-guided bilateral TAPB were performed with 20 ml of 0.22% ropivacaine mesylate injection in each side and ultrasound-guided bilateral RSB were per-formed with 10 ml of 0.22% ropivacaine mesylate injection in each side before surgery.In group T, ultrasound-guided bilateral TAPB were performed with 20 ml of 0.22% ropivacaine mesylate injection in each side and ultrasound-guided bilateral RSB were performed with 10 ml of NS in each side before surgery.In group P,ultrasound-guided bilateral TAPB were performed with 20 ml of NS in each side and ultrasound-guided bilateral RSB were performed with 10 ml of NS in each side before surgery, and PCIA was applied in group P.BP,HR,SpO2 were observed when patients were sent into the op-erating room, 2 minutes before trocar puncture, and 2 minutes after trocar puncture, the consumption of propofol and remifentanil used during the surgery were recorded.The score of visual analogue scale (VAS)during rest and movement were recorded at 2,6,12,24 h after surgery.The patient analgesia satisfaction and the adverse reactions were recorded.Results Compared with group T and group P,group TR had less change of BP before and after trocar puncture(P <0.05).The VAS score was significantly lower in group TR after operation(P <0.05).There were no statistical significant differences of VAS score at 24 h after operation among the three groups.The patient anal-gesia satisfaction was significantly better in group TR than other two groups (P < 0.05 ). Conclusion Ultrasound-guided bilateral transversus abdominis plane block combined with bilateral rectus sheath block is of safety and much efficacy of postoperative analgesia in patients undergoing laparoscopic cholecystectomy.

Objective To investigate the neuroprotective effect of panaxynol on primary cultured cortical neuron against oxidative stress. Methods Viability of panaxynol acted on neuron oxidative stress was monitored by MTT assay and FCM method. Scavenging effects of panaxynol on free radicals were observed in vitro. Effects of panaxynol on SOD activity and GSH-Px, and MDA content in primary neuron injured by H_2O_2 were also determined. Results Panaxynol (2—16 ?mol/L) could dose-dependently protect neuron from oxidative stress induced by H_2O_2; 8 ?mol/L of panaxynol could decrease necrosis and apoptosis rate of neuron significantly (P

Objective To investigate the effects of bone mesenchymal stem cells (BMSCs)transplantation on the neurological function recovery of injured spinal cord and the underlying mechanism.Methods Rats were subjected to contusive spinal cord injury by using NYU spinal cord contusive impactor system ( NYC lmpactor).Seven days after spinal cord injury,the transplantation of BMSCs ( BMSCs group) or injection of PBS ( PBS group) was performed around the epicenter of injured spinal cord in rats.Basso-Beattie-Bresnahan (BBB) score was used to evaluate the function of spinal cord.The cavity volume of the injured spinal cord was measured and the axons in the injury center of spinal cord were examined under transmission electron microscopy.The BMSCs of the green fluorescent protein (GFP)transgenic rats were used to trace the transplanted cells and the survivor of BMSCs in the injured spinal cord and their differentiation into neural cells were observed.A mini-channel implantation model was employed to further investigate the role of BMSCs transplantation on the axonal regeneration.Results The BMSCs group showed a higher BBB score and a smaller lesion volume as compared with the PBS group.Transmission electron microscopy examination displayed that the number of axons in the BMSCs group was far more than that in the PBS group.A great number of BMSCs-GFP were founded around the center of the injured spinal cord at 4 weeks after BMSCs transplantation.lmmunohistochemistry showed that the implanted BMSCs-GFP did not express the surface marker of neurons,astrocytes and oligodendrocytes.In the mini-channel implantation model,NF-positive nerve fibers grew into the BMSCs-seeded channel,while there were no nerve fibers in the channel without seeding of BMSCs.Conclusions The BMSCs transplantation for the injured spinal cord promotes its functional recovery,and the related mechanism is in correlation with BMSCs transplantation inducing axonal regeneration.

Objective To evaluate the effects of different concentrations of sevoflurane anesthesia on longterm learning and memory abilities in neonatal rats.Methods Twenty-seven neonatal Sprague-Dawley rats of both sexes,aged 7 days,weighing 12-20 g,were randomly assigned into 3 groups (n =9 each):control group (C group),2％ sevoflurane group (S1 group) and 3％ sevoflurane group (S2 group).Groups C,S1 and S2 inhaled air,2 ％ sevoflurane and 3 ％ sevofluran for 4 h,respectively.The neonatal rats were reared to 35 days old and underwent open field test,to 36 days old and underwent Morris water maze test,and to 42 days old and underwent continuous multiple-trail inhibition avoidance training.Results Open field test:There was no significant difference in the movement time,movement speed and the time the animals spent in the central square among the 3 groups (P ＞ 0.05).Morris water maze test:Compared with C group,the looking for platform latency on 2nd-5th days in S2 group and on 2nd-3rd days in S1 group was significantly prolonged,and the percentage of time of staying at the platform quadrant was decreased in S1 and S2 groups (P ＜ 0.05 or 0.01).The looking for platform latency on 3rd4th days in S2 group was significantly longer than that in group S1 (P ＜ 0.05).Continuous multiple-trail inhibition avoidance training:The latency detected at 24 h after training was significantly shorter in S1 and S2 groups than in group C (P ＜ 0.05),and in group S2 than in S1 group (P ＜ 0.05).Conclusion Sevoflurane anesthesia decreases the long-term learning and memory function in neonatal rats in a concentration-dependent manner.