ObjectiveTo investigate the effects of etomidate postconditioning on apoptosis in a rat model of focal cerebral ischemia-reperfusion(I/R) injury.MethodsThirty-two pathogen-free male SD rats weighing 250-300 g were randomly divided into 4 groups ( n =8 each) using random number table:group sham operation ( group S); group focal cerebral I/R; group lipid emulsion (vehicle for etomidate) (group L) and group etomidate postconditioning (group Ep).Focal cerebral I/R was induced by inserting a nylon thread with rounded tip into right internal carotid artery.The thread was advanced cranially until resistance was met.Middle cerebral artery was occluded for 2 h in groups I/R,L and Ep.Normal saline,lipid emulsion and etomidate emulsion 20 mg/kg were injected peritoneally at the end of ischemia in groups I/R,L and Ep respectively.The animals were sacrificed at 24 h of reperfusion and their brains were removed for microscopic examination,assessment of apoptosis (by TUNEL) and detection of Bcl-2 and Bax expression ( by immuno-histochemistry).Apoptosis index ( AI =the number of apoptofic neurons/the total number of neurons examined × 100％ ) and Bcl-2/Bax ratio were calculated.Results I/R induced microscopic changes,significantly increased AI and Bcl-2 Bax ratio and up-regulated Bcl-2 and Bax expression in group I/R as compared with group S.Etomidate postconditioning significantly amefiorated brain damage,decreased AI,increased Bcl-2/Bax ratio,up-regulated Bcl-2 expression and down-regulated Bax expression in ischemic cerebral hemisphere in group Ep as compared with group I/R.There was no significant difference in brain damage,AI and Bcl-2 and Bax expression and Bcl-2/Bax ratio between groups I/R and L.ConclusionEtomidate postconditioning can attenuate focal cerebral ischemia-reperfusion injury in rats by inhibiting apoptosis and modulating Bcl-2 and Bax expression.

Effects of epidural block on stress response during eardiopulmonary bypass were studied. Twenty patients, undergoing open heart surgery with cardiopulmonary bypass, were randomly divided into two groups:the control group with intravenous high-dose fentanyl and enflurane inhalation (1%-1.5%);the tested group with epidural block and enflurane inhalation (0.5%-1%). The plasma norepinephine (NE) and epinephrine (E) concentrations were higher in group control than those in tested group during and after CPB,even at the end of operation (P

Objective To investigate the effects of different concentrations of sevoflurane on adhesion and expression of CD24 and CD44v6 in human lung cancer cell line A549.Methods Human lung cancer cell line A549 was obtained from Shanghai Cell Biology Medical Research Institute,Chinese Academy of Sciences and cultured in RPMI1640 culture medium containing 10％ fetal calf serum.The cells were inoculated in 24 well culture plate.After being cultured for 24 h,the cells were randomly divided into 4 groups:control group (group C) and 3 sevoflurane groups exposed to 1.7 ％,3.4 ％ and 5.1％ sevoflurane for 2,4 and 6 h respectively ( groups S1,S2,S3 ).The cells were cultured for another 48 h.Cell adhesion rate was detected by adhesion test and the expression of CD24 and CD44v6 mRNA and protein was determined by RT-PCR and flow cytometry.Results Sevoflurane significantly inhibited the cell adhesion rate and down-regulated CD24 and CD44v6 expression in a concentration and duration of exposure-dependent manner.Conclusion Sevoflurane can inhibit cell adhesion through down-regulation of CD24 and CD44v6 expression.

Objective To evaluate the effect of continuous spinal anesthesia with a "catheter-over-needle" system which diminished the leakage of CSF through the hole in the dura alongside the inserted catheter and minimizes the risk of post-dura-puncture headache. Methods Sixty ASA Ⅰ - Ⅱ patients aged over 60 yr, scheduled for transurethral prostatectomy, were randomly divided into two groups of 30 patients in each group: group I continuous spinal anesthesia (CSA); group Ⅱ continuous epidural anesthesia(CEA) . Catheter was placed at L2-3 or L3-4. Both groups received 0.5% bupivacaine for surgery. A loading dose of 1.5-2.5 ml (groupⅠ ) or 8-13 ml (group Ⅱ) was given. If the surgery exceeded 2 h a third of the loading dose was injected. For postoperative analgesia a mixture of 0.125% bupivacaine + 0.0006% fentanyl was used. In group I the PCA setting was loading dose 0.5ml, background infusion at 0.5 ml/h, bolus dose 0.5 ml and lock-out interval 8 min. In group Ⅱ the loading dose was 2 ml followed by background infusion at 2 ml/h and bolus dose was 2 ml with lock-out interval of 15 min. Onset time and level of analgesia were recorded during surgery and VAS pain score and movement of lower extremities (modified Bromage score) were assessed. Postoperative PCA was maintained for 50 h. Results The demographic data including age, height and body weight were comparable between the two groups. There was no significant difference in the duration of surgery between the two groups. The onset of block was significantly faster in group I (3.5 ?2.3) min than that in the group Ⅱ (9.5 ?3.4) min. Motor blockade was less intense in group Ⅱ as assessed by modified Bromage score. Analgesia was more satisfactory in group I as less patients received fentanyl and droperidol iv during surgery in group I . Thetotal amount of bupivacaine used during postoperative analgesia was significantly less in group I , only about one-fifth of the total amount used in group Ⅱ. Two patients complained of headache in group I but in group Ⅱ there was also one patient complaining of headache. Conclusion Continuous spinal anesthesia has the advantage of faster onset of block, better analgesia, more intense motor block with less local anesthetic.

Objective To investigate the effect of intrathecal (IT) dexmedetomidine on the expression of cAMP response element-binding protein phosphorylation (p-CREB) in spinal dorsal horn in a rat model of bone cancer pain. Methods Sixty-four adult female Wistar rats weighing 200-240 g were randomly divided into 4 groups (n = 16 each): sham operation group (group S); bone cancer pain group (group BP); normal saline group ( group NS) ; dexmedetomidine group (group D) . Bone cancer pain was induced by injecting Walker 2S6 mammary gland carcinoma cell suspension (2 ×106 cells/ml) 10μl into the medullary cavity of the tibia in BP, NS and D groups. Groups S and BP received no IT injection. Croups NS and D received IT injection of NS 10 μl and dexme detomidine 5 μg/kg respectively 7 days after successful establishment of the model. Ten animals were selected from each group at 1 day before IT administration (T0), immediately before IT administration (T1 ) and at 1, 6, 12 and 24 h after IT administration (T2-5 ) and paw withdrawal threshold (PWT) to mechanical stimuli was measured with von Frey filaments. The other 6 rats in each group were sacrificed at T4 and the spinal cord was removed for determination of p-CREB expression in the spinal dorsal horn.Results PWT was significantly decreased at T1-5 and pCREB expression up-regulated at T4 in BP, NS and D groups compared with group S ( P ＜ 0.05) . Compared with group BP, PWT was significantly decreased at T2-5 and p-CREB expression down-regulated at T4 in group D ( P ＜0.03), while no significant change in PWT and p-CREB expression was found in group NS (P ＞ 0.05) .Conclusion IT dexmedetomidine can reduce the bone cancer pain through inhibiting the phosphorylation of CREB in rat spinal dorsal horn.

ObjectiveTo investigate the role of T-type calcium channel in the spinal neurotoxicity of intrathecal (IT) lidocaine in rats.MethodsForty-eight adult male SD rats in which IT catheter was successfully implanted,weighing 230-270 g,were randomly divided into 4 groups ( n =12 each):dimethyl sulfoxide (DMSO)group (group D),lidocaine group (group L),mibefradil + lidocaine group (group M),normal saline + lidocaine group (group N).Another 12 rats served as control group (group C).DMSO and 10％ lidocaine 20μl were injected intrathecally in groups D and L respectively.After mibefradil 200 μg/10μl and normal saline 10 μl were injected intrathecally in groups M and N respectively,10％ lidocaine 20 μl was injected intrathecally in the two groups.The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured before IT injection and at 2,4,8 and 12 h and 1,2,3,4 and 5 d after IT injection (T0-9).Four rats were sacrificed at T6 in each group and their lumbar enlargements were removed for microscopic examination.ResultsCompared with group C,no significant change in MWT and TWL was found at each time point in group D,MWT was significantly increased at T1-8 and TWL was significantly prolonged at T1-7 in groups L and N,and MWT was significantly increased at T1-6 and TWL was significantly prolonged at T1-6 in group M ( P ＜ 0.05 ).Compared with groups L and N,MWT was significantly decreased at T1-4 and TWL was significantly shortened at T1-4 in group M ( P ＜ 0.05).Pathological injury was significantly reduced in group M as compared with groups L and N.ConclusionT-type calcium channel is involved in the spinal neurotoxicity of IT lidocaine in rats.

ObjectiveTo investigate the effects of sevoflurane on inhibition of invasive activity and migration of human adenocarcinoma cell line A549 by cisplatin.MethodsThe.human lung adenocarcinoma cell line A549 was obtained from Shanghai Cell Biology Institute,Chinese Academy of Sciences and cultured in RPMI 1640 culture medium containing 10％ fetal calf serum.The cells were inoculated in culture plate and cultured for 24 h and randomly divided into 4 groups:control group; 2.5 ％ sevoflurane group ; cisplatin group and cisplatin + 2.5 ％sevoflurane group.In groups sevoflurane,cisplatin and cisplatin + sevoflurane the cells were exposed to 2.5％sevoflurane or/and cisplatin 10μmol/L for 4 h respectively.The invasive activity of the cells was evaluated by Transwell chamber assay.The migration of the cells was determined by wound healing assay.The expression of MMP-2,MMP-9,Ezrin,and Fascin in the cells was detected by Western blot.ResultsBoth 2.5％ sevoflurane and cisplatin depressed invasive activity and migration of the A549 cells and down-regulated MMP-2,MMP-9,Ezrin and Fascin expression in A549 cells.The inhibitory effects of cisplatin on the A549 cells were potentiated by 2.5 ％ sevoflurane.ConclusionSevoflurane can enhance the inhibition of invasive activity and migration of human adenocarcinoma cell line A549 by cisplatin.

Objective To compare the quality of emergence from TCI of sufentanil and remifentanil supplementing propofol-sevoflurane anesthesia in patients undergoing radical colo-rectal cancer resection.Methods Forty ASA Ⅰ or Ⅱ patients of both sexes aged 40-64 yr undergoing elective radical colo-rectal cancer resection were allocated into 2 groups ( n =20 each):sufentanil group (group S) and remifentanil group (group R).Anesthesia was induced with propofol TCI at plasma concentration (Cp) of 4.0 μg/ml in both groups and sufentanil TCI (effect-site concentration Ce =0.4 ng/ml ) or remifentanil TCI ( Cp =4.0 ng/ml).Tracheal intubation was facilitated with vecuronium 0.1 mg/kg.The patients were mechanically ventilated (VT =8-10 ml/kg,RR =12-16 bpm).PErCO2 was maintained at 30-40 mm Hg.Anesthesia was maintained with propofol TCI-sevoflurane supplemented with sufentanil (Ce=0.25 ng/ml) or remifentanil (Cp=2.5 ng/ml).The depth of anesthesia was maintained at Narcotrend index of 37-56 by adjusting Cp of propofol TCI and sevoflurane concentration.The infusion of sufentanil was discontinued at 40 min before the conclusion of the operation while remifentanil was administered until the end of surgery.The incidence of postoperative adverse events,the time from the end of operation to eye openg and the time to extubation were recorded.Reesults The two groups were comparable with respect to demographic data.Neither group developed prolonged emergence and respiratory depression but the time from the end of operation to eye opening and the time to extubation were significantly longer in group S than in group R.The incidence of hypertension and tachycardia,agitation,shivering aad coughing were significantly lower in group S than in group R.Conclusion The quality of emergence from sufentanil supplementing propofol-sevoflurane anesthesia is higher than that from remifentanil.

Objective To preliminarily evaluate the role of Ras homolog gene (Rho)/Rho-associated coiled coil-forming protein kinase (ROCK) signaling pathway in propofol-induced inhibition of metastasis of human gastric cancer cells.Methods Human gastric cancer MKN-45 cells cultured in vitro,with the concentration of 1.0× 106 cells/ml,were seeded in culture plates,and incubated for 24 h.The plates were then randomly divided into 4 groups using a random number table:control group (group C),propofol group (group P),lysophosphatidic acid group (group L) and propofol + lysophosphatidic acid group (group PL).Group C received no administration.In group P,propofol at the final concentration of 16 μg/ml was given.In group L,lysophosphatidic acid at the final concentration of 1 μmol/L was administered.In group PL,propofol and lysophosphatidic acid were given with the final concentration of 16 μg/ml and 1 μmol/L,respectively.All the cells were then incubated for another 24 h.The migration of cells was determined by wound healing assay,and cell migration rates were calculated.The invasion of cells was determined by Transwell assay,and the invaded cells were counted.The expression of matrix metalloproteinases-2 (MMP-2),MMP-9,RhoA,and ROCK1 in cells was detected by Western blot.Results Compared with group C,cell migration rates and the number of invaded cells were significantly increased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was up-regulated in group L,and cell migration rates and the number of invaded cells were decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group P.Compared with group L,cell migration rates and the number of invaded cells were significantly decreased,and the expression of MMP-2,MMP-9,RhoA and ROCK1 was down-regulated in group PL.Conclusion Inhibition of RhoA/ROCK1 signaling pathway is involved in the mechanism by which propofol decreases metastasis of human gastric cancer cells.

Objective To evaluate the role of TWIK-related K+ channel 1 (TREK-1) in reduction of cerebral ischemia-reperfusion (I/R) injury by sevoflurane preconditioning in mice.Methods Sixty male Kunming mice,aged 8 weeks,weighing 21-29 g,were randomly divided into 5 groups (n=12 each) using a random number table:sham operation group (group S),group I/R,sevoflurane preconditioning group (group SP),TREK-1 small hairpin RNA (shRNA) lentivirus + sevoflurane preconditioning group (group TSP),and negative control shRNA lentivirus + sevoflurane preconditioning group (group NSP).In S,I/R and SP groups,normal saline 15 μl was injected into the lateral cerebral ventricle at 1 μl/min.In TSP and NSP groups,TREK-1 shRNA lentivirus and negative control shRNA lentivirus 15 μl were injected into the lateral cerebral ventricle,respectively,at a rate of 1 μl/min.And 14 days later,S and I/R groups inhaled 100％ oxygen for 60 min,SP,TSP and NSP groups inhaled 2.4％ sevoflurane for 60 min,followed by 15 min washout by inhaling 100％ oxygen,and then cerebral I/R was produced by occlusion of right internal carotid artery for 2 h followed by reperfusion.At 24 h of reperfusion,neurological deficit was scored (NDS).The mice were then sacrificed,and brains were removed to determine the cerebral infarct size (IS),expression of hippocampal caspase-3 and cell apoptosis in brain tissues.Apoptosis index (AI) was calculated.Results Compared with group S,the NDS,cerebral IS,expression of hippocampal caspase-3 and AI were significantly increased in I/R,SP,TSP and NSP groups.Compared with group I/R,the NDS,cerebral IS and AI were significantly decreased,and the expression of hippocampal caspase-3 was down-regulated in SP,TSP and NSP groups.Compared with group SP,the NDS,cerebral IS and AI were significantly increased,and the expression of hippocampal caspase-3 was up-regulated in group TSP,and no significant change was found in the parameters mentioned above in NSP group.Conclusion Sevoflurane preconditioning reduces cerebral I/R injury through activating TREK-1 and inhibiting apoptosis in hippocampal neurons of mice.