ve To investigate the time course of potentiation of rocuronium produced by 1MAC of desflurane or isoflurane. Methods Twenty-four ASA I-II patients aged 18-60 years undergoing elective abdominal operation under general anesthesia were studied. Patients with neuromuscular, liver or kidney disease and those receiving any drug which may affect neuromuscular transmission were excluded. Premedication consisted of intramuscular phenobarbital 0.1 and atropine 0.5mg 30min before operation. Anesthesia was induced with midazolam 0.1-0.2 mg?kg-1, fentanyl 6?g.kg-1 and etomidate 0.3mg?kg-1 .Tracheal intubation was facilitated with rocuronium 0.6mg?kg-1 iv. The degree of neuromuscular block was monitored by measuring muscle response to TOF using accelerography (Biometer) . For maintenance of anesthesia the patients were randomly assigned to receive either propofol + fentanyl (control group) or 1 MAC of desflurane + propofol + fentanyl (desflurane group) or 1 MAC of isoflurane + propofol + fentanyl(isoflurane group). Rocuronium was continuously infused during operation to maintain T1 at 5 % of the control and the infusion rate was recorded every 15 min. Results There were no significant differences among the three groups with respect to sex, age, body weight and duration of anesthesia. In Des and Iso groups the infusion rate of rocuronium was reduced in an exponential manner and maximal potentiation occurred at 90 min of isoflurane or desflurane inhalation. The maximal reduction in infusion rate was 42.7 % in Des group and 37.6% in Iso group. There was no significant difference between the two groups.Conclusions Desflurane and isoflurane can potentiate the muscle relaxation produced by rocuronium in a similar degree and the potentiation is time dependent.

Objective To investigate the change in neuromuscular blocking effect of rocuronium induced by liver dysfunction. Methods Forty patients undergoing elective liver and biliary tract operation under general anesthesia were divided into 2 groups : (A) control group included 20 patients with normal liver function and (B) liver dysfunction group included 20 patients with obstructive jaundice. The premedication consisted of phenobarbital 0.lg and atropine 0.5 mg. Anesthesia was induced with midazolam 0.1 mg?kg-1,fentanyl 6?g?kg-1 and etomidate 0.3 mg?kg-1.The neuromuscular function was monitored by TOF stimulation of the ulnar nerve using accelerograph (Biometer).Rocuronium 0.6 mg?kg-1 was administered iv via the vein in the upper arm.The patients were intubated when T1 was 95% depressed and mechanically ventilated.PETCO2 was maintained at 35-40 mm Hg.The onset time (from the end of injection to T1=0),clinical duration of action (from the end of injection to 25% recovery of T1) and recovery index (T1 from 25% to 95% ) were recorded.MAP, HR and SpO2 were recorded before and at 5 and 10 min after rocuronium injection.Results The demographic data including sex, age and weight were comparable between the two groups. The onset time was (63?19) s in group A and (70?21) s in group B.The difference was not statistically significant. The clinical duration of action was (41?16) min in group A and (67?29) min in group B (P0.05).Conclusion Liver dysfunction induced by obstructive jaundice prolongs the clinical duration of action,but does not significantly affect the onset time of and recovery from rocuronium.

Objective To evaluate the role of oxidative stress in the spinal neurotoxicity induced by ropivacaine in rats.Methods Ninety pathogen-free male Sprague-Dawley rats,weighing 250-320 g,aged 3 months,in which intrathecal catheter was successfully implanted into L5,6 interspace without complications,were randomly divided into 3 groups (n =30 each) using a random number table:control group (group C),ropivacaine group (group R),and antioxidant Tempol group (group T).The rats received 1％ ropivacaine 1.2 μg/g for 8 times at 1.5 h intervals through the catheter in R and T groups,while the rats received the equal volume of normal saline instead in group C.In T group,Tempol 20 μg/g was injected intrathecally at 4,8,12,24,48 and 72 h after the last injection of ropivacaine.The rats were sacrificed at 1,3,5,7 and 14 days after the end of ropivacaine injection,and their lumbar enlargements were removed for TUNEL staining to detect the cell apoptosis.SOD activity was determined by colorimetry and MDA content was measured using TBA photoelectric colorimetry.Apoptosis index was calculated.Results Compared with group C,apoptosis index and MDA content were significantly increased,and SOD activity was decreased in R and T groups.Compared with group R,apoptosis index and MDA content were significantly decreased,and SOD activity was increased in group T.Conclusion Oxidative stress is involved in the development of spinal neurotoxicity induced by ropivacaine in rats.

Objective To evaluate the ischemic postconditioning on endoplasmic reticulum stress during cerebral ischemia/reperfusion (I/R) in rats.Methods Ninety adult male Sprague-Dawley rats,aged 350-450 g,were randomly divided into 3 groups (n =30 each) using a random number table:sham operation group (S group),I/R group,and ischemic postconditioning group (group P).Focal cerebral I/R was induced by electrocoagulation of left middle cerebral artery and 30 min occlusion of bilateral common carotid arteries followed by reperfusion.In group P,bilateral common carotid arteries were subjected to 3 cycles of 30 s reperfusion and 10 s ischemia at the beginning of reperfusion.At 24 h of reperfusion,neurological deficit was scored,and cerebral infarct size was detected by TTC staining.At 6,12 and 24 h of reperfusion,the expression of glucose-regulated protein 78 (GRP78),C/EBP homologous protein (CHOP) and caspase-12 in the ischemic area were measured (using immunohistochemistry).The neuronal apoptosis in the ischemic area was detected by TUNEL.Results Compared with S group,the neurological deficit score was significantly increased,cerebral infarct size was enlarged,the neuronal apoptosis was increased,and the expression of GRP78,CHOP and caspase-12 was up-regulated in I/R and P groups.The neurological deficit score was significantly lower,cerebral infarct size was smaller,the expression of GRP78 was higher at 12 and 24 h of reperfusion,the neuronal apoptosis was lower at 24 h of reperfusion,and the expression of CHOP and caspase-12 was lower in group P than in group I/R.Concluion Ischemic postconditioning can inhibit neuronal apoptosis mediated by endoplasmic reticulum stress during cerebral I/R,which dose not play a leading role in cerebral protection in rats.

Objective To investigate the effects of sevoflurane preconditioning (SP) on acute lung injury induced by lipopolysaccharide (LPS) in rats.Methods Twenty-four male SD rats weighing 220-250 g were randomly divided into 4 groups (n = 6 each): group Ⅰ control (group C),group Ⅱ LPS,group Ⅲ sevoflurane (group Sev) and group Ⅳ SP + LPS.In group Ⅰ and Ⅱ ,normal saline and LPS 5 mg/kg were given Ⅳ 30 min after ventilation respectively.In group Ⅲ and Ⅳ,the animals inhaled sevoflurane (end-tidal concentration 2.4% ) for 30 min followed by 5 min wash-out,and then received iv injection of normal saline and LPS 5 mg/kg respectively.The animals were killed at 6 h after LPS or normal saline administration.Lungs were removed for determination of W/D lung weight ratio,myeloperoxidase (MPO) activity,cytokine-induced neutrophil chemoattractant-1 (CINC-1) content and expression of CINC-1 and CINC-1 mRNA.The severity of lung injury was evaluated using diffuse alveolar damage (DAD) score.Results Compared with group Ⅰ ,W/D lung weight ratio,DAD score,MPO activity and CINC-1 content were significantly increased,and expression of CINC-1 and CINC-1 mRNA up-regulated in group Ⅱ and Ⅲ,while there was no significant difference in the above indices between group Ⅲ and group Ⅰ .Compared with group Ⅱ ,W/D lung weight ratio,DAD score,MPO activity and CINC-1 content were significantly decreased,and expression of CINC-1 and CINC-1 mRNA down-regulated in group Ⅲ.Conclusion Sevoflurane preconditioning can protect the lungs against LPS-induced acute lung injury by inhibiting inflaunnatory response.

Objective To evaluate the accuracy of BIS and anesthetic depth index (CSI) for monitoring levels of sedation induced by different target effect-site concentrations (CT) during TCI of propofol combined with sufentanil. Methods Ninety ASA Ⅰ or Ⅱ patients of both sexes aged 20-49 yr weighing 45-70 kg undergoing elective surgery under general anesthesia were randomly divided into 6 groups (n=15 each): group Ⅰ, Ⅱ, Ⅲ TCI of propofol with CT set at 2, 4 and 6 μg/ml respectively (P1-3);groupⅣ, Ⅴ,Ⅵ sufentanil 0.7 μg/kg + propefol TCI with CT set at 2, 4 and 6 μg/ml (SP1-3). Anesthesia was induced with propefol TCI with CT set at 4 μg/ml in all 6 groups. As soon as the patients lost consciousness, tracheal intubation was facilitated with vecuronium 0.1 mg/kg. The patients were mechanically ventilated. PET CO2 was maintained at 35-45 mm Hg. Anesthesia was maintained with propofol TCI with CT set at 2 μg/ml(in group P1, SP1), 4 μg/ml(in group P2, SP2) and 6 μg/ml(in group P3,SP3) immediately after intubation respectively. Sufentanil 0.7 μg/kg was given iv at 20 min after propofol TCI was started in group SP<1-3. MAP, HR, BIS (Aspect) and CSI (Danmeter Denmark) were continuously monitored and recorded before induction of anesthesia (T0, baseline), at 1 min before tracheal intubation (T1), and at 30 s(T2), 15 min(T3), 30 min(T4), 35 min(T5) and 40 min (T6) after tracheal intubation. Results BIS and CSI values were gradually decreasing at T3-6 in group P1-3 and SP1-3. BIS and CSI values were significantly lower at T4-6 in group SP1 and SP2 than in group P1 and P2. CSI values were significantly lower at T4-6 in group SP3 than in group P3, but there was no significant difference in BIS values at T4-6 between SP3 and P3. Conclusion CSI and BIS can monitor the levels of sedation indueed with TCI of propofol with CT set at 2 and 4 μg/ml when combined with sufentanil 0.7 μg/kg but only CSI can monitor the level of sedation induced by propofol TCI with CT set at 6 μg/ml when combined with sufentanil 0.7 μg/kg.

Objective To investigate the intervention effect of lentivirus expressing human IL-10 (LV-hIL-10) on activated astrocytes.Methods DI TNC1 cell line was treated with different concentrations of lipopolysaccharide (LPS) and time points.The expression of proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukinb-1β (IL-1β) was detected by RT-PCR and ELISA.Moreover,the effect on the expression of proinflammatory cytokines TNF-α and IL-1β was analyzed in DI TNC1 cell lines infected with and without LV-hIL-10.Results The expression of TNF-α and IL-1β was increased in DI TNC1 induced by LPS.The expression of IL-10 was upregulated in DI TNC1 infected with LV-hIL-10.TNF-α and IL-1β were inhibited by IL-10 overexpression in DI TNC1 actived by LPS.Conclusion DI TNC1 is activated by LPS and secretes proinflammatory cytokines TNF-α and IL-1β as immune-like cells,and these activation is inhibited by hIL-10 overexpression.

Objective To construct contains human interleukin-10 gene recombinant lentiviral-vector(LV-IL-10)and to form a basis to further explore the therapy of chronic pain.Methods hIL-10 gene fragment was isolated and amplified from pCYIL-10 plasmid by PCR,and was cloned into pWPXL-GFP.The inserted hIL-10 fragment was verified by Pme I digestion and DNA sequencing.The recombinant plasmid pWPXL-IL-10-GFP,envelope plasmid pMD2.G and packaging plasmid psPAX2 were cotransfected into 293T cells,to pack out lentivirus particle that has the ability of duplicated-deficiency,then virus titer determination was undertaken.Results The 530bp IL-10 gene fragment was amplified from pCYIL-10 plasmid by PCR,and was recombinated into pWPXL-GFP plasmid.DNA sequencing confirmed that the cloned gene segment was 100% homologous to the published hIL-10 sequence in genebank.High titer(2?1010)and highly purified lentiviral particles was obtained.Conclusions The lentivirus vector LV-hIL-10 was constructed successfully,which form a basis of research of chronic pain therapy.

Objective To investigate the effects of intrathecal morphine on cell-mediated immunity. Methods Forty male SD rats weighing 250-300 g were randomly divided into 5 groups ( n = 8 in each group) : sham-operated group (F); saline group (NS) and 3 morphine groups (M1, M2, M3). The animals were anesthetized with intraperitoneal chloral hydrate 300-350 mg?kg-1 . Microspinal catheter was inserted into the subarachnoid space at the lumbar region according to modified Yaksh technique. Correct implantation of the spinal catheter was confirmed by aspiration of CSF. In the morphine groups, after 5 days morphine was continuously infused through the spinal catheter at 2.5 (Ml), 5.0 (M2) and 10 ?g?h-1(M3) for 7 days. In NS group normal saline was continuously infused instead of morphine. On the 7th day 5% formalin 50 fd was injected into the plantar surface of left hindpaw. The number of flinches, lickings and total time of licking were recorded for 60 min. Pain intensity scoring (PIS) (0-3, 0 = no pain, 3 = severe pain) was used to assess the antinociceptive effect of intrathecal morphine. The animals were killed after evaluation of pain intensity. Body weight and spleen weight were measured. Spleen index (spleen weight/body weight) was calculated. T-lymphocyte function was evaluated based on Concanavalin-A (Con A) induced splenocyte proliferation. Modified lactic acid dehydrogenase (LDH) release assay was used to assess NK cell activity. Results The PIS scores were significantly lower in group M1 , M2 and M3 than in F and NS group. The spleen index, splenocyte proliferation induced by Con A and NK cell activity were significantly suppressed in the 3 morphine groups Conclusion Intrathecal morphine has significant antinociceptive effect and suppresses T-lymphocyte proliferation and NK cell activity in a dose-dependent manner

Objective To investigate the effects of continuous spinal anesthesia with different concentrations and doses of ropivacaine on the ultrastructure of the spinal cord and nerve roots. Methods Twenty-four male SD rats weighing 220-280 g were anesthetized with intraperitoneal 10% chloral hydrate 300-350 mg/kg. A polyurethane microcatheter was inserted into the lumbar subarachnoid space according to the technique described by Yaksh. An 8-cm catheter segment was left in the subarachnoid space. The animals were randomized to receive normal saline, 0.5%, 0.75% or 1.0% ropivacaine 40 ? 1 intrathecally 3 times at 1.5 h interval. Six hours after the first intrathecal administration the animals were decapitated and L1 ,2 segment of the spinal cord and nerve roots were immediately removed for electron microscopic examination. Results Electron microscopic examination revealed that in animals which received intrathecal (i.t.) normal saline, 0.5% or 0.75% ropivacaine the neurolemma of the nerve roots and the mitochondria and endoplasmic reticulum of the neurons in the spinal cord were intact, while in animals which received i.t. 1.0% ropivacaine the neurolemma was stratified and partly disrupted and there were swelling of endoplasmic reticulum and vacuole degeneration. Conclusion Six hours continuous spinal anesthesia with 1.0% ropivacaine may be injurious to the spinal cord and nerve roots.