Objectivc To study the effects of ketamine and MK-801 on lipopolysaccharide (LPS)-inducedexpression of intercellular adhesion molecule-1 (ICAM-1 ) and the translocation of nuclear factor-kappa B (NF-?B)into nuclei of human umbilical vein endothelial cells (HUVECs). Methods The endothelial cells obtained fromhuman umbilical vein by digestion with collagenase 1 were cultured at 37℃ in a 5 % CO_2-95% room airatmosphere for 7 days. The cultured human umbilical vein endothelial cells (HUVECs) wer randomly divided into(1) control group in which nothing was added to the RPMI-1640 culture medium; (2) LPS group in which us 1?g?ml~(-1) was added to RPMI-1640; (3) ketamine group was further divided into 4 subgroups according to theconcentration of ketamine added: 12.5 (KⅠ), 25 .0 (KⅡ), 100 (KⅢ) and 300?mol?L~(-1) (KⅣ); (4) MK-801group was further divided into 4 subgroups M Ⅰ-Ⅳ, according to the different concentrations of MK-801 added(1 .25, 2.50, 10, 30?mol?L~(-1)). In one set of experiment in ketamine and MK-801 groups after addition ofketamine and MK-801 to the RPMI-1640 culture medium, the HUVECs were incubated for 30 min at 37℃, thenLPS1?g?ml~(-1) was added and incubated for 18 h in a 5 % CO_2 atmosphere at 37℃. The HUVECs were thenharvested for determination of ICAM-1 expression by flow cytometry. In another set of experiment the culturedHUVECs were stimulated with LPS 1?g?ml~(-1) for 2 h in the absence or presence of ketamine (12.5, 25 .0, 100and 300?mol?L~(-1) ) or MK-801 (1.25, 2.50, 10 and 30?mol?L~(-1)). The translocation of NF-?B p65 into nucleiwas detected by immunohistochemistry technique. Results In group K Ⅱ, KⅢ and KⅣ the upregulation ofICAM-1 and translocation of NF-?B into nuclei of HUVECs induced by LPS were significandy reduced (P0.05). Conclusion Ketamine can suppress LPS- induced HUVEC activation at the higher concentrations (≥25?mol?L~(-1)). The inhibitory effects of ketamine ismost likely not mediated through NMDA receptor interactions.

Objective To evaluate the efficacy and safety of target-controlled remifentanil infusion combined with cervical plexus block for anterior cervical decompression surgery.Methods Twenty ASAⅠ or Ⅱpatients aged 30-64 yr undergoing anterior cervical decompression were studied.After a succegsful cervical plexus block,TCI of remifentanil was started at a target plasma concentration(CP)of 1.5 ng/ml 5 min before operation.The remifentanil CP was adjusted according to the patient's response to surgical stimulation and increased or decreased by 0.2 ng/ml each time until Ramsay sedation score reached 2-3 or verbal pain score(VPS)reached 0-1.TCI of remifentanil was discontinued 5 min before the end of surgery.MAP,HR,SpO2,BIS,Ramsay sedation score and VPS were monitored and recorded before cervical plexus block(To,baseline),at 10 min after cervical plexus block(T1),5 min(T2),30 min(T3)after skin incision,when the response to tracheal traction was significant during operation(T4)and at the end of operation(T5).The highest remifentanil Cp and the side effects such as respiratory depression,muscle rigidity,nausea/vomiting and pruritis that occurred were recorded.Remits MAP,SpO2 and BIS were not significantly changed during operation as compared to the baseline values at T0.HR was significantly increased at T2 as compared with the baseline.The Ramsay score reached 2-3 and the VPS reached 0-1 in the majority of patients in group R.No marked side effects were detected during TCI of remifentanil.The remifentanil CP ranged between 1.5-5 ng/ml and the mean CP during operation was(3.4±1.0)ng/ml.Conclusion TCI of remifentanil of low concentration combined with cervical plexus block can safely and effectively induce awake analgesia in patients undergoing anterior cervical decompression surgery.

Objective To investigate the cerebral protective effect of intracarotid infusion of propofol in patients undergoing resection of cerebral gliomas. Methods Sixty ASA Ⅰ- Ⅲ patients with cerebral glioma aged 40-64 yr weighing 48-73 kg were enrolled in this study. Forty patients undergoing resection of glioma under general anesthesia were randomly divided into 2 groups ( n = 20 each): intracarotid propofol group (group IA ) and intravenous propofol group (group Ⅳ). Twenty patients undergoing biopsy of glioma under local infiltration anesthesia with 2% lidocaine 15-20 md served as control group (group C). In IA and Ⅳ groups anesthesia was induced with TCI of propofol and remifentanil. Tracheal intubation was facilitated with rocuronium 0.6 mg/kg. The patients were mechanically ventilated. PErCO2 was maintained at 35-45 mm Hg. Anesthesia was maintained with TCI of propofol and remifentanil and intermittent iv boluses of rocuronium. In group IA internal carotid artery was cannulated after induction of anesthesia and propofol was administered by TCI via carotid artery while remifentanil was administered by TCI via peripheral vein. BIS was maintained at 40-60 during operation. ECG, MAP, HR, SpO2, PETCO2 and BIS were continuously monitored. MAP and HR were recorded before induction of anesthesia (T1) ,during skin incision (T2 ), at the end of operation (T3), during extubation ( T4 ). The glioma specimens were obtained for microscopic examination and determination of aquaporin 1 and aquaporin 4 ( AQP1, AQP4) expression by immunohistochemistry. Results MAP and HR were significantly decreased at T2 and T3 as compared with the baseline at T1 in group Ⅳ ( P ＜ 0.05), while there was no significant change in MAP and HR after induction of anesthesia in group IA ( P ＞ 0.05). The expression of AQP1 and AQP4 was down-regulated in IA and Ⅳ groups compared with group C (P ＜0.05). The propofol consumption during anesthesia was significantly less in group IA than in group Ⅳ (P ＜0.05). There was no significant diffe-rence in AQP1 and AQP4 expression, the amount of remifentanil and recuronium consumed and duration of operation betweenIA and Ⅳ groups ( P ＞ 0.05). Concltsion Intracarotid propofol can decrease the amount of propofol needed for maintenance of anesthesia as compared with intravenous administration and attenuate brain edema,indicating cerebral protective effect.

When applied to the inspection of the organophosphorus and carbamate pesticides, acetylcholinesterase has a high sensibility and a high activity. The sensibility is related to its activity, selectivity, amount, temperature and so on. With acetylcholinesterase liquor prepared, this paper discusses the relationship between the concentration of organophosphorus pesticide and its inhibition effect on acetylcholinesterase, and the relationship between different concentrations, temperatures of acetylcholinesterase and the inhibition ability. The experiment data present the theory basis of the practical application of acetylcholinesterase to the inspection of the pesticide.

Objective: To compare the efficacy of bupivacaine alone or combined with fentanyl, midazolam or tramadolduring PCEA. Methods:Sixty patients scheduled for abdominal hysterectomy under combined epidural and spinal anesthesiawere randomly divided into four groups. Group A received 0. 125 % bupivcaine, group B 0. 125 % bupivacaine + fentanyl(2.5tg/ml), group C 0.125 % bupivacaine + midazolam(0.5mg/ml), group D 0. 125 % bupivacaine + tramdol(3mg/ml).PCEA parameters were a loading dose of 6mi, a bolus dose of 3mi, a lockout interval of 30 min and continuous infusion of2ml/h. The total drug dosage was recorded for up to 24h after operation. The number of PCEA demand, visual analogue painscales(VAS), sedation scales, the incidence of nausea and vomiting, respiratory rate (RR) and mean arterial pressure (MAP)were measured at 4h, 8h, 12h and 24h postoperatively. Results: The total drug dosage, number of button pressed and VAS ingroup A were significantly higher than those in the other groups( P < 0.01 ), which was the least in group D. The sedationscales were the highest in group C. There was a higher incidence of nausea and vomiting in group B. Conclusions: Bupivacainecombined with fentanyl, midazolam or tramadol used for PCEA produces higherquality of pain relief than bupuvacaine alone.

Objective To investigate the change in the phosphorylation of vanilloid receptor 1 (VR1) in dorsal root ganglion (DRG) in rats with inflammatory pain (IP)-morphine tolerance. Methods Twenty 8-12 months old male SD rats in which intrathecal (IT) catheters were successfully implanted without complication were randomly divided into 4 groups (n =5 each): group NS, IP + normal saline (NS) 10 μl IT twice a day ×7 days; group M0 ,intact rats + morphine 10 μg/kg ( 10 μl) IT twice a day × 7 days; group M1 , IP + morphine 10 μg/kg (10 μl) IT once; group M2 ,IP + morphine 10 μg/kg(10 μl) IT twice a day × 7 days. IP was induced by injecting complete Freund's adjuvant (CFA) into the ankle joint of the left hindlimb. IT morphine or NS was started on the 3rd day after induction of IP. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL)were measured after catheterization, before and at 1-7 days of IT consecutive administration. The rats were sacrificed after last pain threshold measurement. The phosphorylated VR1 (p-VR1) protein expression in DRG was determined by Western blot. Results There was no significant difference in the baseline PWL measured before induction of IP among the 4 groups. Morphine tolerance developed in group M0 and M2. The expression of p-VR1 in DRG was highest in group M2. Conclusion The phosphorylation of VR1 in DRG in rats with IP tolerance is increased, which is involved in the development of morphine tolerance.

Objective To investigate effects of hydrogen sulfide on hepatic ischemia-reperfusion injury in rats.Methods Thirty healthy male SD rats weighing 220-250 g were randomly divided into sham operation group (S group),ischemia-reperfusion group(IR group) and different doses of hydrogen sulfide groups (H2S1～3 groups),every group contains six rats.In S group hepatic portal was only exposed but not ligated.In IR group the left and middle lobes of hepatic pedicle,portal vein and hepatic artery were clamped for 1 h and then reperfuse.H2 S1～3groups received intraperitoneal injection of NaHS 14,28,56 μmol/kg at 5 min before reperfusion.Blood samples were collected for measuring the activity of alanine transaminase (ALT) and aspartate transaminase (AST) in serum at 6 h after reperfusion.Liver tissue samples were collected for measurement the glutathione (GSH) content and pathologic examination.Results Compared with S group,the activity of ALT and AST in serum was increased,GSH content in liver tissue decreased in IR group ; Compared with IR group,the activity of ALT and AST in serum was decreased,GSH content in liver tissue increased in H2 S1～3 groups.Hepatic tissue pathologic injury was reduced in H2 S1～3 groups as compared with IR group.Conclusion Hydrogen sulfide can reduce hepatic ischemia-reperfusion injury in rats.

Objective To investigate the changes in the expression of nerve growth factor (NGF) and brain-derived neurotrophic (BDNF) in the dorsal root ganglion (DRG) and spinal dorsal horn following peripheral inflammatory hyperalgesia induced by formalin injected into the plantar region of the right hindpaw in rats. Methods Twenty-four adult SD rats weighing 250-400 g were studied. Peripheral inflammatory hyperalgesia was induced by an intraplantar injection of 5% formalin into right hindpaw. The animals were randomly divided into 4 groups (n=6 in each group), group A:control; group B:2 h after formalin injection; group C:24 h after formalin injection and group D: 48 h after formalin injection. Pain response was recorded. The expression of NGF and BDNF in the inflamed skin, DRG and spinal dorsal horn was detected using immuno-histochemistry technique and image analysis method. Results There were significant bi-phasic nociceptive responses induced by intraplantar injection of formalin in rats. The expression of NGF started to increase 2 h after injection, in the inflamed skin, ipsilateral DRG and dorsal horn neurons and reached the peak level at 24 h after injection. The expression of BDNF in ipsilateral DRG and dorsal horn neurons was unchanged 2 h after injection and started to increase at 24 h after injection. There was a positive correlateion between the expression of NGF and BDNF in ipsilateral DRG neurons.Conclusion NGF is not only an important transmitter in the peripheral mechanicsm of inflammatory pain but also involved in central sensitization through facilitating expression of BDNF in dorsal horn neurons.

Objective To investigate the effects of propofol on cultured primary neurons isolated from fetal Wistar rats against anoxic-reoxygenated injury and its neuro-protective mechanisms at cellular level. Methods Neuronal cells were isolated from brains of fetal Wistar rats and cultured for 12 days. The cultured neuronal cells were randomly divided into 4 groups : (Ⅰ) control group; (Ⅱ) anoxic-reoxygenated group in which neurons were exposed to 95% N2 + 5% CO2 at 37?for 3O min; (Ⅲ) propofol pretreatmenl group in which propofol was added to the culture medium (the final concentrations of propofol were 14 ?mol?L-1) 1 h before exposure to anoxia. (Ⅳ) propofol pretreatment group (the final concentrations of propofol were 56 ?mol?L-1) . Neuronal activity was detected by MTT analysis and NO output was assayed with nitrate reductase method at 1, 2, 4, 6 and 24 h after reoxygenation. The synthesis of heat shock protein (Hsp)70 mRNA was measured by in situ hybridization technique and the synthesis of Hsp70 was measured by immuno-histochemical technique at 1, 3, 8, 24, 48 h and 72 h after reoxygenation.Results (1) 30-min anoxia decreased neuronal activity, increased NO output and significantly increased the synthesis of Hsp70 mRNA and Hsp70. The expression of Hsp70 mRNA reached its peak at 24 h after reoxygenation and that of Hsp70 at 48 h after reoxygenation. (2) Propofol pretreatment significantly increased neuronal activity at 1, 2, 4, 6 and 24 h after reoxygenation and decreased NO output at 1, 2 and 4 h after reoxygenation compared with those in anoxia-reoxygenated group. (3) The synthesis of Hsp70 mRNA was significantly increased and accelerated by pretreatment with both concentrations of propofol but the synthesis of Hsp70 was significantly increased and accelerated by pretreatment with 56?mol?L-1 propofol only. Conclusion Propofol pretreatment can inhibit anoxia-reoxygenation injury to neurons by decreasing NO output and increasing expression of Hsp70 through inducing the synthesis of Hsp70 at both transcription and translation levels.

Objective To study the changes in the expression of GABA and its receptors in the dorsal horn of rat spinal cord induced by hind paw formalin injection. Methods Twelve healthy male SD rats weighing 300-325 g were randomly divided into two groups: (A) control group (n=6) and (B) peripheral inflammatory hyperalgesia group in which 5% formalin 50?l was injected subcutaneously into the plantar region of right hind paw to produce persistent pain(n=6). The animals were killed 24h after formalin injection. L_(4-6) segment of the spinal cord was removed. The number of GABA immuno-reactive cells was examined by immuno-cytochemistry technique and the exprpession of GABA_(A?3) and GABA_(B1) receptor mRNA in the spinal dorsal horn were determined by in situ hybridization. Results In control group(A), GABA immuno-reactive cells and GABA_(A?3) and GABA_(B1) receptor mRNA were observed throughout the lumbar spinal dorsal horn. The density of GABA immuno-reactive cells and GABA_(B1) receptor mRNA was highest in the superficial laminae Ⅰ-Ⅲ; while the GABA_(A?3) receptor mRNA was evenly distributed in the spinal dorsal horn. In group B, 24h after formalin injection there was a significant increase in the GABA immuno-reactive cells in the ipsilateral spinal dorsal horn. The expression of GABA_(A?3) and GABA_(B1) receptor mRNA were significantly increased in bilateral dorsal horn compared to group A. The three parameters were positively correlated and their locations in the spinal dorsal horn were not significantly different from those in group A. Conchusion GABA and its receptors may play an important role in nociceptive modulation.