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 evaluate the use of laparoscopic operation in gynecological acute disease. Methods 56 cases of gynecological acute disease patients were treated with different laparoscopic operation according to pathogenetic condition. Results All were exelcymosised urinary canal, liquid diet, out-of-bed actived 6h post operation, ambulation 10h later,no infective fever,postoperative hospital stay 3～5d[mean (3.3?1.1d)] and incisal opening healing well. Conclusion Laparoscope is an effective and safe operation in gynecological acute disease.

Objective To study the effect of IL-8 on cell proliferation and invasion,and to analyze the correlations between chemokine and epidermal growth factor receptor(EGFR)signaling pathways in breast carcinoma cells.Methods IL-8 secretion responded to treatment with rhEGF and anti-EGFR and expression of its receptors CXCR1,CXCR2 in MDA-231 cells were measured by ELISA and immunocytochemistry,respectively.Effect of rhIL-8 and neutralizing antibody on cell proliferation and invasion were analyzed by using MTT and matrigel invasion assay.EGFR transactivation stimulated with rhIL-8 and neutralizing an tibody was assessed by Western blot using anti-phosphotyrosine antibody.Results MDA-231 cells released hish level of IL-8 and two receptom of IL-8(CXCR1 and CXCR2)both expressed on cell membrane.Exogenous IL-8 and its neutralizing antibody did not significantly influence the proliferation of breast carcinoma cells,but rhIL-8 stimulated invasive activity in MDA-231 cells and its neutralizing antibody inhibited the in vasive activity(P＜0.05).EGF and anti-EGFR both inhibited the secretion of IL-8 in breast carcinoma cells,and IL-8 had no effect on EGFR phosphorylation,but anti-IL-8 induced transactivation of EGFR after 24h.Conclusion IL-8 contributes to tumor progression in breast carcinoma through its enhancement of in vasive activitv but not act as an autocrine growth factor.The correlation of competitive inhibition rather than cross-talk is found between G protein coupled receptor(GPCR)-mediated IL-8 signaling pathway and EGFR pathway in breast carcinoma.

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.

Objective To evaluate the effects of the right stellate ganglion block on the expression of β3adrenoceptor (β3-AR) in rabbits with heart failure.Methods Forty-eight Japanese white rabbits of both sexes,weighing 2.5-3.0 kg,were randomly divided into 3 groups (n =16 each):sham operation group (group S),heart failure group (group HF) and right stellate ganglion block group (group RSGB).Heart failure was induced by occlusion of left anterior descending branch of coronary artery and confirmed by ultrasonic cardiography 4 weeks later.A PE-10 catheter was inserted into the right stellate ganglion for administration of drugs.0.25％ bupivacaine 2 ml was injected through the catheter once a day for 2 weeks in group RSGB,while the equal volume of normal saline was injected instead of bupivacaine in S and HF groups.The left ventricular end-diastolic diameter (LVEDD),left ventricular end-systolic diameter (LVESD),ejection fraction (EF) and left ventricular fractional shortening (LVFS) were measured at 1 day before ligation (T0),before catheter insertion (T1),before 8th administration (T2),and 1 day after the last administration (T3).Eight rabbits were sacrificed at T1 and T3 in each group and myocardial specimens were obtained from the apex of the left ventricle for determination of the expression of β3-AR by Western blot.Results Compared with group S,the LVEDD and LVESD were significantly enlarged and LVEF and LVFS were decreased at T1-3,and the expression of β3-AR was up-regulated at T1,3 in groups HF and RSGB (P ＜ 0.05).Compared with group HF,the LVEDD and LVESD were significantly decreased,LVEF and LVFS were increased,and the expression of β3-AR was significantly down-regulated at T3 in group RSGB (P ＜ 0.05).Conclusion The right stellate ganglion block can improve the cardiac function of rabbits with heart failure through down-regulating the expression of β3-AR in myocardium.

ObjectiveTo establish a rat model of nerve damage induced by intrathecal(IT) lidocaine.MethodsFifty-five adult male SD rats weighing 200-220 g were randomly divided into 5 groups (n =11 each):group normal control (group C); group dimethyl sulfoxide (DMSO)-the solvent(group D) and groups IT 5％,10％,15％ lidocaine (groups L5.10.15 ).IT catheter was successfully implanted without complication in groups D,L5,L1o,L15.DMSO,5％,10％ and 15％ lidocaine 20 μl were injected IT in groups D,L5,L10,L15 respectively.Motor dysfunction of hindlimb was assessed and scored (0 =normal,2 =complete block) and paw withdrawal threshold to mechanical stimulation (von Frey filaments) (MWT) and paw withdrawal latency to thermal nociceptive stimulus (TWL) were measured before (baseline) and at 1,2,3,4,5,7 d after IT administration in 8 animals in each group.Three animals in each group were sacrificed at 1 d after IT administration.The lumbar segment (L4-5) was removed for microscopic examination.ResultsThere was no significant difference in motor dysfunction score,MWT and TWL among groups C,D and L5.MWT was significantly increased and TWL prolonged at 1 and 2 d after IT administration in group L10,while in group L15 motor dysfunction score was significantly increased at 1,2 d after IT administration and MWT was significantly increased and TWL prolonged at 1,2,3 d after IT administration.There was significant histologic damage to spinal cord in groups L10 and L15.Conclusion Nerve damage can be induced by IT 10％ lidocaine.

Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the up-regulation of expression of Cav3.2 T-type calcium channels in spinal cord in a rat model of neuropathic pain (NP).Methods Forty-eight male Sprague-Dawley rats,aged 3 months,weighing 220-250 g,were randomly divided into 6 groups (n =8 each)∶ sham operation group (group S),group NP,dimethyl sulfoxide group (group D) and different concentrations of a specific CaMK Ⅱ inhibitor KN93 groups (groups K1-3).NP was produced by chronic compression of dorsal root ganglion.The rats in groups D and K1-3 received a single intrathecal injection of dimethyl sulfoxide and KN93 15,30,60 nmol/L (10 μl),respectively,on 5th day after NP.Paw withdrawal threshold to von Frey filament stimulation (MWT) and paw withdrawal latency to thermal nociceptive stimulus (TWL) were measured before NP,before intrathecal injection on 5th day after NP,and at 30 and 60 min and 3,6 and 8 h after intrathecal injection on 5th day after NP (T1-7).The rats were sacrificed after the measurement of pain threshold at T7 and their lumbar enlargements were removed to detect the expression of Cav3.2 mRNA and protein using Western blot and RT-PCR.Results Compared with group S,MWT was significantly decreased,TWL was shortened and the expression of Cav3.2 mRNA and protein was up-regulated in NP,D and K1-3 groups (P ＜ 0.05).Compared with NP group,MWT was significantly increased,TWL was prolonged and the expression of Cav3.2 mRNA and protein was down-regulated in a concentration-dependent manner in K1-3 groups (P ＜ 0.05),and no significant change was found in the parameters mentioned above in group D (P ＞ 0.05).Conclusion CaMK Ⅱ is involved in the development and maintenance of chronic NP by up-regulating the expression of Cav3.2 T-type calcium channels in rat spinal cord.

Objective To evaluate the role of calcium/calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) in the neuronal damage induced by lidocaine.Methods SH-SY5Y cells were seeded in 96-well plates (100 μl/hole) with a density of 5 × 105/ml and randomly divided into 4 groups (n =63 each):normal culture group (C group),CaMK Ⅱ inhibitor KN93 (K group),lidocaine group (L group) and KN93 + lidocaine group (KL group).KN93 (final concentration 1 μmol/L) was added to the culture medium and the cells were then cultured for 24 h in group K.Lidocaine (final concentration 10 mmol/L) was added to the culture medium and the cells were then cultured for 24 h in group L.KN93 (final concentration 1 μmol/L) and lidocaine (final concentration 10 mmol/L) were added to the culture medium and the cells were then cultured for 24 h in group KL.The cell morphology was examined with microscope after 24 h of incubation.The viability of cells was measured by MTT assay before incubation and at 1,6,12 and 24 h of incubation.The apoptosis in the cells was assessed by flow cytometry.The apoptotic rate was calculated.Results Compared with C and K groups,the cell viability was significantly decreased and the apoptotic rate was increased in L and KL groups (P ＜ 0.05).The cell viability was significantly higher and the apoptotic rate was lower in group KL than in group L (P ＜ 0.05).There was no significant difference in the cell viability and apoptotic rate between C group and K group (P ＞ 0.05).The pathological changes were obviousin group L and significantly reduced in group KL.Conclusion CaMK Ⅱ is involved in the neuronal damage induced by lidocaine.

Objective To investigate the effects of post-operative analgesia with oxycodone or morphine for patients undergoing colon cancer radical surgery on platelet activation and cellular immunity.Methods Forty colon cancer patients scheduled for radical surgery, 23 males and 17 females, ASA physical status Ⅰ or Ⅱ, were randomly divided into 2 groups (n=20 each): oxycodone group (group O) and morphine group (group M).Patient-controlled intravenous analgesia (PCIA) was used for post-operative analgesia.PCIA solution contained oxycodone 1 mg/kg and tropisetron 6 mg in 100 ml normal saline in group O or morphine 1 mg/kg and tropisetron 6 mg in 100 ml normal saline in group M.Blood samples were obtained from the patients at 5 min before anesthesia induction (T0), 4 h after surgery (T1), 24 h after surgery (T2) and 48 h after surgery (T3).The levels of glycoprotein (GP)Ⅱb/Ⅲa, P-selection (CD62P), natural killer (NK) cells, NKT cells, and natural Treg (nTreg) cells were detected.The platelet aggregation rate (PAR) was determined.Results Compared with T0, the levers of GPⅡb/Ⅲa, CD62P, PAR and nTreg cells were significantly higher at T1 in group O and at T1, T2 in group M (P<0.05).Compared with T0, the levels of NK and NKT cells were decreased significantly at T1 in group O and at T1-T3 in group M (P<0.05).The levels of GPⅡb/Ⅲa, CD62P, PAR and nTreg cells at T2 and T3 in group O were decreased significantly as compared with group M (P<0.05).The levels of NK cells, NKT cells at T2 and T3 in group O were significantly higher than those in group M.Conclusion Post-operative analgesia with oxycodone for patients undergoing colon cancer radical surgery exhibits a more significant effect of decreasing platelets activity and presents a less disturbance on cellular immunity as compared with morphine.