Objective To investigate the effect of different doses of dexmedetomidine(Dex)on sevoflurane consumption in patients undergoing laparoscopic oophorocystectomy.Methods Eighty ASA Ⅰ or Ⅱ patients aged 25-50 yr with body mass index 18-25 kg/m2 undergoing laparoscopic oophorocystectomy were randomly divided into 4 groups (n =20): control group (group C),low dose Dex group(group DL),medium dose Dex group(group DM) and high dose Dex group(group DH).Normal saline 20 ml and Dex 0.3,0.6,0.9μg/kg was infused iv over 10 min at 10 min before skin incision in groups C,DL,DM and DH,respectively.End-tidal sevoflurane concentration (ETsev) was recorded before Dex administration(T1 ),skin incision(T2 ),immediately after pneumoperitoneum (T3 ),10 min of pneumoperitoneum(T4 ) and the end of surgery (T5 ).Duration of anesthesia,consumption of sevoflurane,emergence time,extubation time were recorded and restlessness at 10 min after extubation was also recorded.The concentrations of blood glucose and corticosteroid were measured by quickly by glucose analyzer and radio-immunity gefore anethesia induction (T0) and at T3,T4,T5 respectively.Results The consumption of sevoflurane per hour,ETsev at T2-5,concentrations of blood glucose and corticosteroid at T3-5 were decreased gradually in groups C,DL,DM and DH ( P ＜ 0.05).The emergence time and extubation time were shorter and the incidence of restlessness was lower in groups DL,DM and DH than in group C ( P ＜ 0.05 ).Conclusion Dexmedetomidine can reduce the consumption of sevoflurane in a dose-dependent manner in patients undergoing laparoscopic oophorocystectomy.

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.

Objective To evaluate the role of interleukin-4 receptor (IL-4R) in renal fibrosis following renal ischemia-reperfusion (I/R) injury in mice.Methods Twelve male wild type BALB/C mice and 12 IL-4Rα gene-knockout mice,aged 8-10 weeks,weighing 20-30 g,were used in the study.The mice of either type were divided into 2 groups (n =6 each) using a random number table:sham operation group (group S) and group I/R.In group I/R,renal I/R was induced by occlusion of the right renal artery for 1 h with atraumatic microclips followed by 2 weeks of reperfusion.The right renal artery was only isolated in group S.At 2 weeks of reperfusion,blood samples were taken from the orbital vein for determination of the concentrations of serum blood urea nitrogen (BUN) and creatinine (Cr).The renal tissues were obtained,and the renal fibrosis area was measured by Sirius Red staining.The expression of fibronectin (FN),collagen Ⅰ (COL-Ⅰ) and α-smooth muscle actin (α-SMA) in renal tissues was detected by immunofluorescence.The expression of signal transducer and activator of transcription 6 (STAT6) and phospho-STAT6 in renal tissues was determined by Western blot.The ratio of phoshop-STAT6 to STAT6 was calculated to reflect the phosphorylation of STAT6.Results Compared with group S of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly increased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly up-regulated,and the phosphorylation of STAT6 in renal tissues was significantly increased in group I/R of wild type and IL-4Rα KO mice (P＜0.05).Compared with group I/R of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly decreased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly down-regulated,and the phosphorylation of STAT6 in renal tissues was significantly decreased in group I/R of IL-4RαKO mice (P＜0.05).Conclusion The mechanism of renal fibrosis following renal I/R injury is partially related to IL-4R,and IL-4R results in renal fibrosis through promoting activation of STAT6 signaling pathway in mice.

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 construct rat TRESK gene recombinant adenovirus expression vector.Methods TRESK full-length cDNA was cloned from rat dorsal root ganglion cells and confirmed by RT-PCR and sequencing. pAd/CMV/V5-DEST-TRESK was then constructed under the control of CMV-promotor. DH5α colibacillus was translated and the positive recombinants were subsequently identified by PCR and DNA sequencing. 293T cells were cotransfected and packed to produce adenovirus. Results The titer of virus was tested using Hole-by-dilution titer method. The full length of TRESK from rat dorsal root ganglion cells is 781 bp. It was demonstrated that the DNA sequencing was completely consistent with TRESK sequencing of rat recorded in GeneBank. The PCR amplification of the pAd/CMV/V5-DEST-TRESK gDNA was matched with pAD-GFP blank vector as anticipated. The titer of the concentrated virus was 1.31×109 TU/ml. Conclusion Rat TRESK gene recombinant adenovirus vector is constructed successfully.

Objective To evaluate the changes in the expression of diplopore potassium ion channel TRESK mRNA in dorsal root ganlion (DRG) in rats with neuropathic pain (NP) .Methods Thirty-two male SD rats weighing 220-250 g were randomly divided into 2 groups ( n = 16 each) : group sham operation (group S) and group NP. NP was induced by ligation and severance of left tibial and common fibular nerves according to the technique described by Decosterd. Eight rats in each group were sacrificed 1 day before and 14 day after operation and their L4,5 DRGs in the operated side were isolated for determination of TRESK mRNA expression by RT-PCR. In the remaining 8 rats in each group paw withdrawal threshold to mechanical stimuli ( MWT) and paw withdrawal latency to a thermal nociceptive stimulus (TWL) were measured at 1 day before (baseline) and 1, 3, 5, 7, 14 day after operation. Results MWT was significantly lower in group NP than in group S. The TRESK mRNA expression in L4,5 DRGs in the operated side was significantly decreased after operation as compared with the baseline before operation in group NP and was significantly lower in group NP than in group S. Conclusion The development and maintenance of NP may be closely related with down-regulation of TRESK mRNA.

Objective To determine the half-effective target plasma concentration(EC50)of remifentanil inhibiting airway response when combined with propofol by TCI in patients undergoing fiberoptic bronchoscopy.Methods Forty ASAⅠorⅡ patients,aged 20-64 yr, undergoing elective fiberoptic bronchoscopy, were randomly divided into 2 groups (n = 20 each).Anesthesia was performed with TCI of remifentanil and propofol in both groups. The target effect site concentration of propofol was 3 μg/ml.The target effect site concentration of remifentanil was determined by up-and-down sequential hial. The target effect site concentration of remifentanil was set at 5 μg/ml in the first patient and the ratio of the target concentrations between the two consecutive patients was 1.1. BIS ≤ 60 was defined as the suitable depth of anesthesia in group A.The airway response≤grade Ⅱ was defined as the suitable depth of anesthesia in group B. The EC50 and 95% confidence interval (CI) required to inhibit the airway response were calculated in the two groups.Results The EC50 and 95% CI of remifentanil required to inhibit the airway response were 4.50μg/L (95% CI 3.88-5.36 μg/L)in group A and 4.10μg/L(95% GI 3.31-5.00 μg/L) in group B. The EC50 of remifentanil inhibiting airway response was significantly higher in group A than in group B. Conclusion The EC50 of remifentanil inhibiting airway response is 4.10 μg/L when combined with propofol by TGI (effect site concentration 3μg/ml)in patients undergoing bronchoscopy. BIS is not a suitable index assessing the depth of propofol-remifentanil anesthesia.

Objective To investigate the effect of sevoflurane preconditioning on TREK-1 channel expression in hippocampus after focal cerebral ischemia-reperfusion (I/R)in rats and the mechanism.Methods Thirty-six male SD rats weighing 240-280 g were randomly divided into 3 groups(n=12 each):group Ⅰ sham operation (group S),group Ⅱ I/R and group Ⅲ sevoflurane preconditioning (group Sevo).Focal cerebral ischemia was produced by inserting a 4-0 nylon thread with rounded tip into right internal jugular vein.The nylon thread was the nylon thread Wag about 18-20 Innl.The right middle cerebral artery(MCA)Wag occluded for 2 h and then released for 24 h reperfusion.The Sevo group inhaled 2.4% sevoflurane for 30 min at l h before ischemia.Neurological deftcits were assessed and scored at the end of 24 h reperfusion (the higher was the score,the severer was the deficit).The cerebral infarct size was determined by TTC staining and the TREK-1 mRNA in hippocampus by RT-PCR.Results The cerebral infarct size was significantly smaller and the neurological deficit scores were significantly lower in Sevo group than in I/R group.The TREK-1 mBNA expression was significantly up-regulated in Sevo group as compared with I/R group.Conclusion Sevoflurane preconditioning Can protect the brain against I/R injury by activating TREK-1 in hippocampus.

Objective To evaluate the role of T?type calcium channels in up?regulation of spinal Ca2+∕calmodulin?dependent protein kinase Ⅱ ( CaMKⅡ) expression in rats with neuropathic pain. Meth?ods Forty?eight male Sprague?Dawley rats, weighing 230-270 g, in which intrathecal catheters were suc?cessfully implanted, were divided into 4 groups ( n=12 each) using a random number table: sham opera?tion group (group S), neuropathic pain group (group NP), normal saline group (group NS), and T?type calcium channel blocker mibefradil group ( group M ) . The model of neuropathic pain was established by chronic compression of the dorsal root ganglion ( DRG) . Normal saline 20μl and mibefradil 200μg ( dilu?ted to 20μl in normal saline) were injected intrathecally at 5 days after compression of the DRG in NS and M groups, respectively. Before intrathecal catheter implantation ( T1 ) , before compression of the DRG ( T2 ) , at 5 days after compression of the DRG and before intrathecal administration ( T3 ) , and at 30, 60, 120 and 240 min after intrathecal administration ( T4?7 ) , the mechanical paw withdrawal threshold ( MWT) and thermal paw withdrawal latency ( TWL) were measured. The rats were sacrificed after the last measure?ment of the pain threshold at T7 , and the lumbar enlargement segments of the spinal cord were harvested for determination of CaMKⅡ expression by Western blot. Results Compared with group S, the MWT was significantly decreased, and TWL was significantly shortened at T3?7 , and the expression of spinal CaMKⅡ was significantly up?regulated in NP and M groups (P<0.05). Compared with group NP, the MWT wassignificantly increased, and TWL was significantly prolonged at T4?6, and the expression of spinal CaMKⅡwas significantly down?regulated in group M (P<0.05), and no significant change was found in the parame?ters mentioned above in group NS (P>0.05). Conclusion T?type calcium channels are opened, the intra?cellular free calcium ion concentrations are increased, and activated spinal CaMKⅡ is involved in the de?velopment of neuropathic pain in rats.

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.