Objective To evaluate the effect of intrathecal administration of ?-conopeptide SO3 on inducible nitric oxide synthase(iNOS)expression of spinal cord and the ligated sciatic nerve in a rat model with chronic constriction injury(CCI).Methods 40 male SD rats were randomly divided into 4 groups of 10 animals each.Rats in the N group served as controls;in group C 4 loose ligatures were placed around the right sciatic nerve for 14 days;in group CN,normal saline 1?l/h was injected intrathecally slowly for 7 days seven days after the ligation;in group CS,?-conopeptide SO3 30ng/h was administered intrathecally slowly for 7 days seven days after the ligature.Local expression of iNOS was assayed in samples taken from injured nerves(between and distal to the CCI site)and the spinal cord using Western blotting analysis,with GAPDH as an internal reference.Results A 130 kDa band,corresponding to iNOS protein was detected in the middle and distal sections of the injured nerves and the spinal cord.The iNOS immunoreactivity was inhibited by continuous intrathecal injection of ?-conopeptide SO3.There was no difference in the expression of iNOS between group CN and group C.Conclusion The expression of iNOS in the spinal cord and injured nerves of CCI rats was enhanced.Intrathecal injection of ?-conopeptide SO3 can inhibit the expression of iNOS.The data suggested that N-type calcium channel blocker took part in the expression of iNOS.

Objective To observe the effect of dexmedetomidine on inflammation, oxidative stress and lung injury in lipopolysaccharide( LPS)-induced septic mice.Methods Forty eight male adult BALB/c mice were randomly divided into three groups (n=16): normal control group (Ctrl), sepsis group (Sep), and Dex group.Ae septic mice model was established by LPS 20 mg/kg,and Dex 30μg/kg injected intraperitoneally at 0.5 h after LPS injection.The concentrations of serum IL-6 and IL-10 were detected at 2 h and 6 h after LPS injection while myeloperoxidase ( MPO ) activity and malondialdehyde( MDA) content of lungs were detected and weight dry ratio ( W/D) of lungs was calculated at 6 h after LPS injection.Pathological changes were observed in left lung HE stained with optical microscopy at 6 h after LPS injection. Results Compared with Sep group, the concentrations of serum IL-6 decreased significantly(P <0.05), while the concentrations of IL-10 increased significantly(P<0.05) at 2 h and 6 h after LPS injection in Dex group.MPO activity, MDA content and W/D of lungs decreased significantly(P<0.05) at 6 h after LPS injection in Dex group.The injury to the lung was lightened significantly under optical microscopy in Dex group.Conclusion Dex protects against LPS-induced ALI in septic mice by inhibiting systemic inflammatory response, reducing lung tissue inflammatory infiltration and oxidative stress.

AIM: To compare the blocking effect of ropivacaine and bupivacaine on sodium channels of rat dosal root ganglia(DRG) using whole cell recording technique. METHODS: Rat DRG neurons were enzymatically isolated , tetrodotoxin-sensitive(TTX-s) and tetrodotoxin-resistant (TTX-r) sodium currents of DRG were recorded by whole cell recording.Drugs were given in bath solution.The concentrations of ropivacaine were 10,30,100, 1 000 ?mol?L~ -1 and bupivacaine were 10,30,100,300 ?mol?L~ -1 . The recording number in each dose group was six. RESULTS: CsCl in extracellular fluid and TEA in intracellular fluid were used to block the potassium channels. Sodium currents were recorded when the holding potential was - 70 mV and a serials of pulse with step 10 mV and duration 70 ms was given.TTX-s sodium channel was recorded in 80.1 % large DRG cells and TTX-r sodium channel was recorded in 92.4 % medium and small DRG cells,of which 56.3 % cells had no response to 1 ?mol?L~ -1 TTX. The half-maximal blocking concentrations of ropivacaine on TTX-r sodium channel was 65.7 ? 6.1 ?mol?L~ -1 , which was much lower than that on TTX-s sodium channel 246.8 ? 11.2 ?mol?L~ -1 (P 0.05 ). CONCLUSION: Ropivacaine preferentially blocks TTX-r sodium channel.Selective blocking of TTX-r and TTX-s sodium channel was one of the reasons of seperation of sensation and motion when it is used in epidural anesthesia.

Objective To observe the effects of propofol and etomidate on inflammation and ox-idative stress in septic mice.Methods Sixty-four male adult BALB/c mice were randomly divided into four groups:normal control group (N),sepsis group (S),propofol treatment group (P)and etomid-ate treatment group (E).The septic mice model was established by lipopolysaccharide (LPS,20 mg/kg)intraperitoneal injection,and propofol (60 mg/kg)or etomidate (10 mg/kg)was injected in the abdominal cavity at 0.5 h after LPS injection.Serum interleukin-6 (IL-6)concentrations and in-terleukin-10 (IL-10)concentrations were measured at 2 h and 6 h after LPS injection;malondialde-hyde (MDA)content of lung,liver and kidney tissue was measured at 6 h after LPS injection. Results Compared with group N,serum IL-6 concentrations increased significantly (P <0.05),and IL-10 concentrations decreased significantly (P <0.05)at 2 h and 6 h after LPS injection in group S;MDA content of lung,liver,kidney increased significantly (P <0.05 )at 6 h after LPS injection in group S;Compared with group S,serum IL-6 concentrations decreased significantly (P <0.05),and IL-10 concentrations increased significantly (P < 0.05 )at 2 h and 6 h after LPS injection in both group P and E;MDA content of lung,liver,kidney decreased significantly (P <0.05 )at 6 h after LPS injection in group E,but only MDA content of lung decreased significantly (P <0.05)at 6 h af-ter LPS injection in group P;Compared with group P,serum IL-6 concentrations was significantly lower (P <0.05),and IL-10 concentrations was significantly higher (P <0.05)at 2 h and 6 h after LPS injection in group E;MDA content of lung,liver,kidney was significantly lower (P <0.05)at 6 h after LPS injection in group E.Conclusion Both propofol and etomidate injected in the abdominal cavity can reduce injury of inflammatory and oxidative stress in septic mice induced by LPS,and the effect of etomidate is more significant.

Objective To review our experiences on perioperative anesthetic management for patients who received percutaneous nephroscopic peripancreatic necrectomy for acute necrotizing pancreatitis.Method The clinical data on 18 patients with acute necrotizing pancreatitis who received percutaneous nephroscopic peripancreatic necrectomy in our hospital from August 2008 to January 2011 were retrospectively analyzed.Results There was a marked fluctuation in hemodynamic status of the patients which required the use of vasoactive drugs during perioperative period.PETCO2 significantly increased after pneumoperitoneum.Tracheal extubation was possible in 11 patients immediately after surgery in the operation room,while 7 patients required tracheal intuhation to be transported back to the surgical intensive care unit (SICU).Conclusion Most patients who underwent percutaneous nephroscopic peripancreatic necrectomy had a varying degree of shock and multi-organ injury before operation.Proper anesthetic induction and maintenance,correct use of vasoactive drugs and lung protective ventilation strategy,and active fluid resuscitation are the keys to good perioperative anesthetic management and to improve treatment results.

Objective To explore the anesthetic effects of repeated administration of propofol combined with vitamin C in mice. Methods Forty mice were subjected to daily intraperitoneal injections of 80 mg/kg propofol (P80 group), 70 mg/kg propofol and 50 mg/kg vitamin C (P70+Vc50 group), 55 mg/kg propofol and 100 mg/kg vitamin C (P55+Vc100 group), or 50 mg/kg propofol and 200 mg/kg vitamin C (P50+Vc200 group) for 6 consecutive days, and the anesthesia induction time and anesthesia duration were recorded. Results Compared with the P80 group, the mice in P55 + Vc100 group and P50 + Vc200 group showed significantly shorter anesthesia duration on the first 3 days (P<0.05). In all the groups, anesthesia duration was significantly shortened in the following days compared with that on day 1 (P<0.01);anesthesia duration was shorter on day 3 than on day 2 in P50+Vc200 group (P<0.01), and was shorter on days 4, 5, and 6 than on day 2 in all the groups (P<0.01). In all the groups, the rate of loss of righting reflex (LORR) decreased gradually with time in a similar pattern. Conclusions Vitamin C can reduce the dose of propofol without obviously affecting the anesthetic effect to reduce the incidence of drug tolerance and potential dose-related side effects of propofol.

Objective To investigate the protective effects of dexmedetomidine (Dex) against glutamate-induced cytotoxicity in PC12 cells and its mechanism.Methods PC12 cells were treated with varying concentrations of dexmedetomidine 1 h before exposure to a high concentration of glutamate.The cell viability was measured by MTT assay,and LDH release,MDA content and SOD activity were measured.The level of ROS was tested by DCFH-DA staining and flow cytometry.The level of intracellular Ca2+ was detected by Fluo-8 staining and flow cytometry,and the mitochondrial membrane potential (MMP) was determined with JC-1 staining and flow cytometry.Results Within the concentration range of 0.01 to 100 μrnol/L,Dex dose-dependently protected PC12 cells against glutamate-induced cytotoxicity.Treatment with 100 μmol/L Dex significantly increased the cell viability to (86.6±2.2)％ of that of the control cells (P＜0.01) and decreased LDH release to 1.4±0.1 folds of the control level (P＜0.01).In PC12 cells exposed to glutamate,Dex pretreatment significantly reduced MDA content (P＜0.01),enhanced SOD activity (P＜0.01),inhibited ROS overproduction (P＜0.01),reduced intracellular Ca2 + level (P＜0.01) and maintained a stable MMP (P＜0.01).Conclusion Dexmedetomidine can protect PC12 cells against glutamate-induced injury possibly in relation with its anti-oxidative activity,inhibitory effect on intracellular calcium overload and protective effect of the mitochondria.

Objective To explore the anesthetic effects of repeated administration of propofol combined with vitamin C in mice. Methods Forty mice were subjected to daily intraperitoneal injections of 80 mg/kg propofol (P80 group), 70 mg/kg propofol and 50 mg/kg vitamin C (P70+Vc50 group), 55 mg/kg propofol and 100 mg/kg vitamin C (P55+Vc100 group), or 50 mg/kg propofol and 200 mg/kg vitamin C (P50+Vc200 group) for 6 consecutive days, and the anesthesia induction time and anesthesia duration were recorded. Results Compared with the P80 group, the mice in P55 + Vc100 group and P50 + Vc200 group showed significantly shorter anesthesia duration on the first 3 days (P<0.05). In all the groups, anesthesia duration was significantly shortened in the following days compared with that on day 1 (P<0.01);anesthesia duration was shorter on day 3 than on day 2 in P50+Vc200 group (P<0.01), and was shorter on days 4, 5, and 6 than on day 2 in all the groups (P<0.01). In all the groups, the rate of loss of righting reflex (LORR) decreased gradually with time in a similar pattern. Conclusions Vitamin C can reduce the dose of propofol without obviously affecting the anesthetic effect to reduce the incidence of drug tolerance and potential dose-related side effects of propofol.

Objective To investigate the protective effects of dexmedetomidine (Dex) against glutamate-induced cytotoxicity in PC12 cells and its mechanism.Methods PC12 cells were treated with varying concentrations of dexmedetomidine 1 h before exposure to a high concentration of glutamate.The cell viability was measured by MTT assay,and LDH release,MDA content and SOD activity were measured.The level of ROS was tested by DCFH-DA staining and flow cytometry.The level of intracellular Ca2+ was detected by Fluo-8 staining and flow cytometry,and the mitochondrial membrane potential (MMP) was determined with JC-1 staining and flow cytometry.Results Within the concentration range of 0.01 to 100 μrnol/L,Dex dose-dependently protected PC12 cells against glutamate-induced cytotoxicity.Treatment with 100 μmol/L Dex significantly increased the cell viability to (86.6±2.2)％ of that of the control cells (P＜0.01) and decreased LDH release to 1.4±0.1 folds of the control level (P＜0.01).In PC12 cells exposed to glutamate,Dex pretreatment significantly reduced MDA content (P＜0.01),enhanced SOD activity (P＜0.01),inhibited ROS overproduction (P＜0.01),reduced intracellular Ca2 + level (P＜0.01) and maintained a stable MMP (P＜0.01).Conclusion Dexmedetomidine can protect PC12 cells against glutamate-induced injury possibly in relation with its anti-oxidative activity,inhibitory effect on intracellular calcium overload and protective effect of the mitochondria.

OBJECTIVETo explore the anesthetic effects of repeated administration of propofol combined with vitamin C in mice.

METHODSForty mice were subjected to daily intraperitoneal injections of 80 mg/kg propofol (P80 group), 70 mg/kg propofol and 50 mg/kg vitamin C (P70+Vc50 group), 55 mg/kg propofol and 100 mg/kg vitamin C (P55+Vc100 group), or 50 mg/kg propofol and 200 mg/kg vitamin C (P50+Vc200 group) for 6 consecutive days, and the anesthesia induction time and anesthesia duration were recorded.

RESULTSCompared with the P80 group, the mice in P55 + Vc100 group and P50 + Vc200 group showed significantly shorter anesthesia duration on the first 3 days (P<0.05). In all the groups, anesthesia duration was significantly shortened in the following days compared with that on day 1 (P<0.01); anesthesia duration was shorter on day 3 than on day 2 in P50 + Vc200 group (P<0.01), and was shorter on days 4, 5, and 6 than on day 2 in all the groups (P<0.01). In all the groups, the rate of loss of righting reflex (LORR) decreased gradually with time in a similar pattern.

CONCLUSIONVitamin C can reduce the dose of propofol without obviously affecting the anesthetic effect to reduce the incidence of drug tolerance and potential dose-related side effects of propofol.

Anesthesia ; Anesthesia Recovery Period ; Anesthetics, Intravenous ; administration & dosage ; pharmacology ; Animals ; Ascorbic Acid ; administration & dosage ; pharmacology ; Drug Tolerance ; Mice ; Propofol ; administration & dosage ; pharmacology