Objective To explore the effect and significance of propofol combined with a small dose of butorphanol in anesthesia abortion surgury.Methods Retrospective analysis of 2145 cases of the propofol combined with a small dose of butorphanol on the anesthesia abortion surgery of the anesthesia effect,side effects,anesthesia,surgery time,recovery time,discharge time,cost,etc.Results The excellent rate of narcotic analgesia was 99.9％,the satisfaction rate of the patients was 100％,4.5％ incidence of adverse events,mainly body movements and allergies.The average amount of anesthetic propofol was ( 95 ± 15) mg,the butorphanol was 0.6mg;the operative time was (5.4 ±1.6) min,the patients alert in ( 1.8 ± 0.6) min,and discharged from the hospital 0.5 to 1 hour after the surgery.Conclusion The propofol combined with a small dose of butorphanol used in anesthesia abortion surgery has good curative effects,safety,low incidence of side effects,cheap price.

Objective To compare the polysaccharide content of pseudostellaria heterophylla which produced in various areas and in different parts of them. Methods The polysaccharide content of pseudostellaria heterophylla was determined by phenol-sulfuric acid method. Results The polysaccharide content of pseudostellaria heterophylla produced in Fujian is the highest, Jiangsu and Guizhou are second-class. The polysaccharide content has some disparity in the bodies and in the roots of pseudostellaria heterophylla. Conclusions The polysaccharide content in the bodies differs 1.96% with that in the roots. This experiment provides theory foundation for scientific preparation of pseudostellaria heterophylla.

Objective To investigate the effect of intrathecal hyperbaric bupivacaine on spinal cord neurons apoptosis in diabetic neuropathic rats.Methods Thirty-two healthy male Sprague-Daw-ley rats weighing 220-300 g,8 normal rats randomly served as control group (group C),the other rats were intraperitoneal injection 1% streptozotocin (STZ)60 mg/kg to induce diabetic neuropathic (DN),and last induced thirty-seven diabetic neuropathic rats.group C and diabetic neuropathic rats administer intrathecal catheter,respectively.Twenty-four rats in which DN was successfully intrathe-cal catheter were randomly divided into 3 groups (n=8):hyperbaric bupivacaine group (group HB), isobaric bupivacaine group (group IB),glucose group (group G).Hyperbaric bupivacaine 10 μl were injected intrathecally in groups C and HB respectively,isobaric lidocaine 10 μl were injected intrathe-cally in group IB,10% glucose 10 μl were injected intrathecally in group G,once daily for 3d.After rats each administration 2 min,motor block duration were recorded;The paw withdrawal threshold to von Frey filament stimulation (PWT)were measured before induced diabetes model (T1 ),before in-jected intrathecally (T2 ),after 30 min administered 1 d (T3 ),2 d (T4 ),3 d (T5 )and end administered 4 d (T6 ).All rats were sacrificed at T6 and their lumbar intumescential spinal cord tissue were re-moved for microscopic examination.And using TUNEL assay to measure spinal neuronal apoptosis. Results PWT was lower at T2-5 in groups HB,IB and G comparing with T1 (P <0.05 ).Comparing with group C,the motor block duration was significantly prolonged(P <0.05)and spinal cord neuro-nal apoptosis cells were increased(P <0.05)in group HB.Comparing with group IB,the motor block duration was significantly prolonged(P <0.05)and spinal cord neuronal apoptosis cells were increased (P <0.05)in group HB,too.PWT was increased at T6 in group HB at T2-T5 (P <0.05).Group G did not appear motor block and spinal cord neuronal apoptosis.Conclusion Intrathecally hyperbaric bupi-vacaine can promote spinal cord neuronal apoptosis in diabetic neuropathic rats.

Objective To investigate the effects of Saikosaponin A (SSA)on cognitive function and cAMP/CREB signaling pathway and expression of BDNF in mice after traumatic brain injury. Methods Sixty SD male mice were randomized into three groups:shame operation group (group S, n =20),trauma group (group T,n =20)and SSA treatment group (group A,n =20).Mice received an administration of SSA 5 mg/kg (group A)or equal volume saline (group S,group T)immediately and once daily for 5 consecutive days after trauma.The cognitive function was detected by Morris wa-ter maze test on day 1,3,7 and 14 after trauma.The hippocampal tissues were harvested after be-havioral tests and homogenized for measuring the levels of brain derived neurophic factor (BDNF)and cyclic AMP (cAMP)by ELISA as well as the levels of cAMP-response element binding protein (CREB)and phosphorylation-cAMP-response element binding protein (pCREB)by western bolt. Results Compared with group S,the escape latency and swimming distance were significantly pro-longed in group T on day 1,3,7 and 14 and group A on day 1,3 after trauma (P <0.05 );while compared with group T,they were significantly shorter in group A on day 7,14 after trauma (P <0.05).Compared with group S,the levels of BDNF,cAMP,CREB and pCREB were significantly de-creased in group T(P < 0.05 ).Compared with group T,the levels of BDNF,cAMP,CREB and pCREB were significantly increased in group A (P <0.05).Conclusion SSA can significantly improve cognitive dysfunction in mice after traumatic brain injury,and the mechanism may be related to the activation of cAMP/CREB signaling pathway and up-regulation of BDNF.

Objective To evaluate the effect of hyperbaric factor on lidocaine-induced apoptosis in spinal neurons in rats with diabetic neuropathic pain.Methods Healthy male Sprague-Dawley rats,weighing 220-300 g,were used in the study.Diabetic neuropathic pain was induced by high-sugar high-fat diet + intraperitoneal 1％ streptozotocin (STZ) 30 mg/kg and confirmed by blood glucose level ＞ 16.65 mmol/L at 3 days after STZ injection and then intrathecal catheter was placed.Twenty-four rats with diabetic neuropathic pain in which IT catheters were successfully implanted were randomly divided into 3 groups (n =8 each):hyperbaric lidocaine group (group HL),isobaric lidocaine group (group IL),and glucose group (group G).Another 8 rats in which IT catheters were successfully inserted served as control group (group C).2％ hyperbaric lidocaine 10 μl (in C and HL groups),2％ isobaric lidocaine 10 μl (in group IL),or 10％ glucose 10 μl (in group G) was injected intrathecally once a day for 3 consecutive days.The duration of motor block was recorded at 2 min after each administration.The paw withdrawal threshold to von Frey filament stimulation (PWT) was measured before STZ injection (T1),before IT injection (T2),at 30 min after administration on 1st,2nd and 3rd days and on day 5 after the end of administration (T3-6).All the rats were sacrificed at T6 and their L4,5 segments of the spinal cord were removed for microscopic examination.The apoptosis in spinal neurons was detected using TUNEL assay.Results Compared with the baseline value at T1,PWT was significantly decreased at T2-5 in HL,IL and G groups.PWT was significantly higher at T6 than at T2-5 in group HL.Compared with group C,the duration of motor block was significantly prolonged and the apoptotic index was increased in group HL.Compared with group IL,the duration of motor block was significantly prolonged and the apoptotic index was increased in group HL.Conclusion Hyperbaric factor can promote lidocaine-induced apoptosis in spinal neurons in rats with diabetic neuropathic pain.

Objective To evaluate the effect of perioperative administration of dexmedetomidine on postoperative ileus after laparocolectomy.Methods Sixty patients scheduled for abdominal surgery were randomly divided into two groups,30 in each group.Group D received dexme-detomidine administeration at a loading dose of 0.6 μg/kg for 10 minutes before induction,followed by an infusion rate of 0.5 μg·kg-1 ·h-1 to 30 min before the end of surgery.The control group re-ceived saline instead of Dex.After the surgery,Group C received intravenous sufentanyl 2 μg/kg, while group D sufentanyl 2 μg/kg combined with Dex 2 μg/kg.Heart rate variability (HRV)were detected before Dex infusion (T0 ),10 minutes after intubation (T1 ), 10 minutes after CO 2 insufflation (T2 ),1 hour after CO 2 insufflation (T3 ),10 minutes after CO 2 desufflation (T4 ),and 10 minutes after extubation(T5 ).The plasma concentrations of epinephrine(E)and norepinephrine (NE)were determined at T0 ,T3 ,T5 ,T7 and T1 0.The recovery of bowel function was evaluated in terms of the first time to fart and intake food.Results Compared with T0 ,HRV of power (TP), high-frequency (HF)power,low-frequency (LF)power and the ratio of LF/HF power were signifi-cantly decreased at T1-T4 in group C and at T1-T5 in group D.The plasma concentrations of E and NE were higher at T3 ,T5 ,T7 and T1 0 in both group C and group D (P <0.05).Compared with T1 ,TP, LF and the ratio of LF/HF were increased at T2-T4 (P <0.05).Compared with group C,TP,LF and the ratio of LF/HF were decreased at T2-T5 ,The plasma concentrations of E and NE were decreased at T3 ,T5 ,T7 and T10 and the time of first flatus was earlier(P <0.05).Conclusion The perioperative ad-ministration of dexmedetomidine during laparocolectomy facilitated the early recovery of bowel func-tion after surgery and decreasede the time of postoperative ileus.

Objective To evaluate the role of C-Jun N-Terminal kinase (JNK) signaling pathway in dexmedetomidine-induced reduction of spinal neurotoxicity induced by lidocaine in rats.Methods Seventy-two adult male Sprague-Dawley rats, weighing 280-320 g, in which intrathecal catheters were successfully implanted without complications, were randomly divided into 6 groups (n =12 each) using a random number table: control group (group C);SP600125 (JNK signaling pathway blocker) group (group SP);dexmedetomidine group (group D);lidocaine group (group L);dexmedetomidine + lidocaine group (group DL);SP600125+lidocaine group (group SPL).Dimethyl sulfoxide (DMSO) 20 μl was injected intrathecally in group C.SP600125 30 μg and 10％ lidocaine 20 μl were injected intrathecally in SP and L groups, respectively.At 20 min after intrathecal injection of 10％ lidocaine, dexmedetomidine 75 μg/kg was injected intraperitoneally in group DL, and SP600125 30 μg was injected intrathecally in group SPL.Dexmedetomidine 75 μg/kg was injected intraperitoneally in group D.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured before intrathecal catheters were implanted (T0), before intrathecal administration (T1), and at 4, 8 and 12 h and 1, 2, 3, 4, 5 and 6 days after intrathecal administration (T2-10).At 24 h after intrathecal administration, 6 rats randomly selected from each group were sacrificed.The lumbar segment (L4-5) of the spinal cord was removed for detection of cell apoptosis (by TUNEL) and phosphorylated JNK (p-JNK) expression (by Western blot).The apoptotic index was calculated.Results Compared with group C, no significant change was found in the MWT, TWL, apoptotic index and expression of p-JNK in SP and D groups (P＞0.05), the MWT at T2-8 in group L, at T2-6 in group DL and at T2-5 in group SPL were significantly increased, the TWL at T2-8 in group L, at T2-5 in group DL and at T2-4 in group SPL were prolonged, and the apoptotic index and expression of p-JNK were increased in DL, SPL and L groups (P＜0.05).Compared with group L, the MWT was significantly decreased, and the TWL was shortened at T2-8, and the apoptotic index and expression of p-JNK were decreased in DL and SPL groups (P＜0.05).Conclusion The mechanism by which dexmedetomidine mitigates spinal neurotoxicity induced by lidocaine is related to inhibited activation of JNK signaling pathway in rats.

Objective To explore the similarities and differences between finger photoplethysmogram (PPG) and CSI in monitoring the depth of anaesthesia in Chinese adults under general anaesthesia. Methods Ninety-three patients, ASA ⅠorⅡ, aged 20-67, under general anaesthesia were enrolled. Anaesthesia was induced with target-controlled infusion (TCI) of propofol. The initial TCI concentration of propofol was set at 0.5 mg·L-1 followed by increments of 0.5 mg·L-1 at 3-min interval until the score of Modified Observer's Assessment of Alertness/Sedation Scale (MOAAS)reached 0. PPG and CSI were continuously monitored and their values were recorded every 2-4 seconds. MOAAS was recorded every 30 seconds to evaluate the sedation level in the study period. ResultsFor the periodfrom pre-induction to pre-intubation, the difference of photoplethysmogram amplitudevalues had statistical significance between level 4 and level 3, level 3 and level 2 of MOAAS (P<0.05). CSIvalues declined along with the decrease of MOAAS levels and were statistically different between every two neighboring levels of MOAAS (P < 0.05). Photoplethysmogram amplitude (PPGA) and pulse beat interval (PBI) values showed significant differences before and after intubation, pre- and post-incision (P < 0.05). Conclusions PPGA and PBI appear to be suitable to monitor the nociceptive component of balanced general anesthesia , while the CSI exhibits a good performance in monitoring the sedation or hypnotic component of balanced general anesthesia , thusthe combination of PPGA and CSI would benefit the monitoring of the adequacy of depth of anaesthesia.

Objective To evaluate the role of p38 MAPK signal transduction pathway in dexmedetomidine against neurotoxicity induced by bupivacaine.Methods Seventy-two adult male SD rats,successfully implanted with intrathecal catheter without complications,were randomly divided into 6 groups: control group (group C);p38MAPK inhibitor group(group SB);dexmedetomidine group (group D);bupivacaine group (group B);dexmedetomidine and bupivacaine group (group DB);p38MAPK inhibitor and bupivacaine group (group SBB).DMSO 20 μl were injected intrathecally in group C;p38MAPK inhibitor 30 μg and 5% bupivacaine were respectively injected intrathecally in group SB and B;group DB and SBB were respectivel pretreated with dexmedetomidine 75 μg/kg intraperitoneally and p38MAPK inhibitor 30 μg intrathecal injection 20 min before intrathecally injected 5% bupivacaine.Dexmedetomidine 75 μg/kg was injected intraperitoneally in group D.Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured before intrathecal catheter was implanted (T0),before intrathecal administration (T1) and at 4,8 and 12 h and on 1,2,3,4,5 and 6 days after intrathecal administration (T2-T10).At 24 h after intrathecal administration,6 rats were randomly chosen from each group and sacrificed.The lumbar segment (L4-5) of the spinal cord was removed for detecting neuronal apoptosis (by TUNEL) and phosporylated p38MAPK(p-p38MAPK) expression (by Western blot).Results Compared with T0,MWT was significantly increased and TWL was prolonged at T2-T9 in group B,MWT at T2-T7 was significantly increased and TWL at T2-T6 was prolonged in group DB,MWT was significantly increased and TWL was prolonged at T2-T5 in group SBB (P<0.05).Compared with group C,no significant difference was found in MWT,TWL,the apoptotic index and expression of p-p38MAPK in groups D and SB.MWT was significantly increased and TWL was prolonged at T2-T9 in group B,the apoptotic index and expression of p-p38MAPK were significantly increased in group B (P<0.05).Compared with group B,MWT and TWL at T2-T9,the apoptotic index and expression of p-p38MAPK were significantly decreased in groups DB and SBB (P<0.05).Conclusion Dexmedetomidine can inhibit spinal neurotoxicity induced by bupivacaine in rats via inhibiting apoptosis in spinal cord,and inhibition of p38 MAPK signal transduction pathway may be involved in the underlying mechanism.

Objective To investigate the role of Rho/Rock signaling pathways in ventilator-in-duced lung injury in rats.Methods Ninety-six male SD rats,weighing 300-350 g,were equally and randomly divided into four groups using a random number table (n =24 each):control group (group C),fasudil group (group F),high tidal volume group (group H)and high tidal volume + fasudil group (group HF).Rats in group C and group F received no mechanical ventilation,rats in group H and group HF were intubated and mechanically ventilated (VT = 40 ml/kg,RR = 40 beats per minutes,FiO 2 =40%)for 4 h.The animals in group F and group HF were given intraperitoneal in-jection of fasudil 10 mg/kg at the time 1 h before mechanically ventilated.Six rats were chosen in each group at the time before ventilation (T0 )and at 4,8,24 h after ventilation (T1-T3 ),and blood sam-ples were taken for determination of the levels of serum tumor necrosis factor-α (TNF-α),IL-6 and IL-10,lungs were removed,bronchoalveolar lavage fluid (BALF)was collected to examine protein content,wet/drying (W/D)ratio was determined,which were then stained with haematoxylin and e-osin and examined under microscope,the pathological changes of lungs were scored.Myeloperoxidase (MPO)activity in lung tissue was determined by spectrophptometry.Protein and gene expression of RhoA and Rock2 in the lung tissue were detected by Western blot and reverse transcription PCR (RT-PCR).Results Compared with group C,the serum TNF-α,IL-6 and IL-10,BALF protein content, W/D ratio,the pathological scores,MPO activity,the expression of RhoA,Rock2 protein and mR-NA were significantly increased in group H and HF at T1-T3 (P <0.05 ).Compared with group H, the serum TNF-αand IL-6,BALF protein content,W/D ratio,the pathological scores,MPO activi-ty,the expression of RhoA,Rock2 protein and mRNA were significantly decreased,and the serum IL-10 was significantly increased in group HF at T1-T3 (P <0.05).Conclusion Fasudil can attenuate ventilator-induced lung injury in rats,and the mechanism may be associated with inhibition of the Rho/Rock signaling pathways reducing the inflammatory response.