Objective To investigate the effect of epidural anesthesia for painless labor on the birth process and newborn,and to provide a reference for the implementation of painless labor.Methods From January 2013 to January 2015 in our hospital,102 pregnant women were randomly divided into observation group and control group, 51 cases in each group.The observation group used sufentanil combined with ropivacaine for labor analgesia,and the control group received conventional natural childbirth measures for labor.Compared the two groups of maternal analge-sia effect,duration,the rate of vaginal delivery and postpartum 2 hours the amount of bleeding,and compared the two groups of fetal distress and neonatal asphyxia incidence.Results The maternal effect rate and total efficiency in the observation group were 62.75%,96.08%,which were significantly higher than those of the control group (P <0.05).In the observation group,the first birth process was (251.82 ±93.64)min,the second stage of labor was (54.72 ±2.561)min,which were significantly less than those of the control group (P <0.05 );birth rate of the observation group was 74.51%,postpartum 2 hours bleeding (227.52 ±31.73)mL,fetal distress occurred rate was 1.96%,newborn asphyxia occurrence rate was 1.96%,and compared with the control group,the differences were not statistically significant (P >0.05).Conclusion Epidural block anesthesia of painless labor can effectively relieve the pain of delivery,reduce maternal labor and the second stage of history,and has good safety of mother to child,it is worth popularization and application.

Aim To investigate the effects of propofol and lidocaine on P2X7-gated currents and the interaction of both drugs.Methods RAW2647 macrophages were cultured,whole-cell patch clamp technique was used to record the P2X7-gated currents induced by ATP with two times EC50 level under 1~100 ?mol?L-1 propofol or 10~1 000 ?mol?L-1 lidocaine. Then,propofol of IC50 level and lidocaine with 10~1 000 ?mol?L-1 were administered,and the P2X7-gated currents were recorded.Results Propofol and lidocaine could inhibit P2X7-gated currents in a concentration-dependent manner,and the IC50 level was (36.5?5.3) ?mol?L-1 and (223?34) ?mol?L-1,respectively. Lidocaine with high concentration (300 ?mol?L-1,1 000 ?mol?L-1) following the administration of propofol of EC50 level could increase the P2X7-gated currents(P

Objective To explore the correlation between the prealbumin synthetic rate and liver function damage in patients with liver cirrhosis resulted from hepatitis. Methods The prealbumin synthetic rate was measured using isotope tracer technique of 15 N-lysine injected by intravenous followed by intravenous drop at constant rate in 23 patients with liver cirrhosis and 12 healthy subjects. Results Prealbumin synthetic rate in the patients decreased significantly than that in normal control(P

Objective To investigate the effect of thiopental sodium (TPS) on spontaneous and KCl-evoked glutamate release from prefrontal cortical synaptosomes in rats and the effect of bicuculline on this effect ofTPS.Methods SD rats of both sexes (200-250 g) were decapitated and brains were removed. The prefrontalcortex was dissected and added to ice-cold sucrose solution and homogenized. The homogenate was centrifuged at1000 g at 0℃-4℃ for 5 min. The supernatant was again centrifuged at 12 000 g for 20 min. The sediment wascrude synaptosomes, which was added to artificial cerebro-spinal fluid (ACSF). The crude synaptosomes weredivided into 5 groups (n = 8): control group and 4 TPS groups. In control group no TPS was added while in TPSgroups different concentrations of TPS was added and the final concentration of TPS was 10, 30, 100, 300?mol?L~(-1) respectively. The synaptosomes were then placed with or without KCl in water bath at 37℃ for 15 min. Thespontaneous or KCl-evoked glutamate release was measured using high-performance liquid chromatograph (HPLC).In another set of experiment bicuculline 0. 1 mmol?L~(-1) was added to ACSF in each group before 15 min water bathto see if it could antogonize the effect of TPS on glutamate release. Results TPS 30, 100 and 300 ?mol?L~(-1)could significantly inhibit the spontaneous or KCl-evoked glutamate release compared with control group (P0.05). Bicuculline 0. 1 mmol?L~(-1) had no effect on the glutamate release in control group but could antagonize the inhibitory effect of TPS on glutamate release. Afteraddition of bicucculline the glutamate released in control group was not significantly different from that in the TPSgroups.Conclusion TPS sodium can inhibit the spontaneous or KCl-evoked glutamate release from prefrontalcortical synaptosomes in a concentration-dependent manner. The inhibitory effect is mediated by GABA_A receptors.

AIM: To investigate the dynamic changes of ATPases and NOS activities and NO production at different anesthesia phases using thiopental and propofol andifferent anesthetic phases (induction, anesthesia, restoration, and awake), the activities of NOS and ATPase and NO production in cortex and brain stem were meagroup. RESULTS: Ca2+ -ATPase and Na+ ,K+ -ATPase activities in the cortex and brain stem were significantly decreased after administration ofthiopental and propofol,especially at induction, anesthesia, or even restoration phase of thiopental group (P＜0.05, P＜0.01) and at anesthesia phase of propofol group (P＜0.05). NOS activities and NO production decreased from induction to restoration phase with thiopental and propofol anesthesia (P＜0.01). The parameters were returned near to the normal at awaken phase. CONCLUSION: Activities of ATPases and NOS and the production of NO may mediate the anesthesia effects of thiopental and propofol in the rat cortex and brain stem.

Objective To investigate the effects of propofol on P2X7 receptor activition and IL-1β production induced by endotoxin in murine RAW264.7 macrophages. Methods RAW264.7 macruphages were treated with LPS (1 μg/ml) for 4 h to induce the production and release of IL-1β, and pretreated with BBG (specific P2X7 receptor antagonist) 1 μmol/L or propofol 1-100 μmol/L for 20 min before LPS stimulation, and IL-1β release was measured using ELISA kit. Whole-cell patch clamp technique was used to record the P2X7-gated currents induced by 1 mmol/L ATP, the cells were exposed to propofol with 1-1 000 -μmol/L for 4 min, and the IC_(50) level of propofol was achieved. Western blot technique was used to measure the production of pro-lL-1β protein and IL-1β protein intracellularly after LPS treatment for 4 h under different concentrations of propofol. Results IL-1β was released from RAW264.7 macrophages after LPS stimulation, which was decreased by propofol, and the IC_(50) level of propefol was (24±3) μmol/L. P2XT-gated currents were inhibited by propofol, and the IC_(50) level was (33±5) μmol/L. Pro-IL-1β protein intracellularly was up-regulated after LPS stimulation, and propofol with 3-100 μmol/L decreased the up-regulation of pro-IL-1β intracellularly induced by LPS. Conclusion Propefol could inhibit IL-1β release from RAW264.7 macrophages treated by LPS, which is mediated by inhibiting P2X7 receptor activition and decreasing the production of pro-IL-1β intracellularly.

Objective To explore the recovery rate of exhale CO 2 and energy expenditure in the patients with cirrhosis.Methods The recovery rate of exhale CO 2 and energy expenditure in fourteen patients with cirrhosis and eleven healthy subjects were measured by using NaH 13 CO 3 as tracer.After overnight fast,all subjects were intravenously given NaH 13 CO 3 at a primed constant rate of infusion for two hours after a saturating dose infusion.Amount of 13 CO 2 in exhale air was measured using stable isotope mass spectrometry analysis,and the recovery rate of exhale CO 2 and energy expenditure were calculated.Results The recovery rate of exhale CO 2 in patients with Cirrhosis was (80 7?0 26)%,and in healthy control subjects was (78 3?0 84)%,which showed a significantly different between the two groups(P0 05)[(30 2?2 4)Kcal?kg -1 ?d -1 and (28 4?3 5)Kcal?kg -1 ?d -1 ,respectively].Conclusions The results provide theoretical basic to calculate meals for nutritional therapy in the patients with cirrhosis.

Aim To investigate the effect of thiopental sodium on the release of glutamate and GABA from synaptosomes of rats prefrontal cortex. Methods Synaptosomes were made from rats prefrontal cortex and incubated with artificial cerebral and spinal fluid (aCSF), then divided into five groups: group base release (Base), group thiopental sodium 10 ?mol?L -1 (THS 10), group thiopental sodium 30 ?mol?L -1 (THS 30), group thiopen tal sodium 100 ?mol?L -1 (THS 100) and group thiopental sodium 300 ?mol? L -1 (THS 300). Various concentrations of thiopental sodium were added to aC SF, the release of glutamate and GABA were performed under 37℃ and measured using reversed-phase high-performance liquid chromatography (RP-HPLC). When Ca 2+-independent release of glutamate and GABA were studied, Ca 2+ was omitted from aCSF.Results Compared with Base, thiopental sodium 30 , 100 and 300 ?mol?L -1 inhibited Ca 2+-dependent release of gluta mate evoked by KCl or veratridine significantly (P

Objective To study the clinical value of combined detection of D-dimer,PT,FIB and Cyc-C in the patients with nephrotic syndrome(NS) complicating thromboembolism.Methods Sixty-five patients with clinically diagnosed NS(observation group) in the Huangshi Municipal Central Hospital from April 2013 to March 2016 were selected and divided into the non-thromboembolism group(group A,45 cases) and thromboembolism group(group B,20 cases).Contemporaneous 43 individuals undergoing physical examination served as the control group(group C).The levels of Cys-C and 24 h urine protein were tested by the electrochemical luminescence method;meanwhile PT,FIB and D-dimmer levels were detected by the nephelometry method.Their changes in the patients with NS complicating thromboembolism were observed.Results The levels of Cys-C,24 h urine protein and D-dimer in the observation group were significantly higher than those in the control group (P＜0.01).The difference of PT and FIB levels were not statistically significant(P＞0.05);the D-dimer and Cys-C levels in the observation B group was significantly higher than that in the observation A group(P＜0.05),moreover the D-dimer level was positively correlated with Cys-C.Conclusion D-dimer and Cys-C can be used as the predictive factors of thromboembolism occurrence in NS patients.

Aim To investigate the role of TNF-αin propofol-induced neuronal apoptosis and long-term cog-nitive impairment in neonatal rats .Methods Seven-day-old SD rats were randomly divided into 3 groups:Control group ( n =12 ) , P ( single ) group ( n =6 ):propofol 50 mg · kg -1 was injected intraperitoneally (ip.)once;P(repeated) group(n=6):propofol 50 mg · kg -1 was injected ip.once daily, and for seven times. Hippocampal TNF-αlevel was measured 2 hours after propofol anesthesia , there were two time points(n=6) in Control group as control levels (post-natal day 7 for P ( single ) group and postnatal day 13 for P ( repeated ) group ) .In another experiment , 7-day-old rats were randomly divided into 5 groups:Con-trol group; P ( single ) group; P ( repeated ) group; P ( single ) +ETN group: ETN ( etanercept ) 0.4 mg · kg -1 was injected intracerebroventricularly 30 min be-fore propofol administration; P ( repeated ) +ETN group:ETN 0.4 mg· kg -1 was injected intracerebrov-entricularly 30 min before the 1st and 4th administration of propofol , which was injected ip .for seven times , once daily .Hippocampal neuronal apoptosis was detec-ted at postnatal day 7 [ P ( repeated ) and P ( repeated )+ETN groups not involved at this time point ] , 13, 21 and 35 , cognitive function was measured at postnatal day 36 to 41 using Morris water maze test .Results Propofol with different exposure times could increase hippocampal TNF-αlevels(P<0.05,P<0.01);in P ( single ) group, active caspase-3 positive neurons in hippocampal pyramidal cell layer were much greater than control level only at postnatal day 7 ( P<0.05 ) , there were no changes of escape latency or platform crossing times compared with control ( P>0.05 );in P ( repeated ) group, active caspase-3 positive neurons were more significantly increased at postnatal day 13, 21 and 35 than those in control group ( P<0.01 ) , es-cape latency was increased or platform crossing times were decreased more significantly than control in Morris water maze test ( P <0.01 ); after etanercept was ad-ministered intracerebroventricularly , there were no sig-nificant changes of active caspase-3 positive neurons , escape latency and platform crossing times after propo-fol anesthesia compared with control ( P>0.05 ) .Con-clusion TNF-αmediates hippocampal neuronal apop-tosis and long-term cognitive impairment induced by propofol in neonatal rats , and long-term cognitive im-pairment may be related with persistent neuronal apop-tosis.