Objective To evaluate the effect of intelligentized patient-controlled analgesia ( PCA) management on the quality of postoperative analgesia in the patients. Methods A total of 6601 patients who underwent postoperative PCA from January 1, 2015 to December 31, 2017 searched from the intelli-gentized PCA system database were selected as intelligentized PCA management group ( I group) , and then were divided into 3 subgroups according to the year: 2015 subgroup ( n=2221 ) , 2016 subgroup ( n=2152) and 2017 subgroup (n=2228). A total of 1235 patients who underwent PCA which was mainly performed by a department of anesthesiology in the postoperative analgesia-related multi-center questionnaire from April 11, 2016 to April 22, 2016 in 12 grade A tertiary hospitals in Guangdong Province were select-ed as the traditional PCA management group (C group). The development of moderate and severe pain, nausea and vomiting, over-sedation at rest and during activity and patient′s satisfaction were recorded on 1st and 2nd days after operation. Results Compared with C group, the incidence of moderate and severe pain, nausea and vomiting and over-sedation at rest and during activity was significantly decreased, and the rate of patient′s satisfaction was increased at each time point after operation in I group ( P<0. 05 or 0. 01) . Com-pared with 2015 subgroup, the incidence of moderate and severe pain at rest and severe pain during activity was significantly decreased in 2016 and 2017 subgroups ( P<0. 05 or 0. 01) , and the incidence of nausea and vomiting was significantly increased in 2017 subgroup ( P<0. 05) . Compared with 2016 subgroup, the incidence of nausea and vomiting was significantly increased in 2017 subgroup (P<0. 05). Conclusion Intelligentized PCA management can improve the efficacy of PCA, mitigates the occurrence of adverse reac-tions and raise the quality of postoperative analgesia in the patients.

Objective To evaluate the effects of edaravone postconditioning and remote ischemic postconditioning on myocardial ischemia/reperfusion (I/R) injury in rats.Methods Forty male Sprague-Dawley rats,aged 8 weeks,weighing 250-300 g,were randomly divided into 5 groups (n =8 each):sham operation group (group S); group I/R; edaravone postconditioning group (group E); remote ischemic postconditioning group (group P); edaravone postconditioning and remote ischemic postconditioning group (group EP).Myocardial I/R was induced by occlusion of anterior desending branch of left coronary artery for 30 min followed by 180 min reperfusion.Edaravone 3 mg/kg was injected intravenously at 1 min before reperfusion in groups E and EP.The animals underwent 10 min ischemia of bilateral hind limbs starting from 20 min of myocardial ischemia in groups P and EP.Left ventricular systolic pressure (LVSP),left ventricular end-diastolic pressure (LVEDP) and ± dp/dtmax were measured and recorded during reperfusion.Results Compared with group S,LVSP and ± dp/dtmax were significantly decreased and LVEDP was increased in the other groups (P ＜ 0.05).LVSP and ± dp/dtmax were significantly higher and LVEDP was lower during reperfusion in groups E,P and EP than in group I/R,and in group EP than in groups E and P (P ＜ 0.05).Conclusion Edaravone postconditioning and remote ischemic postconditioning can alleviate myocardial I/R injury and offers better efficacy than either alone.

Objective To evaluate the role of microglial activation in dorsal root ganglia in a rat model of persistent postoperative pain evoked by skin/muscle incision and retraction (SMIR).Methods Seventy male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 2 groups (n =35 each):group sham operation (group S) and group SMIR.The rat model of persistent postoperative pain evoked by SMIR was established according to the method described by Flatters.Pain behavior was assessed by mechanical paw withdrawal threshold to yon Frey filament stimulation at 1 day before and 1,3,7,12,22 and 32 days after operation.Five animals were sacrificed at each time point in each group for microglia count in dorsal root ganglia.Results Compared with group S,mechanical paw withdrawal threshold was significantly decreased at 3-22 days after operation,and microglia count was significantly increased at 3-12 days after operation in group SMIR (P ＜ 0.05).Conclusion Microglial activation in dorsal root ganglia may be involved in the development of SMIR-evoked persistent postoperative pain in rats.

ObjectiveTo investigate the influence of age on hypnotic target plasma concentration (CT) of dexmedetomidine (Dex) administered by TCI.MethodsSixty ASA Ⅰ - Ⅱ patients aged 18-85 yr undergoing lower abdominal or extremity operation under combined spinal-epidural anesthesia were divided into 2 age groups ( n =30each):18 yr＜groupⅠ＜55 yr (Y) and 65 yr＜group Ⅱ＜85 yr (E).Each group was further divided into 5subgroups (n =6 each) receiving Dex administered by TCI at CT of 0.54,0.64,0.76,0.90,1.07 ng/ml in group Y and 0.36,0.42,0.51,0.60,0.71 ng/ml in group E respectively.Hypnosis was defined as no response to verbal command (OAA/S score ≤2) and loss of eyelash reflex.A quantal response model (probit analysis) was used to calculate the concentration-effect curve and predict plasma EC50 and EC95 (95％CI) of Dex.ResultsEC50 (95％CI) was 0.478(0.424-0.536) ng/ml and EC95(95％CI) 0.641 (0.567-0.816) ng/ml in group E,significantly lower than EC50 (95 ％ CI) 0.738 (0.657-0.827) ng/ml and EC95 (95％CI) 0.990 (0.874-1.267 ) ng/ml in group Y.ConclusionThe EC50 and EC95 of dexmedetomidine for hypnosis were significantly lower in the elderly than in younger patients.

Objective To investigate the effect of dexmedetomidine on norepinephrine(NE)release in midbrain periaqueductal gray(PAG)in a rat model of incisional pain.Methods Twenty-four male Wistar rats in which microdialvsis catheter was successfully placed in the ventrolateral region of PAG without complications were randomly divided into 4 groups(n=6 each):group control(group C);group incisional pain(group IP);group dexmetomidine(group D)and group dexmedetomidine+yohimbine(group DY).Incisional pain was induced by an incision made into the plantar surface of left hindpaw in IP,D,DY groups.Dexmedetomidine 30 μg/kg and dexmedetomidine 30 μg/kg+yohimbine 0.5 mg/kg were given intraperitoneally at 15 min before plantar incision in group D and group DY respectively.Mechanical paw withdrawal threshold(MWT)to von Frey filament stimulation was measured at 30 min before(baseline)and 1,2,3,4 h after operation in C,IP,D groups,and at 30 min before(baseline),and 1 h after operation in group DY.Dialysate samples were collected at 30 min before(baseline)and at evcry 30 min after operation for 4 h via cerebral microdialysis catheter for determination of the NE concentration in C,IP,D groups,and at 30 min before(baseline),30,60 min after operation in group DY.Results Incisional pain significantly decreased MWT and increased the NE concentration in dialysate in group IP.Dexmedetomidine premedication significantly inhibited mechanical hyperalgesia and attenuated incisional pain-induced increase in the NE concentration in dialysate in group D.Yohimbine counteracted effects of dexmedetomidine.Conclusion Dexmedetomidine has analgesic effect though inhibition of NE release from PAG.

Objective To investigate the pharmacodynamics of different local anesthetics administered intrathecally for elderly patients undergoing transurethral resection of the prostate (TURP). Methods Ninety ASA Ⅰ - Ⅲ elderly patients, aged 69-82 yr, with body mass index less than 30 kg/m2 , undergoing TURP under combined spinal-epidural anesthesia, were randomly divided into 3 groups ( n = 30 each): levobupivacaine group (group L), ropivacaine group (group R) and bupivacaine group (group B). Group L, R and B received intrathecai (IT) 0.5 % levobupivacaine, 0.5 % ropivacaine and 0.5 % bupivacaine respectively. The initial dose was 7,10 and 6 mg in group L, R and B respectively. The ratio of two successive doses was 0.9. If the upper sensory block reached T10 within the 20 min after IT injection, the IT analgesia was considered to be effective. The median effective dose (EDs0) and 95 % confidence interval (95 % CI) were calculated by Dixon. Results The ED50 and 95% CI of levobupivacaine, ropivacaine and bupivacaine were 6.781 (95% CI 6.561-7.024) mg, 9.135 (95%CI8.670-9.616) mg and 5.170 (95% CI 5.012-5.333) ng respectively. The relative potency ratio between levobupivacaine, ropivacaine and bupivacaine is 0.76∶0.57∶1.00. ConclusionThe relative potency ratio be tween levobupivacaine, ropivacaine and bupivacaine is 0.76∶0.57∶1.00.

Objective To investigate the effect of morphine on P-glycoprotein (P-gp) expression in mouse brain microvascular endothelial cells. Methods The mouse brain microvascular endothelial cell line b. End3 was purchased from ATCC company (USA) and cultured at 37 ℃ in high glucose serum-free medium RPMI 1640 in 10 cm petri dishes and assigned to one of 3 groups(n = 9 each): Ⅰ control group (group C); Ⅱ morphine group (group M) and Ⅲ PDTC + morphine group (group P + M). In group M the cells were exposed to morphine 1 μg/ml while in group P + M the cells were pre-incubated with PDTC (NF-κB inhibitor) 5 μmol/L for 1 h before treatment with morphine. In group M and P+ M after being treated with morphine 1 μg/ml for 24 h, the cells were collected for determination of P-gp expression and NF-κB p65-abcb1b protein-DNA binding analysis. Results P-gP expression and NF-κB p65-abcb1b protein-DNA binding were up-regulated in group M as compared with group C. The up-regulation was negated by pre-incubation with PDTC in group P + M. Conclusion Morphine can induce up-regulation of the expression of endogenous P-gp in mouse brain microvascular endothelial cells by NF-κB mediated-abcb1 b gene activation.

AIM: To screen the binding proteins to HMGB1 promoter by phage display technique. METHODS: HMGB1 promoter was incubated with phage display library. Unbound phages were eluted and phages bound to HMGB1 promoter were amplified. Twenty individual clones were randomly selected and identified by enzyme-linked immunosorbent assay (ELISA). Positive clones were characterized by DNA sequencing and the sequences were subjected for computer analysis. RESULTS: Positive phages binding to HMGB1 promoter were enriched after 4 rounds of biopanning. Twenty phage clones were selected and eleven clones of which were identified to bind specifically to HMGB1 promoter. The sequences in full length were obtained and searched for homologous sequences from GenBank. Altogether eight coding sequences were obtained, six of which were known proteins including activator protein-1(AP-1) and two of which were uncharacterized ones. CONCLUSION: Several proteins were obtained that bind specifically with HMGB1 promoter. The results will be useful for further studying the expression and regulation mechanism of HMGB1.

Objective To investigate the role of extracellular regulated protein kinase (ERK) signal pathway in mechanical stretch induced high mobility group box 1 protein (HMGB1) expression on alveolar epithelial cells (A549). MethodsA549 cells were cultured and seeded at 1×10~5 cells/ml in 6-well Bioflex cell culture plates. Subsequently, the cells were exposed to cyclic mechanical stretch at 14% (group B) elongation for 4 hours using Flexercell 4000T cell stretching unit. In group C, cells were pretreated with PD98059 for 2 hours before mechanical stretch. Cells in group A without stretch were served as control. The expression of HMGB1 protein and mRNA in A549 cells were detected by immunocytochemisty staining and RT-PCR, respectively. ERK activity was measured by Western blotting method. Results Immunocytochemisty staining indicated that the expression of HMGB1 protein in A549 cells was increased obviously in group B (P<0.05) and decreased in group C (P<0.05). Polymerase chain reaction (RT-PCR) showed that the expression of HMGB1 mRNA was also significantly increased in group B (P<0.05) and decreased in group C (P<0.05). Western blotting analysis confirmed the activation of ERK in A549 cells by mechanical stretch (P<0.05). PD98059, an inhibitor of ERK, might significantly inhibit mechanical stretch induced HMGB1 protein and mRNA expression in A549 cells (P<0.05). Conclusion Mechanical stretch could regulate the expression of HMGB1 gene and protein in A549 cells through ERK signal pathway.

Objective To investigate the role of p38 MAPK pathway in the expression of high mobility group box 1 (HMGB1) in lung tissue in a rat model of ventilator-induced lung injury. Method Twenty-fonr healthy Sprague Dawley (SD) rats were randomly divided into 3 groups (n = 8 each) : group A, spontaneous breathing; group B, small tidal volume ventilation (Vt = 8 mL/kg) and group C, high tidal volume ventilation (Vt = 40 mL/kg). 1he animals in group B and C were mechanically ventilated for 4 hours and all animals were sacri-riced. The lungs were removed for: (1) lung lavage and determination of total protein contnt and WBC and neu-trophil counts in broncho-alveolar lavage fluid (BALF) ; (2) determination of W/D lung weight ratio and myelop-erexidnse (MPO) activity; (3) detennination of HMGB1 protein and mRNA expression and p38 MAPK activity in lung tissue. Differences within the groups were analyzed using One way ANOVA. Results The inflammatory re-sponse as evidenced by total protein (1.77 ± 0.68) g/L and WBC (106.55 ± 28.17) × 10~7/L in BALF, W/D lung weight ratio (7.16±1.02) and MPO activity (3.94±1.21) U/g were significantly higher in group C com-pared with group A (P <0.05); HMGB1 protein (0.64±0.17) and mRNA (1.17±0.45) expression and p38 activity (0.51±0.12) also significantly increased in group C (P <0.05). Of the above indexes, there were no statistical differences between group B and group A (P > 0.05). Conclusions High tidal volume ventilation in-daces acute lung injury, which may be related with upregulation of HMGB1 expression through p38 MAPK signal pathway.