Objective To investigate the changes in gastric intramucosal pH (pHi) and the effect of propofol on microcirculatory perfusion after myocardial ischemia-reperfusion injury in rabbits. Methods Twenty healthy adult rabbits of both sexes, weighing 2.0-2.7kg were randomly divided into two groups: A control group (n=10) and B propofol group (n = 10) . The animals were anesthetized with 2% sodium pentothal iv. Anesthesia was maintained with intermittent iv boluses of fentanyl and vecuronium. The animals were tracheotomized and mechanically ventilated during fluid and propofol infusion. PaCO2 was maintained at 35-40 mm Hg. Right internal jugular vein was cannulated for fluid and propofol infusion. Left carotid artery was cannulated for BP and HR monitoring and blood sampling. TRIP tonometry catheter (14F) was placed in the stomach. Lactated Ringer's solution was infused at 6-8 ml-kg-1 h-1 during experiment. In group B propofol was infused at 5mg-kg-1-h-1 when BP and HR were stabilized for 10 min, chest was opened and heart exposed. Left anterior descending artery (LAD) was tied for 60 min and then released for reperfusion. Hemodynamics and pHi were measured before myocardial ischemia (T0) , 60 min after myocardial ischemia (T1), 60 min (T2), 90min (T3) and 180min (T4) after reperfusion was started. Results There was no significant difference in BP and HR from T0 to T4 between the two groups. pHi decreased significantly after myocardial ischemia-reperfusion injury in both groups. pHi was significantly lower at T3 in propofol group than that in control group (P

Objective To investigate the pharmacokinetics of propofol in children of different ages after a single dose. Methods Thirty-five ASA Ⅰ or Ⅱ children were divided into 3 age groups: group A

Objective To develop a target-controlled infusion (TCI) system incorporating population pharmacokinetics of propofol for children and evaluate its accuracy. Methods The TCI system was composed of a Samsung Q20 laptop computer, Graseby 3500 infusion pump, Stanpump software (Version 1.0 designed by Shafer et al. Stanford) and pharmacokinetic parameter set for propofol in children reported by Lian et al. Twenty-four ASA Ⅰ children undergoing elective orthopedic or urological surgery under general anesthesia were divided into 2 age groups: group A 3-5 yrs ( n = 12) and group B 5-10 yrs (n = 12). Radial artery and internal jugular vein were cannulated. The pediatric patients were sedated with ketamine 4 mg?kg-1 IM (uncooperative patients) or 2 mg? kg-1 Ⅳ( cooperative patients) . Anesthesia was induced with fentanyl 3 ?g?kg-1, propofol by TCI and vecuronium 0.1 mg?kg-1. Target plasma concentration of propofol was set at 3 ?g?ml-1. TCI of propofol was maintained for 60 min. Arterial blood samples were taken at 1, 3, 5, 10, 20, 30, 40, 50 and 60 min after TCI was started and at 2.5, 5, 10, 20 and 30 min after termination of TCI for determination of blood propofol concentration by HPLC. The median performance error ( MDPE) , MDPE without first five minutes ( MDPE1) , median absolute performance error ( MDAPE), wobble and divergence were calculated. Results During the first 40 minutes of TCI there was a remarkable difference between the measured plasma propofol concentration ( Cm) and the target plasma concentration (Cp). The difference was narrowing gradually until the 50 min of TCI. After the termination of TCI the Cm was significantly lower than Cp. The MDPE was 27% in group A and 26% in group B; MDPE1 was 7% (A) and 12% (B) and MDAPE 27% (A) and 26% (B) during TCI. The wobble was 23 % (A) and 24% (B) and the divergence - 0.75%?h-1 (A) and -0.80%?h-1 respectively. Conclusion The bias and divergence of our TCI system for propofol are small and the accuracy is high and a stable plasma concentration of propofol can be maintained in children.

Seven cases scheduled for cesarean section following combined spinal-epidural anesthesia,complicating the premature detachment of placenta,which occurred in the 2nd Affdiated Hospital of Wenzhou Medical College from January 1997 to December 2006,were analyzed to determine the risk factors.The results showed that the supine hypotensive syndrome after combined spinal-epidural anesthesia and anxiety before cesarean section were closely related to the premature detachment of placenta.The incidence rate of the premature detachment of placenta after combined spinal-epidural anesthesia is low,but the prermature of detachment of placenta is severe if it occurs,and the effectively prophylactic measures should be taken,including premedication with midazolam to eliminate anxiety before cesarean section and prevention of supine hypotensive syndrome after combined spinal-epidural anesthesia.

With the development of techniques and methods of medical researches, the ethic review of clinical research has become essential for healthy development of medical research. This article analyseds the practice of ethic reviews of research projects involving human subjects in our hospital and the difficulties in the process are discussed.

Objective To evaluate the effects of curcumin on the activity of NR2B and NR1 in the spinal dorsal horn in a rat model of diabetic neuropathic pain (DNP).Methods Diabetes mellitus was induced by high-sucrose and high-fat diet and intraperitoneal streptozotocin 35 mg/kg,then confirmed by fasting blood glucose level ≥ 16.7 mmol/L 3 days later in male Sprague-Dawley rats.DNP was confirmed by the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) measured on day 14 after streptozotocin administration ＜ 80％ of the baseline value.The rats were then randomly divided into 3 groups (n =27 each) using a random number table:DNP,DNP+ curcumin group (group DCur)and DNP + solvent control group (group DSC).Curcumin 100 mg· kg-1 · d-1 and corn oil 4 ml· kg-1 · d-1 were injected intraperitoneally for 14 consecutive days starting from 14 days after administration of streptozotocin in DCur and DSC groups,respectively.Another 27 normal male Sprague-Dawley rats served as control group (group C) and were fed with normal forage.At 3,7 and 14 days after curcumin injection,MWT and TWL were measured and the lumbar segments (L4-6) of the spinal cord were removed.The expression of pTyr1472-NR2B and pSer896-NR1 in the spinal dorsal horn was determined by immunohistochemistry and Western blot.Results Compared with group C,MWT was significantly decreased,TWL was shortened,and the expression of pTyr1472-NR2B was up-regulated at each time point in group DNP.Compared with group DNP,MWT was significantly increased,and TWL was prolonged at 7 days after curcumin injection,and the expression of pTyr1472-NR2B was down-regulated at 3 days after curcumin injection in group DCur.There was no significant difference in each parameter between DNP and DSC groups,and in the expression of pSer896-NR1 between the four groups.Conclusion The mechanism by which curcumin mitigates neuropathic pain in type 2 diabetic rats may be related to inhibition of up-regulation of pTyr1472-NR2B expression,while unrelated to pSer896-NR1 expression in the spinal dorsal horn.

Objective To evaluate the effect of resveratrol on the cognitive function after isoflurane anesthesia in obese rats.Methods Sixty SPF healthy male Sprague-Dawley rats,aged 4 weeks,weighing 70-80 g,were divided into 4 groups (n=15 each) using a random number table:normal diet plus 30％ O2 group (group N+O),high-fat diet plus 30％ O2 group (group H+O),high-fat diet plus 2％ isoflurane group (group H+I),and reveratrol plus high-fat diet plus 2％ isoflurane group (group R+H+I).Rats were fed a normal diet for 8 weeks in N+O group,while animals were fed a high-fat diet for 8 weeks in H+O,H+I,and R+H+I groups.Starting from 9th week,reveratrol 40 mg · kg-1 · d-1 was given into the stomach through a gastric tube for 7 consecutive days in group R+H+I,while the equal volume of 1％ carboxymethyl cellulose sodium was given instead of reveratrol in the other groups.After the end of drug intervention,animals were exposed to the mixture of 70％ nitrogen and 30％ oxygen for 4 h in N+O and H+O groups or to 2％ isoflurane for 4 h in H+I and R+H+I groups.Ten rats were randomly selected on 2nd day after inhaling isoflurane,and Morris water maze test was performed to assess the cognitive function.Five rats were randomly sacrificed on 3rd day after inhaling isoflurane,brains were removed,and hippocampi were isolated for determination of the expression of brain-derived neurotrophic factor (BDNF),tyrosine kinase B receptor (TrkB) and phosphorylated TrkB (p-TrkB) in hippocampal tissues by Western blot.The p-TrkB/TrkB ratio was calculated.Results Compared with group N+O,the escape latency was significantly prolonged on 3rd and 4th days,the exploration time spent on the original target quadrant was shortened,the expression of BDNF and p-TrkB in hippocampal tissues was down-regulated,and the p-TrkB/TrkB ratio was decreased in group-H+O (P＜0.05).Compared with group H+O,the escape latency was significantly prolonged on 2nd-5th days,the exploration time spent on the original target quadrant was shortened,the expression of BDNF and p-TrkB in hippocampal tissues was down-regulated,and the p-TrkB/TrkB ratio was decreased in group H+I (P＜0.05).Compared with group H+I,the escape latency was significantly shortened on 2nd-5th days,the exploration time spent on the original target quadrant was prolonged,the expression of BDNF and p-TrkB in hippocampal tissues was up-regulated,and the p-TrkB/TrkB ratio was increased in group R+H+I (P＜0.05).Conclusion Resveratrol can mitigates the cognitive dysfunction after isoflurane anesthesia in obese rats,and the mechanism may be related to promoting the activation of BDNF/TrKB signaling pathway.

Objective To investigate the effects of anaesthetic concentration of sevoflurane on TM3 mouse leydig cell viability.Methods TM3 mouse leydig cells were randomly divided into 3 groups ( n =24 dishes each):control group (group C),2％ and 5％ sevoflurane groups (groups SEV1 and SEV2 ).The cells were collected after being exposed to sevoflurane or 95 ％ room air + 5 ％ CO2 for 2,4 or 6 h (T1-3) for microscopic examination with optical binocular inverted microscope.The number of live cells was counted by using cell counting kit8.Gene chips were used to indentify differentially expressed genes between group C and group SEV2 after being exposed to air and 5 ％ sevoflurane for 6 h respectively.Results The leydig cell viability was significantly decreased at T3 in group SEV2 as compared with groups C and SEV1.Morphological changes were found only in group SEV2.A total of 45 genes were identified to be differentially expressed in group SEV2 as compared with group C.The level of expression of prostaglandin-endoperoxidase synthase 2 gene (Ptgs2),chemokine (C-C motif) ligand 2(CCL2) gene and dual specificity phosphatase1 (Dusp1) gene increased by at least 4 times in group SEV2.Conclusion Sevoflurane can inhibit the cell viability of TM3 mouse leydig cell in concentration dependent manner through abnormal expression of Ptgs2,CCL2 and Dusp1 genes.

Objective To investigate the effect of curcumin on apoptosis in hippocampal neurons and the expression of c-Jun N-terminal kinase 3 (JNK3) and postsynaptic density protein 95 (PSD95) in hippocampus during cerebral ischemia-reperfusion (I/R) in rats with spontaneous hypertension (SH) .Methods One hundred and thirty-five male rats (homologous with WKY) with SH and 90 male normotensive WKY rats, weighing 275-325 g,were used in this study. The WKY rats were randomized into 2 groups ( n = 45 each) : sham operation group (WS group) and cerebral I/R group (W-I/R group) . The rats with SH were randomly divided into 3 groups ( n = 45each) : sham operation group (S-S group), cerebral I/R group (S-I/R group) and curcumin group (S-C group) .Global cerebral ischemia was produced by 4 vessel-occlusion method. The bilateral common carotid arteries were only exposed but not ligated in W-S and S-S groups. Intraperitoneal corn oil 10 ml/kg was injected at 30 min of reperfusion in W-I/R and S-I/R groups. Intraperitoneal curcumin 100 mg/kg was injected at 30 min of reperfusion in S-C group. Three animals in each group were sacrificed at 2 h, 6 h, 1 d, 3 d and 7 d of reperfusion and their brains were harvested for determination of apoptosis in hippocampal neurons and the expression of JNK3 and PSD95in hippocampus. Results The number of apoptotic neurons was significantly increased in S-S group compared with W-S group ( P < 0.05) . The number of apoptotic neurons was significantly increased and the expression of JNK3was up-regulated in S-I/R group compared with S-S group ( P < 0.05) . The number of apoptotic neurons was significantly decreased and the expression of JNK3 was down-regulated in S-C group compared with S-I/R group (P <0.05) . There was no significant difference in the expression of PSD95 among all the groups ( P > 0.05) . Conclusion Curcumin can inhibit apoptosis in hippocampal neurons and the mechanism is related to down-regulation of the expression of JNK3 in hippocampus. The mechanism by which curcumin down-regulates the expression of JNK3in hippocampus may not be related to PSD95 pathway.

Objective To investigate the effect of curcumin pretreatment on endoplasmic reticulum stress induced by global cerebral ischemia-reperfusion (I/R) in rats. Methods One hundred forty-four male SD rats weighing 200-250 g were randomly divided into 4 groups (n = 36 each): sham operation group (group S) ; I/Rgroup; curcumin group (group Cur) and vehicle control group (group VC). Global cerebral I/R was produced by four-vessel occlusion technique in S, I/R, Cur, VC groups. Bilateral vertebral arteries were cauterized. Bilateral common carotid arteries were occluded by clipping for 15 min. Curcumin 200 mg/kg was injected intraperitoneally (IP) at 1 h before cerebral ischemia. Global cerebral ischemia was confirmed by unconsciousness and disappearance of papillary and righting reflex. Animals were sacrificed at 12 h, 1,3 and 7 d of reperfusion. Neuronal apoptosis in hippocampal CA1 region was detected by TUNEL assay. Apoptosis index (AI) was calculated. The expression of glucose regulated protein 78 (GRP78) ,growth arrest and DNA damage inducible gene 153 (GADD153) and caspase-12 protein in hippocampal region was assessed by Western blot analysis. Results Cerebral I/R significantly increased AI and GRP78 and caspase-12 protein expression in hippocampus as compared with group S( P <0.05) . Curcumin pretreatment significantly decreased AI, increased GRP78 protein expression and decreased caspase-12 protein expression as compared with group I/R ( P < 0.05) . There was no significant difference in the GADD153 protein expression among Cur, VC and I/R groups ( P > 0.05) . Conclusion Curcumin pretreatment can significantly reduce global cerebral I/R-induced neuronal apoptosis in hippocampus by increasing GRP78 expression and decreasing easpase-12 expression in hippocampus.