To investigate the effect of thiopental sodium on the release of glutamate and gamma-aminobutyric acid (GABA) from synaptosomes in the prefrontal cortex, synaptosomes were made, the spontaneous release and the evoked release by 30 mmol/L KCl or 20 micromol/L veratridine of glutamate and GABA were performed under various concentrations of thiopental sodium (10-300 micromol/L), glutamate and GABA concentrations were determined by reversed-phase high-performance liquid chromatography. Our results showed that spontaneous release and evoked release of glutamate were significantly inhibited by 30 micromol/L, 100 micromol/L and 300 micromol/L thiopental sodium, IC50 of thiopental sodium was 25.8 +/- 2.3 micromol/L for the spontaneous release, 23.4 +/- 2.4 micromol/L for KCl-evoked release, and 24.3 +/- 1.8 micromol/L for veratridine-evoked release. But GABA spontaneous release and evoked release were unaffected. The study showed that thiopental sodium with clinically related concentrations could inhibit the release of glutamate, but had no effect on the release of GABA from rats prefrontal cortical synaptosomes.
Glutamic Acid/*metabolism ; Hypnotics and Sedatives/pharmacology ; Prefrontal Cortex/*metabolism ; Rats, Sprague-Dawley ; Synaptosomes/*metabolism ; Thiopental/*pharmacology ; gamma-Aminobutyric Acid/*metabolism

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.

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 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.

Objective To employ intraoperative discography to determine the injured intervertebral disc segments that can not be identified on the preoperative MRI in patients with cervical spinal cord injury without fracture and dislocation for confirming the responsible segments needing surgical decompression and fusion.Methods The study involved 85 patients with cervical spinal cord injury without fracture and dislocation treated from January 2007 to December 2011,among which sixteen patients had not been identified with the responsible segments by preoperative MRI.The average preoperative Japanese Orthopedic Association (JOA) score was (9.1 ± 1.8) points.There was no obvious fracture or dislocation of the cervical spine on preoperative X-ray film,CT and MRI,but all patients displayed high intense signal in cervical spinal cord on MRI T2 weighted imaging.Besides,MRI revealed hemorrhagic swelling of anterior cervical soft tissue in nine patients and cervical intervertebral disk hernia in all patients.Annulus fibrosus rupture of cervical intervertebral disc with contrast leakage in intraoperative discography of suspected injury segments in all patients under direction of C-arm X-ray machine was set as the injury criterion.The patients with pure ruptured discs received cervical discectomy,interbody fusion and titanium plate fixation.The patients associated with multilevel cervical intervertebral disc hernia or ossification of posterior longitudinal ligament underwent anterior cervical corpectomy,bone graft with titanium cageand titanium plate fixation of ruptured discs.Results Nineteen injured discs were identified eventually by discography,including 2 discs at C3/4,4 at C4/5,8 at C5/6 and 5 at C6/7.Moreover,anterior annulus fibrosus rupture with intact anterior longitudinal ligament was found in 11 patients.The follow-up lasted for (24.4 ± 10.0) months.JOA scores were (13.3 ± 1.5) points and (14.5 ± 1.6) points at two weeks and three months after operation,and (15.1 ± 1.5) points at the last follow-up,indicating a relevant improvement rate of 53％,68％ and 76％ respectively.Mean operation time was 110 minutes and blood loss was 120 ml.Three patients had pain on shoulder and back and one patient had hoarse voice,but all the patients were relieved in two weeks after conservative treatments.No serious complications,such as deep infection,deterioration of neurological dysfunction,vertebral artery injury or internal fixation failure were noticed intra-or post-operatively.Conclusion For the intradiscal rupture that is hard to be determined by the conventional imaging methods,intraoperative discography can be used as an auxiliary method of imaging diagnosis in early surgical determination of responsible segments for cervical spinal cord injury without fracture and dislocation.

To investigate the effect of propofol on the release of glutamate and gamma-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca(2+)-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca(2+)-independent release of glutamate and GABA, no DHK, nipectic acid and Ca2+ were added from aCSF. The release of glutamate and GABA were evoked by 20 micromol/L veratridine or 30 mmol/L KCI. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC). 30, 100 and 300 micromol/L propofol significantly inhibited veratridine-evoked Ca(2+)-dependent release of glutamate and GABA (P < 0.01 or P < 0. 05). However, propofol showed no effect on elevated KCl-evoked Ca(2+)-dependent release of glutamate and GABA (P > 0.05). Veratridine or elevated KCI evoked Ca(2+)-independent release of glutamate and GABA was not affected significantly by propofol (P > 0.05). Propofol could inhibit Ca(2+)-dependent release of glutamate and GABA. However, it has no effect on the Ca(2+)-independent release of glutamate and GABA.
Anesthetics, Intravenous/pharmacology ; Calcium/metabolism ; Glutamic Acid/*biosynthesis ; Hippocampus/*metabolism ; Propofol/*pharmacology ; Rats, Sprague-Dawley ; Synaptosomes/*metabolism ; gamma-Aminobutyric Acid/*biosynthesis

Fast track surgery is referred as the integration of different medical intervention actively during peri-operative period to accelerate the rehabilitation of patients undergoing operation. The propose of fast track surgery has brought about great changes in the treatment mode of many diseases, and the concept has been used in a variety of operations, especially the gastrointestinal surgery. Fast track surgery covers the preoperative appropriate preparation and assessment, sophisticated operative manipulation, and the standardization of postoperative treatment and nursing care. According to clinical trials, fast track surgery is associated with reduced post-operative complications, hospital stay and cost in patients with gastric cancer undergoing surgery. However, some problems exist in the application of fast track surgery in clinical practice, including the multidisciplinary coordination and higher readmission rates etc. A large number of evidence-based clinical trials have confirmed the efficacy of fast track, so we believe that the fast track surgery will be applied more widely.
Digestive System Surgical Procedures ; Humans ; Length of Stay ; Postoperative Complications ; Postoperative Period ; Stomach Neoplasms

ObjectiveTo explore a minimally invasive,reliable,and efficient method for endotracheal intubation to instill lipopolysaccharide (LPS) for preparation of acute lung injury (ALI) in mice.MethodsA total of 80 BALB/C mice was randomly selected into LPS group ( n =40) and control group (Normal saline,NS; n =40).After a successfully endotracheal intubation,each mouse was instilled by LPS (3 mg/kg) in LPS group,and NS ( 1.5 ml/kg) in NS group,respectively.The one-time success rate and final success rate of the endotracheal intubation,and survival rate were recorded.After 24 hours,the total number of cells in bronchoalveolar lavage fluid (BALF) of left lung was counted with light microscope.The cells were classified and counted after Wright's stain.Total protein concentration in BALF was assayed with a BCA kit.Wet/dry value was calculated after the lung became dry.Artery blood PaO2 was tested and the oxygenation index was counted.ResultsCompared to NS group,the LPS group had the one-time success rate 92.5％,and the final success rate 100％,survival rate 100％,the total number of cells [ ( 10.82±3.51) ×105/mlvs (0.72±0.52)×105/ml.t =-6.294 P ＜0 01]the rate of polymorphonulear leukocytes in total cells [ (93.93 ± 1.77) ％ vs (2.2 ± 0.91 ) ％,t =- 105.565,P ＜ 0.01 ],the rate of mononuclear leukocytes in total cells[ (6.07 ± 1.77)％ vs (97.8 ±0.91 )％,t =- 105.565,P ＜0.01 ],total protein concentration[ (0.49 ± 0.13 ) mg/ml vs (0.29 ± 0.11 ) mg/ml,t =- 2.823,P ＜ 0.05 ],W/D ratio(4.60 ±0.18 vs 4.16 ±0.25,t =-4.793,P ＜0.01 ),PaO2[ (68.57 -±7.23)％ vs(87.00 ±6.33 )％,t =4.571,P ＜ 0.01 ],and oxygenation index [ (326.53± 34.43 )mmHg vs (414.29 ± 30.16)mmHg,t =4.571,P ＜0.01 ].ConclusionsImproved method for endotracheal intubation has high success rate and minimal injury,and instillation of LPS (3 mg/kg)can induce mice ALI successfully.

Objective:To study the relationship among lipoprotein‐associated phospholipase A2 (Lp‐PLA2 ) gene A379V and T403V locus polymorphisms and genetic susceptibility of coronary heart disease (CHD) .Methods:Lp‐PLA2 gene A379V and T403V locus polymorphisms of 160 coronary angiography confirmed CHD patients (CHD group ) and 117 healthy subjects (healthy control group ) were measured using gene sequencing technique .ELISA was used to measure blood lipids and plasma Lp‐PLA2 level in two groups ,and they were compared between two groups . Results:Compared with healthy control group ,there were significant rise in age ,male proportion ,plasma levels of hs‐cTnI ,hsCRP ,TC ,LDL‐C , Lp (a) ,WBC ,mononuclear cells (MNCs) and Lp‐PLA2 [ (119.98 ± 49.41) ng/ml vs .(248.59 ± 76.51) ng/ml] ,and significant reduction in HDL‐C level in CHD group ( P<0.01 all) .The CC , CT , TT genotype and C , T allele were de‐tected all in A379V and T403C locus of two groups .Compared with healthy control group ,there were significant rise in frequencies of CC genotype (1.7% vs .9.3% ) and C allele (13.7% vs .20.3% ) of Lp‐PLA2 gene T403C locus in CHD group , P< 0.05 both . All genotypes and alleles of A379V locus possessed no significant difference between CHD and healthy control group . Conclusion:Plasma Lp‐PLA2 level may be related to CHD risk .Lp‐PLA2 gene T403C locus poly‐morphism possesses certain relationship with genetic susceptibility of CHD .

Objective To evaluate the effects of aspirin-triggered lipoxin A4 (ATL) on lipopolysaccharide (LPS)-induced acute lung injury in mice.Methods Thirty male SPF BALB/C mice,aged 10-12 weeks,weighing 25-30 g,were randomly assigned into 3 groups (n =10 each):normal saline group (group NS),LPS group and ATL groups.ATL 0.1 ml was injected via the tail vein 1 h after intra-tracheal instillation of 3 mg/kg LPS in LPS group.In ATL group,ATL 0.2 mg/kg was injected via the tail vein 1 h after intra-tracheal instillation of 3 mg/kg LPS.At 24 h after instillation,the mice were sacrificed.Bronchoalveolar lavage fluid was collected for determination of the total cell count,proportion of the polymorphonuclear leukocytes,proportion of the mononuclear leukocytes,and concentrations of the total protein,TNF-αt,IL-6,monocyte chemoattractant protein-1 (MCP-1) and IL-10.Lungs were removed for determination of myeloperoxidase (MPO) activity,phosphorylation of p38 mitogenactivated protein kinase (p38 MAPK),c-Jun N-terminal kinase (JNK),and extracellular signal-regulated kinase 1/2 (ERK1/2) in lung tissues and for microscopic examination.The pathological changes of lungs were scored.Results Compared with NS group,the lung injury scores,total cell counts,proportion of polymorphonuclear leukocytes,and concentrations of TNF-α,IL-6 and MCP-1 were significantly increased,and the proportion of mononuclear leukocytes was decreased in LPS and ATL groups,and IL-10 concentrations were decreased,and the concentrations of the total protein,MPO activity,and phosphorylation of p38 MAPK,JNK and ERK1/2 were significantly increased in group LPS (P ＜ 0.05),and no significant change in the concentrations of the total protein,MPO activity,phosphorylation of p38 MAPK,JNK and ERK1/2 was found in group ATL (P ＞ 0.05).Compared with LPS group,the lung injury scores,total cell counts,proportion of polymorphonuclear leukocytes and the concentrations of the total protein,TNF-α,IL-6 and MCP-1 were significandy decreased,the proportion of mononuclear leukocytes and IL-10 concentration were increased,and MPO activity and phosphorylation of p38 MAPK and JNK were decreased (P ＜ 0.05),and no significant change in the phosphorylation of ERK1/2 was found in group ATL (P ＞ 0.05).Conclusion ATL can ameliorate LPS-induced acute lung injury by inhibiting activations of p38MAPK and JNK signal pathways in mice.