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

Background: The prevalence of ulcerative colitis (UC) in China has significantly increased in recent years,and Toll-like receptor 4 (TLR4) may be closely related to the development of UC.Aims: To study the effect of vitamin D3 on expression of TLR4 in the intestinal mucosa in colitis model in rats.Methods: Thirty Sprague-Dawley rats were randomly divided into normal control group,model group and vitamin D3 group.Rats in model group and vitamin D3 group were given trinitro-benzene-sulfonic acid (TNBS) to induce colitis model.Rats in vitamin D3 group were given vitamin D3.HE staining was performed,and disease activity index (DAI) and colon histopathological score were evaluated,the expression of TLR4 was measured by immunohistochemistry.Results: Compared with normal control group,DAI and histopathological score in model group were significantly increased (P＜0.05),and expression of TLR4 was significantly increased (P＜0.05).After giving vitamin D3,DAI and histopathological score were significantly decreased (P＜0.05),and expression of TLR4 was significantly decreased (P＜0.05).Conclusions: The expression of TLR4 is increased in colon tissue in colitis model in rats,which may be involved in the pathogenesis of UC.Vitamin D3 can alleviate intestinal inflammation via inhibiting expression of TLR4,thereby playing a role in the adjunctive therapy of UC.

Objective To explore the values of various surgical techniques in the treatment of secondary hepatocarcinoma.Methods One hundred thirty-four patients with secondary hepatocarcinoma were respectively divided into three groups,hepatectomy(group Ⅰ), other surgical treatments(group Ⅱ) and chemotherapy or/and interventional therapy(group Ⅲ). Retrospective analysis was performed to all patients above mentioned.The three groups were compared each other for survival rate.Results The survival rate among three groups was significantly different.There was a higher survival rate in hepatectomy group.Conclusions Hepatectomy is the most effective method to cure secondary hepatocarcinoma.

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 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

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 observe the role of dual-source CT (DSCT) in the diagnosis of coronary artery fistula. Methods Nine patients with coronary artery fistula were examined with dual-source CT coronary artery angiography. Then the source images were post processed using volume rendering (VR), multiple planar reformation (MPR), maximum intensity projection (MIP) and curved planar reformation (CPR), and sequential segmental analysis of the intracardiac and extracardiac anomalies was performed. Results Coronary artery fistula in all the 9 patients were accurately displayed with DSCT, including 2 with left main trunk to right ventricle fistula, 7 with left main trunk and (or) left anterior descending artery to main pulmonary trunk fistula, 5 with complex coronary-pulmonary artery fistula. Conclusion Dual-source CT coronary artery angiography is convenient, fast, non-invasive, and may be the preferable method for diagnosis of coronary artery fistula.

ObjectiveTo investigate the impacts of sepsis-induced cardiac dysfunction on hemodynamics, organ function and prognosis in the patients with septic shock.Methods A prospective cohort study was conducted in 44 patients suffering from septic shock with the duration< 24 hours admitted to the Department of Critical Care Medicine of Peking University Third Hospital during June 2013 to June 2014. The patients were divided into two groups according to the left ventricular ejection fraction (LVEF) as recorded in echocardiogram at time of admission to the intensive care unit (ICU) as sepsis-induced myocardial dysfunction group (LVEF< 0.50,n= 11) and normal cardiac function group (LVEF≥0.50,n= 33). The cardiac function evaluation and hemodynamics monitoring were performed with echocardiogram and pulse-induced contour cardiac output (PiCCO) on 1, 3, 7 days after the ICU admission. The plasma levels of the biomarkers of myocardial damage, troponin T (TnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were measured, and the parameters representing organ function and the 28-day prognosis were collected as well.Results On the ICU admission, central venous pressure (CVP) and left ventricular end-diastolic diameter (LVEDD) were obviously lower in normal cardiac function group than those of myocardial dysfunction group [CVP (mmHg, 1 mmHg = 0.133 kPa): 10±4 vs. 14±6,P< 0.05; LVEDD (mm): 45.0±5.3 vs. 51.8±7.1,P< 0.01], and there was no significant difference in other hemodynamic parameters between two groups. On the 3rd day, all the cardiac function and hemodynamic parameters showed no significant differences between the two groups. On the 7th day, the cardiac index (CI) and pulmonary vascular permeability index (PVPI) of normal cardiac function group were significantly higher than those of myocardial dysfunction group [CI (mL·s-1·m-2): 63.3±13.3 vs. 48.3±10.0,P< 0.05;PVPI: 1.5 (1.4, 1.9) vs. 1.1 (0.7, 1.1),P< 0.01], and no significant difference was found in the other parameters. The plasma levels of TnT and NT-proBNP were found to have no difference at three time points between two groups. There was no difference in the number or the extent of organ dysfunction, including lung, kidney, liver and coagulation system, between the groups at the time of ICU admission. There was no obvious difference in the 28-day survival rate between the myocardial dysfunction group and normal cardiac function group [81.8% (9/11) vs. 72.7% (24/33),χ2= 0.398, P= 0.528].Conclusions Sepsis-induced myocardial dysfunction is a reversible organ dysfunction. It can directly induce decreased left ventricular systolic function and enlargement of ventricle in patients with septic shock without reducing cardiac output or impairing the functions of other organs, or elevating the mortality rate.

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

Objective To investigate the current situation of healthcare-associated infection(HAI)management in secondary and above medical institutions in Shaanxi Province,analyze development trend,and put forward sugges-tions for improvement.Methods In May-June,2016,170 secondary and above hospitals in 10 cities were selected for surveying through stratified random sampling method.Survey content included basic situation of hospitals,HAI management,HAI monitoring,and so on.Results Available questionnaires were obtained from 165 hospitals (43 tertiary hospitals,and 122 secondary hospitals).Of 165 hospitals,more than 90% have established HAI manage-ment organizations and regulations,but hospital risk management should be paid more attention,only 63.03% of hospitals perfected the risk management system and 66.06% conducted risk assessment.99.09% of hospitals im-plement training on HAI to all staff regularly and 88.41% conducted effective feedback.In the aspect of staff alloca-tion,88.48% of the hospitals assigned enough professionals for HAI management,but only 34.55% have specific training programme for these personnel.Only 33.94% of hospitals have special funds for HAI control;in the aspect of monitoring on HAI,21.21% of hospital installed and used HAI monitoring software;In the aspect of implemen-tation of monitoring programme,about 90% of hospitals developed monitoring on HAI cases and environmental hy-giene,but only 34.55% and 23.64% of hospitals conducted targeted monitoring on intensive care unit and neonatal intensive care unit respectively.Conclusion Organizational structure of HAI management in Shaanxi Province is perfect,relevant rules and regulations are basically established,basic monitoring projects are universal,but the awareness of risk management needs to be strengthened,professional allocation and professional quality develop-ment are both imbalance,informational monitoring is inadequate.