Objective To investigate the gene expression variation of rat kidney uridine diphosphate glucuronatetransferase ugt1a6 related to propofol metabolism in anhepatic phase and to primarily explain the reasons of extrahepatic metabolism characteristic of propofol. Methods A total of 15 male SD rats were distributed randomly to 3 groups (n=5 in each group): control group (group A), devascularization of the hepatic portal for 30 min (group B) and 60 min (group C). Kidney tissues of rats were taken and ugt1a6 mRNA were detected by RT-PCR. Results Gene expression levels of kidney ugt1a6 of groups B and C were significantly higher than group A (P

Objective To observe the changes of propofol blood concentrations in rats during anhepatic phase by continuous constant-speed infusion of propofol and to investigate the extrahepatic metabolism of propofol and the effects of lungs on the extrahepatic metabolism of propofol. Methods When the continuous constant-speed transfusion of propofol was carrying out through the left deep cervical vein, the blood samples of 100 ?l were withdrawn simultaneously from the right deep cervical artery and vein at the flowing time points: 5 min before the dissociation of hepatic portal, immediate devascularization of the hepatic portal, 15 min, 30 min and 60 min after devascularization of the hepatic portal. The propofol blood concentrations were analyzed by HPLC. Results At 15 min, 30 min and 60 min after the devascularization of the hepatic portal, the propofol blood concentrations in the right deep cervical artery and vein were significantly higher than that at 5 min before the dissociation of hepatic portal and immediate devascularization of the hepatic portal (P

Objective To assess the protective effect of remifentanil on cultured human hepatocytes against anoxia-reoxygenation injury. Methods Cultured hepatocytes were divided into 5 groups: group C receiving normoxia as control; groups AR, R, CH, R+CH receiving 15-hour xypoxia followed by 5-hour reoxygenation (group R receiving 5 ng/ml remifentanil, group CH 10 ?mol/L chelerythrine, group R+CH 5 ng/ml remifentanil and 10 ?mol/L chelerythrine before reoxygenation). The content of MDA in the hepatocyte mitochondria were measured. The rate of apoptotic cells was measured by flow cytometry. The expression of protein kinase C mRNA was measured by RT-PCR. Results Anoxia-reoxygenation caused dramatic increase in the content of MDA, the rate of apoptotic cells and the expression of protein kinase C mRNA. The three indexes mentioned above of groups R and CH were between that of groups C and AR (P

Objective To observe the effect of dexmedetomidine on plasma SDF-1 level in in hepatic portal occlusion operation.Methods Fifty patients with live cancer undergoing elective partial hepatectomy were selected,no gender limitation,aged 42 to 71,body mass index(BMI) 18.5 ～ 26.0 kg/m2,ASA grade Ⅱ or Ⅲ.The patients were randomly divided into 2 groups(n=25):control group and dexmedetomidine group.The dexmedetomidine group was performed the pump injection of dexmedetomidine 1 μg/kg at 15 min before induction of anesthesia.After induction the rate was changed to 0.4μg · kg-1 · h-1 until 15 min before the end of operation;the control group adopted the same method for conducting continuous intraverous infusion of the same capaci ty of 0.9％ sodium chloride.The peripheral venous blood was collected in 2 groups at preoperative 1 h (T0),postoperative 1 h (T1),postoperative 1 d (T2),postoperative 3 d(T3).The plasma SDF-1 level was detected by using enzyme-linked immunosorbent assay(ELISA).Results There was no statistically significant difference in liver resection range,blood loss,first porta hepatis vessel occlusion time,anesthesia time and plasma SDF-1 level before surgery between the two groups (P＞0.05).Compared with pre-operation,plasma SDF-11evel at T1,T2,T3 time point was significantly increased (P＜0.05).The plasma SDF-1 level at T1,T2,T3 time point in the dexmedetomidine group was lower than that in the control group(P＜0.05).Conclusion SDF-1 expression is significantly increased during perioperative period in the patients with hepatic portal occlusion operation,and intraoperative continuous dexmedetomidine can significantly reduce the SDF-1 level,which inhibits the chemotaxis and accumulation of inflammatory ceils to some extent.

Objective To establish the model of serum-caused damage to pulmonary microvascular endothelial cells (PMVECs) of mice with renal ischemia-reperfusion (I/R) injury.Methods Mice PMVECs were cultured to measure the standard trans-endothelial electrical resistance (TER) in the monolayer of PMVECs.When PMVECs were cultured and arranged in compact monolayer and TER was achieved,they were divided into 4 groups (n =3 each) using a random number table:serum of normal mice group (NS group) and different concentrations (5％,10％ and 20％) of serum of mice with renal I/R injury groups (IRS5 group,IRS10group and IRS20 group).The PMVECs were cultured for 1 h in the serum-free endothelial culture medium.The 0.8 and 0.2 ml culture medium containing 20％ serum of normal mice were then added to the upper and lower chambers,respectively,in group NS.The 0.8 and 0.2 ml culture medium containing 5％,10％ and 20％ serum of mice with renal I/R injury were then added to the upper and lower chambers in IRS5,IRS10 and IRS20 groups,respectively.100 μg/ml FITC-BSA 100 μl was added to the upper chamber in the four groups.At 3,6,9,12,15,18,21 and 24 h of incubation,the PMVEC monolayer permeability (apparent permeability coefficient,Pa) was detected.Results Compared with NS group,the Pa was significantly increased at 12 and 15 h of incubation in IRS5 group,and the Pa was increased at 6-24 h of incubation in IRS10 and IRS20 groups.Compared with IRS5 group,the Pa at 21 and 24 h in IRS10 group and at 9-24 h in IRS20 group were significantly increased.Conclusion Both 10％ and 20％ serum of mice with renal I/R injury can successfully establish the model of damage to PMVECs,and 20％ serum causes a more severe damage.

Objective To investigate the variation of fentanyl concentration and the gene expression and activity of rat intestinal cytochrome P450 3A1 in anhepatic phase. Methods The experiment was comprised of 2 steps. Step 1: The rats were randomly divided into experimental group (group A2, underwent occlusion of the hepatic portal) and control group (group A1), with 10 rats in each group. Fentanyl blood concentration was analyzed by LC/MS/MS. Step 2: The rats were randomly divided into group B1 (control), group B2 and group B3 (the rats underwent devascularization of the hepatic portal for 30 or 60 min). The levels of CYP3A1 in rat small intestine were assessed with RT-PCR and the enzymic activity of CYP3A1 was detected by fluorometry. Results Fentanyl concentration in anhepatic phase dropped more slowly in group A2 than group A1 (P

Objective To dynamically observe the SDF-1 level in plasma,bone marrow,liver,lung and kidney,and to investigate their significance in obstructive jaundice and its complications. Method 48 male SD rats weighing about 200g were randomly divided into Sham group and CBDL group. The serum ALT ,AST and se-rum total bilirubin(TBIL)were detected at 7 d,14 d and 21 d after operation. General condition of rats in the two groups were observed. ELISA was applied in detecting expression of SDF-1 in plasma and supernate of tissue ho-mogenate. And mRNA expression of SDF-1 at different time was detected by qPCR assay. Results ALT,AST,TB increased rapidly after CBDL operation,the difference was significant compared with Sham group(P <0.05). The SDF-1 expression of plasma,liver tissue,lung tissue in CBDL rats at different time points were significantly higher than in Sham group. No significant difference was found in renal tissue. SDF-1 expression of bone marrow in 7 d,14 d,21 d was significantly lower in CBDL group than in Sham group. Conclusion Expression of SDF-1 in liver and lung tissues of obstructive jaundice rats significantly increased ,and decreased in marrow bone. This change may promote related stem cells mobilization and contribute to the pathological changes of obstructive jaun-dice.

Objective To evaluate the effect of dexmedetomidine on pulmonary microvascular en-dothelial cell(PMVEC)injury induced by the serum of mice with renal ischemia-reperfusion(I∕R)injury. Methods Renal I∕R was induced by clamping bilateral renal pedicles for 60 min followed by 24 h of reper-fusion. Primary PMVECs of mice were divided into 3 groups(n=20 each)using a random number table:control group(group C), serum of mice underwent I∕R group(group I∕R)and dexmedetomidine group (group Dex). PMVECs were cultured with 10% serum of mice underwent sham operation in group C. PM-VECs were cultured with 10% serum of mice underwent I∕R injury in group I∕R. PMVECs were incubated for 3 h with dexmedetomidine at the final concentration of 0.1 μmol∕L before incubation with serum in group Dex. At 24 h of culture or incubation, the cell survival rate was detected by CCK8 assay, cell apoptosis by Hoechst 33258 staining, caspase-3 activity using colorimetric method, and the expression of Bcl-2 and Bax using Western blot. Results Compared with group C, the cell survival rate was significantly decreased, the apoptosis rate and activity of caspase-3 were increased, the expression of Bcl-2 was down-regulated, and the expression of Bax was up-regulated in I∕R and Dex groups(P<0.01). Compared with group I∕R, the cell survival rate was significantly increased, the apoptosis rate and activity of caspase-3 were de-creased, the expression of Bcl-2 was up-regulated, and the expression of Bax was down-regulated in group Dex(P<0.01). Conclusion Dexmedetomidine can reduce PMVEC injury induced by the serum of mice with renal I∕R injury, and the mechanism is related to regulating the expression of Bcl-2 and Bax and inhib-iting mitochondrial apoptosis pathway.

Clinical teaching round is one of main teaching methods during standardized training for residents. However, the particularity of standardized resident training in clinical anesthesia determines that it is difficult to apply the teaching round model of other disciplines. In this study, seven core contents of Mini-Clinical Evaluation Exercise (Mini-CEX) were modified after considering the characteristics of anesthesia specialty and applied to the teaching rounds of standardized training for residents of anesthesia , thus promoting the standardization and improving the quality of anesthesia teaching rounds.

Objective To evaluate the effects of melatonin on the excitability of pyramidal neurons in the prefrontal cortex and the role of melatonin receptor 1 (MT1 R)-cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) signaling pathway.Methods Brains were obtained from male SpragueDawley rats between 14 and 21 days after birth.The brain slices of 350-μm thick were prepared and placed in artificial cerebrospinal fluid.The brain slices were divided into 5 groups (n =6 each) using a random number table method:control group (C group),melatonin group (M group),MT1/2R antagonist luzindole plus melatonin group (L+M group),MT2R antagonist 4P-PDOT plus melatonin group (P+M group) and PKA inhibitor Rp-cAMPS plus melatonin group (R+M group).Cells were perfused for 2 min with artificial cerebrospinal fluid in group C.Cells were perfused for 2 min with 1 μmol/L melatonin in group M.Cells were perfused for 2 min with the mixture of 1 μmol/L MT1/2R antagonist luzindole and 1 μmol/L melatonin in group L+M.Cells were perfused for 2 min with the mixture of 1 μmol/L MT2R antagonist 4P-PDOT and 1 μmol/L melatonin in group P+M.In group R+M,1 mmol/L PKA inhibitor Rp-cAMPS was continuously added to the pipette solution,and cells were perfused for 2 min with 1 μmol/L melatonin.The whole-cell patch-clamp technique was used to record the membrane potential and clamp current of pyramidal neurons in the prefrontal cortex.Results Compared with group C,the clamp current was significantly increased,and the membrane potential was decreased in group M (P＜0.05).Compared with group M,the clamp current was significantly decreased,and the membrane potential was increased in L + M and R + M groups (P＜0.05),and no significant change was found in the clamp current or membrane potential in group P+M (P＞0.05).Conclusion Melatonin inhibits the excitability of pyramidal neutrons in the prefrontal cortex,and the mechanism is related to activating MT1 R-cAMP-PKA signaling pathway.