Objective To assess the possible sequestration of remifentanil by the extracorporeal circuit.Methods Two types of extracorporeal circuits (ECCs) were used-Xijian type I (group A)and AFFINITY(R) NT(group B),while in control group (group C) a glass container was used.The ECC and glass container were filled with priming solution (6%hydroxyethyl starch 1000 ml + lactated Ringer's solution 500 ml).Remifentanil Wag then added to the priming solution with the final concentration of 100 ng/ml.The priming solution was circulated in the closed ECC or stirred the glass container.The concentration of remifentanil in the priming solution was determined at 2,5,10 and 15 min after addition of remifentanil.Results The remifentanil concentration in the priming solution decreased by 75.1%,57.9% and 18.3%at 2 min after addition of the drug in group A,B and C respectively as compared with the baseline value.The remifentanil absorption by ECC was significantly greater in group A than in group B.There was no significant difference in remifentanil concentration at the 4 time points in each group.Conclusion ECC can absorb remifentanil.The remifentanil absorption by Xijian type I is significantly greater than that by AFFINITY(R).

ObjectiveTo investigate the effects of sevoflurane anesthesia on aquaporin-9 (AQP-9) expression in brain tissue after focal cerebral ischemia-reperfusion (I/R) in rats.MethodsSeventy-five male SD rats weighing 230-270 g were randomly divided into 3 groups ( n =25 each):group sham operation (group S) ; group I/R and group sevoflurane anesthesia (group SE).All the animals were tracheally intubated under 2.0％ sevoflurane and mechanically ventilated.Anesthesia was maintained with fentanyl infusion at 25 μg· kg-1 · h-1 after a bolus of fentanyl 10 μg/kg and inhalation of 65％ N2O in O2 in groups S and I/R and with inhalation of 2％ sevoflurane in 35％ O2 in group SE.Focal cerebral ischemin was induced by occlusion of middle cerebral artery for 2 h using a nylon thread with rounded tip which was inserted into the right internal carotid artery and advanced cranially until resistance was met.The neurologic function was assessed and scored (0=no deficit,4 =unable to move,unconscious) and brain edema rate (volume of ischemic hemisphere-volume of contralateral hemisphere ÷volume of contralateral hemisphere × 100％ ) and expression of AQP-9 were determined at 6 h,1,2,3 and 5 d of reperfusion.ResultsFocal cerebral I/R significantly increased neurologic deficit scores,brain edema rate and AQP-9 expression in brain tissue in group I/R as compared with group S.Sevoflurane anesthesia significantly attenuated the I/R-induced increase in neurologic deficit scores and brain edema rate and further increased I/R-induced increase in AQP-9 expression in brain tissue.ConclusionSevoflurane anesthesia can reduce focal cerebral I/R injury by up-regulating the expression of AQP-9 in brain tissue.

Objeetlve To avoid inserting the tip of the central venous catheter into internal jugular vein (IJV) through subclavian vein under ultrasound guidance.Methods sixty breast cancel patients aged 28-63 yr weighing 41-70 kg who needed long-term intravenous infusion and chemotherapy through central venous catheter were randomly divided into 2 groups (n=30 each):control group (group C) and ultrasound group (group U).In group C the insertion of central venous catheter through subclavian vein was guided by pulsatile injection of ice-cold saline.In group U ultrasound detector (type HFL 38/13-6 MH,Sonosite Co,USA) was used to guide the insertion of tbe central vesons catheter.The position of the catheter tip was verified by X-ray radiography.The rate of successful placement at 1st attempt was calculated.Results The tip of the central venous catheter was correctly placed in the vena cava and right atrium in all patients in group U (success rate 100%),while in group C the tip was misplaced in IJV in 6 patients (success rate 80%) and had to be replaced.Conclusion Ultrasound guidance is effective for correct placement of the tip of central venous catheter in the vema cava and right atrium through subclavian vein.

Objective To investigate the effects of remifentanil on large-conductance Ca2+ -activated potassium channel (BKCa) in human mesenteric arterial smooth muscle cells (MASMCs) and the mechanism of the vasorelaxant effect of remifentanil. Methods Human MASMCs were obtained freshly by the method of enzymolysis. BKCa current (IBKCa) was recorded by the whole-cell patch clamp technique. The changes in IBKC. produced by different concentrations of remifentanil (1.2, 4.8, 19.4, 77.4 and 310.0 nmol/L) with the holding potential of + 80 mV were observed. BKCa activation rate was calculated. Results Remifentanil significantly increased IBKCa,moved Ⅰ-Ⅴ curve upward and had no effect on the threshold of activation for IBKCa . With the increase in the concentration of remifentanil, BKCa activation rate increased gradually (P ＜ 0.01), and it remained stable when the concentration reached 19.4 nmol/L. There was no significant difference in the peak time of IBKCa after different concentrations of remifentanil were given (P ＞ 0.05). Logarithmic curve was found to suit the relationship between the concentration of remifentanil and BKCa activation rate and the IC50 concentration was (118 ± 7) nmol/L. Conclusion Remifentanil results in vasorelaxation by activating BKCa in MASMCs in a concentration-dependent manner.

Objective To investigate the mechanism by which remifentanil decreases blood pressure during cardiopulmonary bypass (CPB).Methode Twenty-six ASA Ⅱ or Ⅲ patients (NYHA's classification grade Ⅱ or Ⅲ ) of both sexes and aged 20-55 years were randomized to receive remifentanil (group R, n = 13) or normal saline (group C, n = 13). Remifentanil 10 μg/kg or equal volume of normal saline was administered via a venous reservoir when cardiac arrest was induced with cardioplegic solution. The flow rate resistance (SVR) were measured and arterial blood samples were taken for determination of plasma concentrations of histamine,nitric oxide (NO) and 6-keta-prostaglandin F1α(PGF1α) before T0 and at 5, 10, 15 min (T5.10.15) after remifentanil administration.Results Remifentanil administration was associated with a significant decrease in MAP and SVR at T5 and T10 as compared with the baseline values at T0 ( P ＜ 0.05); whereas in control group, MAP and SVR were significantly increased at T5, T10 and T15 as compared with the baseline values at T0 . There were no significant differences in plasma histamine, NO and PGF1α concentrations between the two groups.Conclusion Remifentanil reduces SVR and causes a decrease in BP but without altering plasma concentrations of histamine, NO or PGl2.

Objective To evaluate the changes in the expression of spinal aquaporin-4 (AQP4) during remifentanil-induced hyperalgesia in a mouse model of incisional pain.Methods Seventy-two pathogen-free healthy adult male CD1 mice,weighing 25-30 g,were divided into 4 groups (n=18 each) using a random number table:control group (group C),incisional pain (group I),remifentanil group (group R) and remifentanil plus incisional pain group (group R+I).Normal saline was infused subcutaneously in group C.An incision was made in the left hind paw in group I.Remifentanil 80 μg/kg was subcutaneously infused for 30 min at a rate of 0.8 ml/h in group R.Remifentanil was infused subcutaneously before establishment of the model in group R+I.The thermal paw withdrawal latency (TWL) and mechanical paw withdrawal threshold (MWT) were measured at 1 day before establishment of the model (T0) and 6 h and 1,2 and 7 days after establishment of the model (T1-4).After measurement of the pain threshold at T3,12 animals were sacrificed randomly,and the lumbar segment of the spinal cord was removed for determination of the distribution and expression of AQP4 by Western blot.Results Compared with group C,the TWL was significantly shortened at T1-3,and the MWT was decreased at T2-4 in R and R + I groups,and the expression of AQP4 was significantly up-regulated at T3 in I,R and R+I groups (P＜0.05).Compared with group I,the TWL was significantly shortened at T2,3,and the MWT was decreased at T2.4 in group R,and the TWL was significantly shortened at T1-3,the MWT was decreased at T2.4,and the expression of AQP4 was up-regulated at T3 in group R+I (P＜0.05).Conclusion The mechanism by which remifentanil induces hyperalgesia is related to up-regulation of AQP4 expression in the spinal cord in a mouse model of incisional pain.

Objective: To investigate the mechanism of Glytan lowering portal pressure induced by biliary liver fibrosis. Methods: SD male rats, 240-260g weight around, were randomly divided into sham-operation group, model group, propranolol group, Glytan high-dose, middle-dose and low-dose group according to the weight. Portal hypertension was induced by common bile duct ligation in rats. After two and four weeks, measured the portal pressure(PP) of each group, observed the histological changes of liver by HE staining, tested liver function and the concentration of endothelin-1 in systemic circulation and mesenteric circulation radioimmnuoassay. Results: After two and four weeks, portal pressure of model group rats increased significantly. Both Glytan and propranolol can decrease PP after two and four weeks, and the pressure-relief effect was similar between the two drugs. HE staining showed that Glytan can significantly inhibit the formation of collagen, promote the recovery of liver tissue structure; liver function indicated a significant decrease in serum AST, ALT, TBIL and Na+ concentration. In addition, Glytan decreased the concentration of endothelin -1 in systemic circulation, increased it in mesenteric circulation after two weeks. Conclusion: Glytan decrease PP by improving liver function and microcirculation, inhibiting collagen formation and water-sodium retention after long-term therapy, ameliorating hyperdynamic circulation at the early stage.

Objective To evaluate the effects of remifentanil post-conditioning on aquaporin-1 (AQP-1) expression during myocardial ischemia-reperfusion (I/R) injury in rats.Methods Twenty-four male.SpragueDawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,and remifentanil post-conditioning group (group RP).Myocardial I/R was induced by 45 min occlusion of left anterior descending branch of coronary artery followed by 24 h reperfusion.Remifentanil 10 μg· kg-1· min-1 was infused over 10 min starting from 10 min before reperfusion in group RP,while the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion,all the rats were sacrificed and their myocardial specimens from left ventricles were obtained for microscopic examination of thepathological changes and for determination of AQP-1 mRNA (using real-time fluorescent quantitative PC R) and AQP-1 protein (by Western blot) expression in the ischemic area and myocardial water content.Results Compared with S group,myocardial water content was significantly increased in the other two groups,AQP-1 mRNA and protein expression was up-regulated in group I/R,and no significant change was found in AQP-1 mRNA and protein expression in RP group.Compared with I/R group,myocardial water content was significantly reduced,and AQP-1 mRNA and protein expression was down-regulated in RP group.Conclusion Remifentanil post-conditioning reduces myocardial I/R injury possibly through down-regulating AQP-1 expression in myocardial tissues of rats.

Objective To explore the effect of remifentanil postconditioning on rats subjected to ischemia reperfusion injury and the relative mechanisms.Methods Seventy-eight Sprague-Dawley rats, weighing 200-250 g, were randomly divided into six groups (n=13): sham group (group S), ischemia/reperfusion group (group IR), naloxone group (group NAL), 5 μg·kg-1·min-1 remifentanil postconditioning group (group R1), 10 μg·kg-1·min-1remifentanil postconditioning group (group R2) and 20 μg·kg-1·min-1remifentanil postconditioning group (group R3).Group IR was given 45 min ischemia in the left descending anterior (LAD), followed by a 24-h period of reperfusion.Groups R1, R2, R3 received 10 min of remifentanil infusion of 5, 10 and 20 μg·kg-1·min-1 after 35 min ischemia followed by a 24 h period of reperfusion.Group NAL was given injection of naloxone 0.1 mg/kg at the point of 25 min myocardial ischemia, after 10 min, then remifentanil 10 μg·kg-1·min-1 for 10 min.The myocardial infarct size and pathological changes of myocardial tissue were observed, serum cTnI, LDH and CK-MB level were measured.Results Compared with group S, serum cTnI, LDH and CK-MB and myocardial infarct size were markedly increased in groups IR, NAL, R1, R2 and R3 (P<0.05), and pathologic injury of myocardial cells were augmented.In comparison with group IR, the indexes were decreased in groups R1, R2 and R3 (P<0.05).Conclusion Remifentanil postconditioning could protect against myocardial ischemia reperfusion injury in rats.The protection may be related to remifentanil activating the opioid receptors.There were ceiling effects of remifentanil postconditioning induced myocardial protection.

Objective To investigate the effect of norcantharidin on growth inhibition and induction of apoptosis of human rectal cancer Colo 320 cells. Methods Norcantharidin (NCTD) in different concentrations were added to rectal cancer Colo 320 cells. Morphological characteristics of apoptosis were observed using the light microscope and transmission electron microscope. The expressions of Bag-1 and Bcl-2 proteins were tested by Western blotting. The growth inhibition of Colo 320 cells on the cell cycle was observed by flow cytometry. Results The apoptosis morphological changes of Colo 320 cells were observed by the light microscope and transmission electron microscopy. Flow cytometry analysis showed that the cell count of G2/M phase in experimental group was higher than that in control group ( <0.05) but the cell counts of G0/G1 and S phases have decreased in experimental group after treatment with NCTD at the concentrations of 5μg/mL, 10μg/mL and 20 μg/mL, and presented dosage dependence relations. The expressions of Bag-1 and Bcl-2 proteins have decreased. Conclusion Norcantharidin has inhibitory effect on rectal cancer Colo 320 cells, and the effect may be related to the cell cycle arrest and apoptosis.