Objective To investigate the effect of dexmedetomidine on minimum alveolar concentration (MAC) of isoflurane required to inhibit the body movement during skin incision. Methods Forty-eight ASA Ⅰ or Ⅱ patients aged 40-60 yr with body mass index of 22-27 kg/m2 undergoing elective upper abdominal surgery under general anesthesia were randomly divided into 3 groups: control group (group C, n = 15);low dose dexmedetomidine group (group D1, n = 17) and high dose dexmedetomidine group (group D2, n = 16). The patients were unpremedicated. Dexmedetomidine 0.4 and 0.8 μg/kg in normal saline (NS) 15 ml was infused over 15 min before induction of anesthesia in D1 and D2 groups respectively. Anesthesia was induced with fentanyl-propofol-succinylcholine. The patients were mechanically ventilated after tracheal intubation. Anesthesia was maintained with isoflurane. MAC of isoflurane was determined by up-and-down technique. The initial end-tidal isofiurane concentration was set at 1.0%, 0.8% and 0.6% in C, D1 and D2 groups respectively. Each time the end-tidal isoflurane concentration was increased/decreased by 0.2%. Skin incision was made after 15 min of equilibration, when the twitch height returned to more than 90% of its control value. Movement of body and limbs including swallowing and coughing were carefully looked for when skin incision was made. MAC of isoflurane was the mean of end-tidal concentration of isoflurane of each crossover pair, and 95 % CI was calculated. Results MAC of isoflurane was significantly decreased in D1 and D2 groups as compared with group C and in group D2 as compared with group D1( P ＜ 0.05 or 0.01 ). Conclusion Dexmedetomidine can significantly decrease MAC of isoflurane required to inhibit the body movement during skin incision in a dose-dependent manner.

Objective To evaluate the effect of chronic alcohol intake on the sedative potency of propofol through investigating the effect of chronic alcohol intake on the half-effective target effect-site concentration ( EC50 )of propofol required for loss of consciousness in patients. Methods Fifty male ASA Ⅰ or Ⅱ patients, aged 25-60 yr, weighing 50-80 kg, scheduled for elective surgery, were divided into 2 groups according to the history of chronic alcoholic intake ( n = 25 each): control group (alcoholic intake per day ＜ 25 g) and chronic alcoholic group (alcoholic intake per day＞45 g, lasting for 2 yr or more). The EC50 and 95% confidence interval (CI)were determined by up-and-down sequential method. The initial target effect-site concentration was 2 μg/nl in chronic alcoholic group and 1.5μg/ml in control group, and the ratio between the two successive concentrations was 1.05. Loss of consciousness was defined as loss of response to verbal command and eyelash stimulation. Results The EC50 of propofol that produced loss of consciousness was 3.92 (95 % CI 3.56-4.63 ) μg/ml in chronic alcoholic group and 2.73 (95%CI 2.26-3.31)μg/ml in control group. The EC50 of propofol was significantly higher in chronic alcoholic group than in control group ( P ＜ 0.05). Conclusion Chronic alcohol intake can increase the EC50 of propofol required to induce loss of consciousness and reduce sedative potency in patients.

Objective To compare the myocardial protective effects of isoflurane versus sevoflurane in patients undergoing off-pump coronary artery bypass grafting (OPCABG). Methods Forty ASA Ⅱ or Ⅲ patients (NYHA Ⅱ or Ⅲ ) of both sexes, aged 40-55 yr, weighing 55-94 kg, scheduled for elective OPCABG, were randomly divided into 2 groups ( n = 20 each): isoflurane group ( group Ⅰ) and sevoflurane group ( group S). Anesthesia was induced with midazolam, sufentanil and vecuronium. Patients were tracheal intubated and mechanically ventilated. Anesthesia was maintained with inhalation of isoflurane or sevoflurane and infusion of sufentanil and vecuronium. In group Ⅰ, the initial end-tidal concentration of isoflurane was 1.2%. In group S, the initial end-tidal concentration of sevoflurane was 1.7 %. BIS value was maintained at 40-50 by adjusting the end-tidal concentration of isoflurane or sevoflurane. The central venous blood samples were collected immediately before skin incision, at the end of surgery, 2 and 24 h after surgery for determination of plasma creatine kinase-MB (CK-MB) activity and cardiac troponin Ⅰ (cTnI) concentration. The adverse cardiovascular events were recorded. Results The incidences of ventricular premature beat, tachycardia, bradycardia, ventricular fibrillation and S-T segment elevation ( ＞0.1 mV) during surgery and the plasma CK-MB activity and cTnI concentration after surgery were significantly higher in group S than in group Ⅰ ( P ＜ 0.05). Conclusion Isoflurane has better myocardial protective effect than sevoflurane in patients undergoing OPCABG.

Objective To investigate the blood-saving effect of tranexamic acid in off-pump coronary artery bypass (OPCAB). Methods Two hundred and sixty ASA Ⅰ- Ⅲ and NYHA Ⅰ- Ⅲ patients of both sexes,aged 18-64 yr, with body mass index 16-22 kg/m2 , undergoing OPCAB, were randomly divided into 2 groups (n = 130 each): control group (group C) and tranexamic acid group (group T) . Anesthesia was induced with iv injection of midazolam 0.1 mg/kg, fentanyl 5-10μg/kg and pipecuronium 0.1 mg/kg. The patients were tracheal intubated and mechanically ventilated. PEr CO2 was maintained at 35-45 mm Hg. A bolus of tranexamic acid 1 g was infused intravenously within 30 min after indution followed by continuous infusion at 400 mg/h until the end of operation in group T. While equal volume of normal saline was given in control group. Anesthesia was maintained with inhalation of isoflurane and intermittent iv injection of fentanyl and pipecuronium. Venous blood samples were taken before induction, at the end of operation and at 24 h after operation for determination of Hb, platelet count (P1t), prothrombin time (PT) and international normalized ratio (INR). The volume of chest tube drainage was collected and recorded at 6 and 24 h after operation. The requirement for transfusion of allogeneic red blood cells and fresh frozen plasma was also recorded. Results There was no significant difference in Hb, Plt, PTand INR at each time point between the two groups ( P ＞ 0.05). The requirement for transfusion of allogeneic red blood cells and fresh frozen plasma was significantly reduced in group T as compared with group C ( P ＜ 0.05 or 0.01 ). No deaths and complications occurred during hospital stay in the two groups. Conclusion Tranexamic acid exerts the blood-saving effect in OPCAB.

Objective To investigate the effect of different excipients of propofol on blood lipids and liver function during orthotopic liver transplantation. Methods Forty ASA Ⅲ- Ⅳ patients aged 40-64 yr weighing 50-75 kg undergoing orthotopic liver transplantation were randomly divided into 2 groups ( n = 20 each): propofol medium-chain triglycerides/long-chain triglycerides (MCT/LCT) group (group M) and propofol LCT group (group L). Anesthesia was induced with penehyclidine 1 mg, midazolam 0.04-0.06 mg/kg, sufentanil 0.6-0.8 μg/kg and propofol 1.5-2.0 mg/kg. Tracheal intubation was facilitated with vecuronium 0.10-0.15 mg/kg. The patients were mechanically ventilated. Anesthesia was maintained with 1%-2% isoflurane, continuous infusion of propofol blood samples were collected after admission into the operation room (T1), before skin incision (T2), at the end of pre-anhepatic phase (T3), at the end of anhepatic phase (T4) and 30 and 240 min of neohepatic phase (T5, T6 )for determination of plasma concentrations of triglyceride (TG), total cholesterol (CH), high-density-lipoproteincholesterol (HDL-C), low density-lipoprotein-cholesterol (LDL-C), and activities of aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The changes in parameters from baseline values were calculated. Results Compared with group L, △TG was significant1y decreased at T4-6 in group M ( P ＜ 0.05 ) . There was no significant difference in △CH, △HDL-C, △LDL-C, △AST and △ALT,plasma concentrations of TG,CH, HDL-C and LDL-C,and activities of AST and ALT between the two groups ( P ＞ 0.05). Conclusion The effect of the two formulations of propofol on liver function is comparable. Propofol MCT/LCT exerts less effect on blood lipids during liver transplantation and is more suitable for this type of surgery.

Objective To investigate the role of mitochondrial ATP-sensitive potassium(mito-KATP)channels in attenuation of ischemia-reperfusion(I/R)injury by lidocaine pretreatment in the isolated rat heart.Methods Adult female Wistar rats weighing 220-250 g were anesthetized with intraperitoneal 3% pentobarbital 35 mg/kg.Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95%O2-5%CO2 at 37 ℃.Twenty-four isolated rat hearts with I/R injury were randomly divided into 3 groups(n = 8 each):group I/R,lidocaine group(group L)and lidocaine + glibenclamide group(group LG).After 10 min of equilibration,group C,L and LG received 20 min of perfusion with K-H solution,K-H solution containing lidocaine 2.5 mg/L and K-H solution containing lidocaine 2.5 mg/L + glibenclamide(a blocker of mito-KATP channels)10 μmol/L,respectively,then subjected to 30 min of ischemia followed by 60 min of reperfusion.HR,left ventricular developed pressure(LVDP),+ dp/dtmax and - dp/dtmax were recorded at the end of equilibration(T0)and at 15,30,45 and 60 min of reperfusion(T1-4).Coronary effluent was collected at T0 and T4 for determination of lactate dehydrogenase(LDH)and creatine kinase(CK)activities.Myocardial tissues were obtained from cardiac apex at T4 for determination of Na+ -K+ -ATPase and SOD activities and MDA and Ca2+ contents.Results Compared with group I/R,HR,LVDP,+ dp/dtmax and - dp/dtmax were significantly increased,CK and LHD activities were decreased,Na+ -K+-ATPase and SOD activities were increased,and MDA and Ca2+ contents were decreased in group L(P ＜0.05).Compared with group L,HR,LVDP,+ dp/dtmax and -dp/dtmax were significantly decreased,CK and LHD activities were increased,Na+ -K+ -ATPase and SOD activities were decreased,and MDA and Ca2+ contents were increased in group LG(P＜0.05).Conclusion The mechanism by which lidocaine pretreatment attenuates I/R injury to the isolated rat heart is related to mito-KATP channel opening.

Objective To investigate the effects of combination of propofol and whole-body hypoxic preconditioning on lung ischemia-reperfusion(I/R)injury in rats and the mechansim involved.Methods Ninety male SD rats weighing 250-320 g,were randomly divided into 5 groups(n=18 each): sham operation group(group S),lung I/R group(group I/R),propofol preconditioning group(group P),whole-body hypoxic preconditioning group(group WBHP),and combination of propofol and whole-body hypoxic preconditioning group(group PW).The animals were anesthetized with intraperitoneal 3% pentobarbital 30 mg/kg,tracheostomized and mechanically ventilated.Lung I/R injury was produced by occlusion of hilum of the left lung for 45 min followed by reperfusion.Propofol was continuously infused iv at 30 mg·kg-1·h-1 30 min before ischemia in group P.In group WBHP,5 times of WBHP were performed before ischemia.In group PW,propofol was infused iv at 30 mg· kg-1·h- 1 and 5 times of WBHP were performed 30 min before ischemia.Six rats from each group were killed at 30 min,1 h,and 4 h of reperfusion(T1-3).The lungs were then removed for determination of the contents of TNF-α,IL-1,IL6 and MDA,and activities of SOD.The W/D lung weight ratio was calculated.Results Compared with group S,the contents of TNF-α,IL-1,IL-6 and MDA and W/D ratio were significantly increased at T1-3,and SOD activity was significantly decreased at T1-3 in the other four groups(P＜0.05).The contents of TNF-α,IL-1,IL-6 and MDA and W/D ratio were significantly lower at T1-3 ,and SOD activity was significantly higher at T1-3 in group P,WBHP and PW than in group I/R(P ＜ 0.05).The contents of TNF-α and IL-6 and W/D ratio at T2,3 and contents of IL-1 and MDA at T3 were significantly lower,and SOD activity was significantly higher at T2,3 in group PW than in group P and WBHP(P＜0.05).There was no significant difference in the parameters metioned above between group P and WBHP(P＞0.05).Conclusion The combination of propofol and WBHP can protect the lungs from I/R injury,the efficacy is better than that of either of them alone,and it may be related to the enhancement in the inhibiton of inflammatory reaction and improvement in the antioxidant effect.

Objective To investigate the effect of peroxisome proliferator-activated receptor α agonist Wy14643 on mechanical ventilation-induced lung injury in rats.Methods Thirty-two healthy male SD weighing 250-300 g were randomly divided into 4 groups(n = 8 each): group Ⅰ control(group C);group Ⅱ mechanical ventilation(group V)and group Ⅲ,Ⅳ pretreated with different doses of Wy14643(group W1 ,W2).The animals were anesthetized with intraperitoneal 3% pentobarbital 30 mg/kg and tracheostomized.The femoral artery and external jugular vein were cannulated for blood sampling and drug administration.Group C received no mechanical ventilation.In group V,W1 and W2 the animals were mechanically ventilated for 2 h(VT 40 ml/kg,RR40 bpm,I:E=1:2,FiO2 21%).In group W1 and W2 Wy14643 1 and 3 mg/kg were administered iv at 1 h before mechanical ventilation.Arterial blood samples were collected at 1 and 2 h of mechanical ventilation for determination of PaO2/FiO2.Serum SOD activity and MDA concentration were measured at the end of 2 h mechanical ventilation.The animals were then killed and the lungs removed for microscopic examination,lung lavage and W/D lung weight ratio.The MIP-2 and TNF-α concentrations in BALF were measured.Results Two hour mechanical ventilation significantly decreased serum SOD activity and increased serum MDA concentration,W/D lung weight ratio and TNF-α and MIP-2 concentrations in BALF as compared with group C.Wy14643 pretreatment significantly attenuated these mechanical ventilation-induced changes in group W1 and W2 in a dose-dependent manner.Conclusion Wy14643 can attenuate mechanical ventilation induced lung injury in rats and it is related to the dose.

Objective To investigate the effects of remifentanil postconditioning on apoptosis in hippocampal neruons in a rat model of cerebral ischemia-reperfusion(I/R)and the mechanism involved.Methods Twentyfour male SD rats weighing 250-300 g were randomly divided into 4 groups(n = 6 each): sham operation group (group S);global cerebral I/R group(group I/R);remifentanil 0.6μg·kg- 1·min-1+global cerebral I/R group (group R1)and remifentanil 1.8μg·kg-1·min-1 + global cerebral I/R group(group R2).Global cerebral ischemia was induced by 10 min occlusion of bilateral common carotid combined with hypotension.In group R1 and R2,remifentanil at 0.6 and 1.8μg·kg-1·min-1 were infused for 5 min before ischemia respectively.The cognitive function was tested with Morris water maze and step-down tests from the day 3 to day 8 after reperfusion.When Morris water maze test was finished,rat brains were removed for HE staining and determination of the expression of caspase-3 in hippocampal CA1 region by immuno-histochemistry.Apoptosis in neurons in hippocampal CA1 region was detected by TUNEL assay.Results Compared with group S,the cognitive function was significantly decreased and the number of apopotic neurons in hippocampus CA1 region increased in group I/R,R1 and R2,and the expression of caspase-3 was up-regulated in group I/R(P＜0.05).Compared with group I/R,the cognitive function was significantly increased,the expression of caspase-3 was down-regulated,and the number of apopotic neurons in hippocampus CA1 region was significantly decreased in group R1 and R2(P＜0.05).Conclusion Remifentanil postconditioning can improve the cognitive function through down-regulating caspase-3 expression and inhibiting the apoptosis in hippocampal neruons in a rat model of cerebral I/R.

Objective To investigate the role of A2B adenosine receptor(A2BAR)in 6% HES 130/0.4-induced reduction of pulmonary capillary permeability in a rat model of sepsis.Methods Fifty male SD rats weighing 250-300 g were randomly divided into 5 groups(n = 10 each): group Ⅰ sham operation(group S);group Ⅱ sepsis(group CLP);group Ⅲ ,Ⅳ,Ⅴ low,medium,high dose HES(group H1,2,3).The animals were anesthetized with intraperitoneal pentobarbital sodium 50 mg/kg.Left carotid artery and left femoral vein were cannulated for MAP and HR monitoring and fluid and drug administration.Sepsis was induced by cecal ligation and puncture (CLP).6% HES 130/0.4 7.5,15.0 and 30.0 ml/kg were infused iv over 2 h in group H1,2,3 respectively at 4 h after CLP.The animals were sacrificed at 6 h after CLP.The lungs were isolated for determination of pulmonary capillary permeability(by iv Evans blue injection),the expression of A2BAR and the contents of cAMP,protein kinase A(PKA),TNF-α,IL-6 and IL-10 in the lung tissue.Results CLP significantly increased pulmonary capillary permeability,A2BAR expression and cAMP,IL-6 and TNF-α contents in the lung tissue in group Ⅱ as compared with group S.0.6% HES 130/0.4 significantly reduced pulmonary capillary permeability,increased A2BAR expression,cAMP,PKA and IL-10 and decreased IL-6 and TNF-αcontents in the lung tissue in group H1,2,3 as compared with group CLP.6% HES 130/0.4 decreased pulmonary capillary permeability and up-regulated A2BAR expression in a dose-dependent manner.6% HES 130/0.4 15.0 ml/kg was most effective in increasing cAMP and PKA contents in the lung and depressing inflammatory response.Conclusion 6% HES 130/0.4 decreases pulmonary capillary permeability in a rat model of sepsis by up-regulating A2BAR expression in lung tissue.