Objective:To investigate the influence of electroacupuncture on auditory evoked potential index (AAI) during propofol sedation.Methods: According to propofol effect site concentration, 24 patients for operation were randomly allocated to group 1 (1.0 μg/mL), group 2 (1.5 μg/mL) and group 3 (2.0 μg/mL). Propofol was administered intravenously, points Hegu (LI4) and Neiguan (PC6) were electro-acupunctured, and changes in AAI were recorded.Results:AAI significantly rose in all groups during the initial several minutes after electro-acupuncture and significantly fell in group 2 at 20 min after electro-acupuncture(P＜0.05).Conclusion:AAI can sensitively reflect pain response during electro-acupuncture and electro-acupuncture can strengthen propofol sedation at its medium concentration.

Objective To investigate the protective effect of desflurane preconditioning on human umbilical vein endothelial cells against anoxia-reoxygenation(A/R)injury.Methods The human umbilical vein endothelial cell line(ECV304)was provided by the Liver Cancer Institute,Zhongshan Hospital,Fudan University.ECV304 cells were randomly divided into 5 groups:group Ⅰ normal control;group Ⅱ A/R;group Ⅲ A/R+rhTNF-α;group Ⅳ Des + A/R and group Ⅴ Des + A/R + rhTNF-α.In group Ⅱ-Ⅴ the cells were exposed to 95% N2 + 5% CO2 in an incubator for 30 min followed by 60 min reoxygenation.In group Ⅲ and Ⅴ rhTNF-α(10 ng/ml)10 μl was added to the cells as soon as reoxygenation was started,while in group Ⅳ and Ⅴ the cells were pretreated with 7.2% desflurane for 30 min followed by 10 min washout before A/R.Apoptosis in endothelial cells was detected by fluorescence flow cytometry and TUNEL.Endothelial cells were examined with electron microscope for apoptosis and necrosis.Results The rates of apoptosis in the endothelial cells were significantly higher in A/R group and A/R + rhTNF-α group than in control group.Desflurane preconditioning significantly attenuated apoptosis in the endothelial cells induced by A/R and A/R + rhTNF-α respectively.Electron microscopy showed that there were significantly more necrotic cells in A/R group and A/R + rhTNF-α group.However in the two desflurane preconditioning groups(Ⅳ and Ⅴ)the cells were in a state of duplication and self-repairing.Conclusion Preconditioning with 30 min 7.2% desflurane can attenuate the A/R-induced injury to human umbilical vein endothelial cells.

ObjectiveThe purpose of this study was to evaluate the effect of prostaglandin E1 (PGE1) on blocking the development of acute respiratory distress syndrome (ARDS) induced by acid aspiration. MethodsTwenty new Zealand rabbits were used. Dilute HCl was instilled into right bronchus of the rabbits. The rabbits were then divided randomly into two groups: injury group and treatment group. In injury group ( n = 10) rabbits received no treatment except mechanical ventilation. In treatment group ( n = 10) immediately after acid instillation the rabbits received an intravenous bolus of PGE1 followed by a continuous infusion. Blood gas, airway pressure and dynamic and static compliance were measured before and after acid instillation. Blood samples were taken from artery for determination of 6-k-PGF1α, TXB2, NO2-/NO3- and ET-1. The animals were killed and the wet/dry lung weight (W/D) ratio and total protein of bronchoalveolar lavage fluid(BALF) of right lung were measured. Microscopic examination of the lung was done. ResultsIn treatment group PaO2 was significantly higher than that in injury group after acid instillation. Plasma 6-k-PGF1α and NO2-/NO3- levels were significantly higher in treatment group while plasma TXB2 and ET-1 levels were significantly lower. W/D ratio and TP of BALF of right lung were significantly lower in treatment group. The inflammatory changes were diffuse in injury group while in treatment group they were localized and less severe. Conclusions PGE1 can lessen severity of ARDS induced by acid aspiration. It may protect pulmonary vascular endothelial cells through maintaining the balance between PGI2 and TXA2 and that between NO and ET-1 .

Objective To investigate the effects of nitric oxide (NO) inhalation on the expression of TNF-?,IL-8 and CD11b mRNA in lung tissue during acute respiratory distress syndrome (ARDS) induced by intravenous injection of endotoxin in dogs.Methods Twelve pure bred beagle dogs of both sexs weighing 8-12.5 kg were randomly divided into 2 groups: NO group received mechanical ventilation with NO inhalation (n = 6) and control group received only mechanical ventilation ( n = 6) . Sepsis and ARDS were induced by intravenous injection of endotoxin as described in detail in our previous paper. Hemodynamics and pulmonary oxygenation were monitored and shunt fraction was calculated. At the end of experiment the animals were sacrificed and lung tissue was obtained aseptically and stored in the liquid nitrogen at - 180℃ . The total RNA was extracted. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of TNF-?,IL-8 and CD11b mRNA. The total RNA was reversely transcripted to cDNA. Then the cDNA was amplified by PCR. The product of PCR was scanned by gel-image analysis system.?-action was used as internal control. Semi-quantitative method was adopted for measurement of TNF-? ,IL-8 and CD11b mRNA expression. Results The expression of TNF-?, IL-8 and CD11b mRNA in lung tissue was significantly decreased in NO group compared with those in control group.Conclusion NO inhalation reduces expression of TNF-?, IL-8 and CDllb mRNA in lung tissue during ARDS induced by intravenous endotoxin.

Objective To investigate the effect of propofol on apoptosis at different time points after focal cerebral ischemia-reperfusion (I/R) in a rat model of reversible middle cerebral artery occlusion (MCAO). Methods Sixty male SD rats weighing 240-260g were randomly divided into 2 groups ( n = 30 each): propofol group received intraperitoneal (i. p.) propofol 80 mg ?kg before MCAO and control group received equal volume of normal saline instead of propofol. The animals were anesthetized with 10% chloral hydrate 350mg?kg-1 i.p. . The right external, internal and common carotid artery were exposed. A 4-0 nylon thread with rounded tip was inserted via external carotid artery into internal carotid artery and threaded cranially until resistance was felt. MCAO was maintained for 90 min before reperfusion. The animals were killed and brains removed for detection of apoptotic neurons using TUNEL staining combined with electronic microscopic examination at 3 h, 6 h, 24 h, 3 days, 5 days and 7 days after reperfusion was started ( n = 5 at each time point in both groups) . Results In control group the ratio of apoptotic neurons peaked at 24 h of reperfusion and then gradually decreased; while the ratio of TUNEL positive neurons kept on increasing indicating a shift from apoptosis to necrosis after 24 h reperfusion. The ratio of TUNEL positive neurons and apoptosis were significantly lower in propofol group than in control between 6 h to 3 days after reperfusion was started. Conclusion Propofol pretreatment attenuates apoptosis induced by focal cerebral I/R and the maximum effect is reached and maintained between 6 h to 3 days of reperfusion.

Objective To investigate the effect of intraoperative hypothermia and warming on hemostasis using thromboelastography(TEG)during radical esophagus cancer operation performed under general anesthesia combined with thoracic epidural block.Methods Sixteen ASA Ⅰ or Ⅱ patients undergoing elective radical esophagus cancer operation were randomly allocated to one of two groups(n=8 each):control group and warming group.The patients were unpremedicated.The operating room temperature was set at 21℃.Epidural catheter was placed at T_(7,8) and advanced 4 cm into epidural space.Correct epidural placement was confirmed by a test dose of 4 ml 1% lidocaine.0.375% bupivacaine was used during operation.General anesthesia was induced with fentanyl,thiopental and succinylcholine and maintained with isoflurane inhalation and intermittent i.v.boluses of vecuronium after endobronchial intubation with double lumen catheter.The patients were mechanically ventilated (V_T=8-10 ml?kg~(-1),RR=10-12 bpm,I:E=1:2,FiO_2=100%).In warming group TC-2000 wanning system (Thermacave,USA)was used.The lower part of the body was warmed for 45 min before induction of anesthesia (temperature was set at 38℃).After induction warming was continued(temperature was set at 43℃).In control group no wanning was provided.The fluid infused during operation was all warmed to 37℃.Tympanic temperature measurement was started from 20 min before induction and recorded every 10 min afterwards.TEG was performed before induction of anesthesia(T_0) and at 150 min after induction(T_1).The blood samples were divided into 2 aliquots of which one was tested at 37℃ and the other at patient's actual core temperature.Results The two groups were comparable with respect to age,sex,body weight duration of operation and the amount of fluid infused during operation.At T_1 the tympanic temperature was 34.7?0.4℃ in control group and 36.5?0.3℃ in warming group.At T_1 in control group the reaction time(R)and clot formation time(K)were significantly prolonged and a angle was significantly reduced when TEG was measured at core temperature compared with those measured at 37℃ (P＜0.05).At T_1 when TEG was measured at core temperature R and K were significantly shorter and a angle was significantly wider in warming group than in control group (P＜0.05).There was no significant difference in MA between the two groups at T_1.Conclusion Mild hypothermia developed during operation can impair bemostasis.Maintenance of normal body temperature(core temperature)during operation is necessary.

Objective To investigate the effect of isoflurane administered before ischemia on polymorphonuclear neutrophil (PMN) infiltration and expression of adhesion molecules in the lung injured by ischemia-reperfusion.Methods One-hundred and twenty male SD rats weighing 250-350 g were randomly divided into 4 groups ( n = 30 each) :Ⅰ sham operation group (S) ;Ⅱ I/R group in which hilum of left lung was clamped for 45 min and then undamped for reperfusion; Ⅲ Iso + I/R in which 1 MAC isoflurane was inhaled for 30 min before ischemia and Ⅳ Iso + S in which 1 MAC isoflurane was inhaled for 30 min without I/R. The animals were anesthetized with intraperitoneal pentobarbital 50 mg?kg-1 then tracheostomized and mechanically ventilated with 100% O2(VT= 10-15 ml?kg-1) . PaCO2 was maintained at 35-45 mm Hg. Right jugular vein and left carotid artery were cannulated for BP monitoring, blood sampling and fluid and drug administration. Anesthesia was maintained with ketamine 10 mg?kg-1?h-1 and vecuronium 0.1 mg?kg-1?h-1. 1 MAC isoflurane (1.38% in rats) was inhaled for 30 min before hilum of left lung was clamped with an atraumatic clamp. Left lung ischemia was maintained for 45 min then the left lung was released for reperfusion. MAP was monitored and blood gases were analyzed during experiment. The animals were killed at the end of 45 minute ischemia and at 30, 60 and 120 min reperfusion and left lung was removed for: (1) determination of W/D lung weight ratio, myeloperoxidase (MPO) activity and expression of ICAM-1 mRNA; (2) light and electron microscopic examination; (3) broncho-alveolar lavage (BAL). BAL fluid (BALF) was collected and the number of cells, percentage of PMN and total protein concentration in BALF and the expression of CD18 on PMN surface were determined. Results The W/D lung weight ratio, MPO activity and expression of ICAM-1 mRNA in the lung tissue, the percentage of PMN and TP concentration in BALF and the expression of CD18 on PMN surface were all significantly increased during reperfusion in I/R group but isoflurane pretreatment significantly attenuated the I/R induced increases. Histological examination showed that the I/R induced lung injury was also ameliorated by isoflurane pretreatment. Conclusion Inhalation of isoflurane before ischemia could protect the lungs against I/R injury by inhibiting the PMN infiltration and expression of ICAM-1 mRNA and CD-18.

120 g?L-1. The estimated intraoperative blood loss was 1 000-1 500 ml. The patients were randomly divided into 3 groups ( n = 16 each): group Ⅰ lactated Ringer's solution (LR); group Ⅱ LR-6% HES and group Ⅲ colloid (6% HES). Blood was removed from radial artery after induction of anesthesia. The target Hct was 28% . The volume of blood removed = body weight (kg)?7.5 ? (preop Hct -target Hct) / 0.5?(preop Hct + target Hct). The removed whole blood was replaced with lactated Ringer's solution in a three to one ratio in group Ⅰ or with 6% HES in a one to one ratio in group Ⅲ. In group Ⅱ half of the removed whole blood was replaced with LR and the other half with 6% HES. The EVLW, HR, BP, Cardiac index (CI) and dp/dtmax were monitored by PiCCO and recorded before induction of anesthesia (T0), immediately after induction of anesthesia (T1), immediately after and 15 min after ANH (T2,3), immediately before and after reinfusion (T4,5) . Hct, colloid osmotic pressure and blood gases were also measured and recorded. Results The 3 groups were comparable with respect to M/F ratio, age, body weight and the volume of whole blood removed. MAP, HR, SpO2 and CVP were stable during operation in all 3 groups. Hct was significantly decreased after ANH as compared with the baseline at T0 in all 3 groups. The osmotic pressure was significantly decreased after ANH in group Ⅰ and Ⅱ and was significantly higher in group Ⅱ and Ⅲ than in group Ⅰ after ANH. CI and dp/dtmax were significantly decreased after ANH as compared to the baseline at T0 in all 3 groups. There was no significant difference in EVLW, PaO2 and [ HCO3- ] among the 3 groups. Conclusion Moderate ANH with crystalloid or colloid has little effect on EVLW and oxygenation in patients with normal cardio-pulmonary function.

Objective To compare the efficacy of postoperative noninvasive positive pressure ventilation ( NPPV ) plus standard medical therapy ( SMT) with SMT alone in patients with moderate to severe chronic obstructive pulmonary disease ( COPD )Methods Twenty-four patients, after upper abdominal or thoracic surgery, who suffered from COPD and moderate to severe respiratory insufficiency, were randomly allocated to receiving SMT alone (oxygen, aminophylline infusion, nebulized beta-2 agonists and anticholinergics, antibiotics administration and chest physiotherapy; control group ,n=12) or NPPV in addition to SMT(NPPV group ,n=12) NPPV was intermittently given with an air-cushioned face mask under the continuous positive airway pressure of 3 cmH 2O and FiO2 of 35%Results There were not significant differences in baselines between both groups 8 patients in control group ( 667%) and all patients in NPPV group recovered with initial therapy with statistically significant difference (P

Objective To research the different protective effects of general anesthesia combined with thoracic epidural anesthesia on experimental myocardial infarctionMethods Rabbits of experimental group were anesthesitized with 1% sodium pentobarbitone (30 mg/kg, iv) Following tracheal intubation, epidural catheter was put into at T_ 6-7 with the anterior end of the catheter reaching at T_ 2-3 After the epidural anesthesia was made sure to be effective, the anterior descending branches of left coronary artery were ligated Blood samples were collected before ligation, 15, 30, 60, 120, 180 and 240 min after ligation All procedures of control group were similar to those of experimental group except for thoracic epidural anesthesia Nitric oxide (NO), creatine kinase(CK), lactate dehydrogenase (LDH), aspartate transaminase (AST), superoxide dismutase (SOD) were detected The changes of the activities of CK and LDH, and NO level during the research course in both groups were analyzed with liner regression Results The regression coefficients of CK, LDH and NO in the experimental group were significantly lower than those in control group In the experimental group the activities of CK and LDH decreased markedly, NO level increased significantly as compared with those in control groupConclusions General anesthesia combined with thoracic epidural anesthesia produces the protective effects on the myocardial infarction and the stress-induced injury