Objective To investigate the changes of cognitive function after major non-cardiac surgery and the relationship between the postoperative cognitive dysfunction(POCD)and the intraoperative cerebral oxygen metabolism in the elderly.Methods Sixty-four patients(49 male,12 female)aged 65-85 yr undergoing elective major non-cardiac surgery were enrolled in this study.A battery of four neuropsycbological tests was administered 2-3 days before and 7 days after surgery by an experienced psychometrician.A postoperative deficit in any test was defined as a cognitive decline by more than or equal to the preoperative standard deviation of that test in all patients.As long aft any patient showed cognitive decline in two or more tests.this situation was defined as POCD.Blood samples were taken from radial artery and internal jugIIlar vein simultaneously for blood gas analysis immediately (T1) and 2 h (T2) after induction of anesthesia,and just before leaving postanesthesia care unit (T3).The ratio of cerebral blood flow to cerebral oxygen metabolic rate(CBF.CMR02)was calculated.Results Sixty-one patients completed postoperative neuropsychological tests and 10 cases(16.4%)had POCD.Logistic regression analysis showed that the abnormality of CBF/CMR02 during operation was associated with the occurrence of POCD.Conclusion The occurrence of POCD after major non-cardiac surgery is related to the abnormality of cerebral oxygen metabolism during operation.

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 analyze the risk factors associated with postoperative respiratory failure (PRF) in elderly patients undergoing noncardiac surgery. Methods In a prospective randomized joint study, 582 patients conforming to the criteria established by the four medical centers were enrolled for analysis. Univariate analysis and multivariate logistic regression analysis were used to examine the relations between perioperative risk factors and PRF. PRF was defined as mechanical ventilation after operation lasting for more than 48h or reintubation and mechanical ventilation within 6h after extubation.Results Fifty-one patients developed PRF (8.8%) . Multivariate logistic regression analysis identified that the type of surgery, ASA physical status classification, history of COPD and plasma albumin upper abdominal surgery and peripheral vascular surgery. The reason that neurosurgery topped the list was that most neurosurgical patients suffered from severe head injury and postoperative mechanical ventilation was prolonged because of coma. Our study showed that physical status was also a significant predictor of PRF. According to ASA classification, one class higher increased the risk by 6.325 time s. Conclusion Based on these predictors of PRF, in high risk elderly patients necessary measures can be taken to decrease the development of PRF.

Objective Neutrophils (PMNs) play an important role in the myocardial injury-induced by ischemia/reperfusion. The purpose of the study was to assess the role of PMN in anoxia/reoxygenation (A/R) injury to primary cultured myocytes and the protective effects of desflurane preconditioning (DPC) .Methods Myocytes obtained from ventricle were cultured in MEM medium for 3 days. The cultured myocytes were then randomly divided into 4 groups : group Ⅰ A/R; group Ⅱ PMNs + A/R; group Ⅲ DPC + A/R and group Ⅳ DPC + PMNs + A/ R. In all four groups the cultured myocytes were subjected to anoxia by being incubated in a tightly closed incubator filled with 95 % N2 + 5 % CO, for 2 h, followed by one hour reoxygenation (95 % O2 + 5 % CO2). In group Ⅱ and Ⅳ 5.0 ? 106 ml -1 PMNs isolated from peripheral blood or bone marrow were added to the medium during the one hour reoxygenation. In group Ⅲ and Ⅳ the myocytes were exposed to 9 % desflurane for 1 h before A/R. The activities of lactic dehydrogenase (LDH) and creatine kinase (CK) and the concentration of cardiac troponin (cTnT) in the supernatant were measured before and at the end of the experiment. Cell survival rate, beating rate and arrhythmia rate of the cultured myocytes were also calculated under phase-contrast microscope before and at the end of the experiment.Results A/R caused significant increase in LDH and CK-MB activities, cTnT concentration and arrhythmia rates and decrease in beating rates except in group Ⅲ . The differences in LDH, CK-MB activities and arrhythmia rates between the baseline value and the value obtained at the end of the experiment were significantly lower in group Ⅳ than those in group D but still higher than those in group Ⅰ . The cell survival rate was significantly higher in group Ⅳ than that in grorp Ⅱ . Conclusion Neutrophil accentuates A/R injury while desflurane preconditioning attenuates neutrophil-mediated A/R injury to primary cultured myocytes.

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 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

Objective To research the stress to experimental myocardial infarction under general anesthesia combined with thoracic epidural anesthesia(TEA) Methods Nine rabbits in experimental group were anesthetized with 1% sodium pentobarbitone with tracheal intubation after sectioned, and after the epidural catheters was put into to make sure that the epidural anesthesia was effective, the anterior descending branches of their left coronary artery were ligated All procedures in control group were similar to those of experimental group except for thoracic epidural anesthesia The blood samples from left common carotid artery before ligation were taken 15,30,60,120,180 and 240min after ligation, to measure the plasma levels of monoamine neurotransmitters with high performence liquid chromatography, the Ag Ⅱ and cortisol levels with radioimmunoassay TNFa content in non infarction myocardium was assessed with immunohistochemistry Results There were no differences in NE and 5 HT levels between both groups before ligation Thirty min after the ligation, NE level in experimental group remained unchanged, but in control group increased markedly(P

Objective The purpose of this study was to evaluate the effect of prostaglandin E 1 (PGE 1) on blocking the development of acute respiratory distress syndrome (ARDS) induced by acid aspiration. Methods Twenty 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 PGE 1 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-PGF 1?, TXB 2,NO 2 -/NO 3 - 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. Results In treatment group PaO 2 was significantly higher than that in injury group after acid instillation. Plasma 6-k-PGF 1? and NO - 2/NO - 3 levels were significantly higher in treatment group while plasma TXB 2 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 PGI 2 and TXA 2 and that between NO and ET-1 .