Objective:To observe whether the in-flow anesthetic gas absorber can reduce the recovery time after stopping inhalation of enflurane or isoflurane. Methods: In fixed tidal volume, minute volume and fresh gas flow, the recovery time of isoflurane or enflurane anesthesia with or without in-flow anesthetic gas absorber were compared after closing the vaporizer.Results: With in-flow anesthetic gas absorber, the time for anesthetic gas concentration in circle to reduce the MAC to 0.3was 3.3±0.5 min for isoflurane, which was significntly shorter than that without absorber (20±0.3min) ( P＜0.01 ) and the time for enflurane was 3.5±0.5min and 25±0.1min respectively. Conclusion:Anesthetic gas absorber can reduce the recovery time of either enflurane or isoflurane inhalational anesthesia significantly.

Objective To investigate the effect of different doses of propofol on cytokines-tumor necosis factor-? (TNF-?), interleukin-6 ( IL-6 ), interlenkin-8 ( IL-8 ), during systemic inflammatory response syndrome (SIRS) .Methods Fifty-six male Wistar rats weighing 190-220g were anesthetized with intraperitoneal 2.5% pentobarbital 30mg.kg-1 . The animals were randomly divided into 4 groups of 14 animals each: group A received intraperitoneal saline 10ml.kg-1 followed by intravenous infusion of saline (2ml.h-1 ); group B received intraperitoneal LPS 1mg.kg followed by intravenous infusion of saline(2ml.h-1 ) ; in group C propofol was infused iv at 75?g.kg-1.min for 4h after intraperitoneal LPS injection; in group D propofol was infusion iv at 150?g.kg-1 .min-1 for 4h after intraperitoneal LPS injection. Blood samples were taken before experiment and 1, 2, 3, 4h after saline or propofol infusion for determination of serum TNF-? (cytotoxin stain method) and IL-6, IL-8 (ELISA) concentration.Results Serum concentrations of TNF-?, IL-6 and IL-8 induced by LPS increased significantly in group B as compared with those in group A. Propofol decreased the level of cytokines and delayed the peak values of TNF-? and IL-8. Conclusion Propofol used in the early stage of SIRS has some protective efficacy.

Pathologic pain is a common suffering and does great harm to people health. Therefore it is important to search some suitable targets for pain management. Recently it has been shown that activated inflammatory cells and glia are strongly implicated in the pathologic pain. Cyclic 3',5'-adenosine monophosphate,a universal intracellular second messenger,has been proven to inhibit the activity of inflammatory cells and glia by enhancing its activity,further to control pathologic pain. This review presents the current understanding of the underlying mechanisms for the inhibitive effect of cAMP signal pathway in inflammatory cells and glia,and the effect of phosphodiesterase inhibitors used for relieving pathologic pain.

Objective To investigate the effectiveness of entropy in measuring the level of sedation during target controlled infusion (TCI) of propofol in patients of different ages. Methods Twenty-nine ASA Ⅰ-Ⅱ patients undergoing elective surgery under general anesthesia were divided into two age groups: Ⅰ adult group (20-64 yr) (n = 16) and Ⅱ the aged group (65-85 yr) ( n = 13). The patients were unpremedicated. The level of sedation was assessed using OAA/S scale. Propofol was given by TCI. The effect-site concentration (Ce) of propofol was set first at 1 ?g?ml-1 and then increased step by step by 0.5 ?g?ml-1 every 60 seconds until Ce reached 6 ?g?ml-1. Response entropy ( RE), state entropy ( SE), BP, HR, SpO2 were monitored and recorded at each Ce, before intubation, and immediately and 1, 2, 3, 4, 5, 10 min after intubation. The predictive performance of entropy was evaluated by prediction probability (Pk) .Results The two groups were comparable with respect to sex (M/F ratio), body weight and body weight index (kg?m-2). The RE and SE values decreased as Ce increased. The difference between RE and SE was also reduced. In adult group when Ce reached 2.0 ?g?ml-1, the RE and SE values were lower than the baseline values ( P

Objective To investigate the effects of propefol on β-amyloid protein(β-AP)-induced injury to cultured rat cortical neurons.Methods Eighteen days pregnant SD rats were anesthetized with ether.The fetal rats were obtained under sterile condition and decapitated. Cortices were then dissected under dissecting microscope.Cortical neurons were isolated according to the method described by Velly LJ et al and cultured for 7 days.There were 5×104 neurons in each well (200 μl).The experiment included 2 parts.In part T 15 wells of neurons were randomly divided into 5 groups(n=3 each ) : group I control(C);group II β-AP 25 μmol/L; group III and IV 2 propofol pretreatment groups (PP1,PP2) and greup V propofol treatment (PT).In group PPt propofol 50 μmol/L was added to the culture medium 24 h before the addition of β-AP 25 μmol/L and the neurons were incubated for another 24 h.In group PP2 propofol 50 μmol/L and μ-AP 25 μmol/L were added to the culture medium simultaneously and the neurons were then incubated for 24 h.In group PT propefol 50 μmol/L was added to the culture medium at 6 h after the addition of β-AP 25 μmol/L and the neurons were incubated for another 18 h.In part Ⅱ 18 wells of neurons were randomly divided into 6 groups(n=3 each):group I control (C) ; group IIβ-AP 25 μmol/L; group III intralipid; group IV,V,and VI 3 prepofol treatment groups (P1,P10,P50).In intralipid group equal volume of 10% intralipid was added to the culture medium at 6 h after β-AP 25 μmol/L and the neurons were then incubated for another 18 h.In group IV- VI propofol 1,10 and 50 μmol/L were added at 6 h alter β-AP 25 μmol/L respectively and the neurons were incubated for another 18 h.The amount of lactic dehydrogenase (LDH) released was measured.Neuronal viability was assessed by MTT assay.The neuronal apoptosis was detected using Hoechst33342 staining and TUNEL technique,and the.apoptosis rate was calculated.Results In part Ⅰ there was no significant difference in the amount of LDH released between group Ⅱ(β-AP) and the 2 propofol pretreatment groups(Ⅲ,Ⅳ).The amount of LDH released was significantly lower in group Ⅴ (propofol treatment) than in group β-AP(Ⅱ).In part Ⅱ the amount of LDH released was significantly lower,neuronal viability higher and the apoptosis rate was lower in group P50 than in group Ⅱ(β-AP).Conclusion Propofol 50 μmol/L given after β-AP can attenuate β-AP induced injury to cultured rat cortical neurons while prophylactic administration of propofol can't.

Dexmedetomidine( DEX) is a pure potent, highly se-lective and highly specific agonist ofα2-adrenergic receptors with sedative, analgesic and sympatholytic properties. The sedative effect mimics natural sleep of“arousable” and“cooperative” se-dation without respiratory depression. Due to the above properties and advantages, DEX has received adequate attention in clinical practice and its spectrum of application is also expanding. In re-cent years, it is proved that DEX is neuroprotective not only in animal researches but also in clinical studies. The neuroprotec-tion of DEX and its related mechanism will be briefly reviewed in this paper.

Objective To compare the effect of target-controlled infusion (TCI) and manual controlled infusion (MCI) of propofol in out-patients undergoing gastroscopy with the sedative depth monitoring by bispectral index (BIS).Methods Forty-eight patients with physical status Ⅰ-Ⅱ scheduled for an elective gastroscopy under general anesthesia were enrolled in this study. All patients were randomly divided into two groups, group T (n=24) and group M (n=24). Before induction, all patients were received a single dose of fentanyl (1 ?g/kg) intravenously. With the monitoring of BIS, the gastroscope was inserted in by the time of BIS value less than 60. Patients in group T received a propofol infusion with the initial plasma concentration of 1 ?g/ml and then the dose was titrated upward by 0.5 ?g/ml each time till the BIS values was less than 60 and then propofol was maintained at a concentration of 2-3 ?g/ml. In the group M, propofol was infused at a rate of 4 g/h until the BIS was less than 60 and then propofol was administrated at a rate of 4-6 mg?h -1?kg -1. During the period of gastroscopy, the sedation depth was maintained by BIS value of 40 to 60. The infusion was stopped by the end of biopsy in both groups. The time from induction to put in the endoscopy, the examination maintenance and the duration of anesthesia, the induction and total amounts of propofol infused were recorded and the average infusion rate was calculated. Results The induction time was significantly shorter in group T than in group M. The duration of examination, time from the induction to opening the eyes and time from induction to the orientation were not significantly different between two groups. Propofol consumption for induction and maintenance was much higher in group M than in group T. The average infusion rate was not significantly different in both groups. The BIS values were almost same at the beginning of gastroscopy and at opening the eyes. The plasma concentration and effect-site concentration were (4.25 ?0.94) ?g/ml and (1.78?0.66)?g/ml at the time of beginning of gastroscopy; while being (1.34?0.39) ?g/ml, ( 1.77?0.40) ?g/ml at the time of opening the eyes. There were 3 cases in group T and 7 cases in group M had sidereactions during the gastroscopy, respectively, but all were mild. Conclusions BIS could be a good sedative depth monitor in total intravenous anesthesia in out-patients gastroscopy. Target-controlled infusion system can help us to get accurate depth of anesthesia quickly and stably, and decrease the consumption of propofol and side effects as well.

Aim To investigate the effects of propofol on focal cerebral ischemia and the changes of protein kinase C isoform ?(PKC?) expression in rats brain. Methods Male SD rats were randomly allocated into five groups: Ⅰ: sham group, Ⅱ: injury group, Ⅲ: propofol (25 mg?kg-1) plus injury group, Ⅳ: propofol (50 mg?kg-1) plus injury group, Ⅴ: intralipid plus injury group. The focal cerebral ischemia was induced by 3 h of middle cerebral artery occlusion (MCAO) and 24 h of reperfusion. 30 min before reperfusion, propofol and intralipid were infused intraperitoneal of the rats in groups Ⅲ, Ⅳ, Ⅴ, respectively. After 24 h of reperfusion, rats were weighted and the neurological deficit was assessed by 5-point scale. Brain pathologic changes were observed by HE staining, the method of terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL) was carried out for the assessment of neural apoptosis, and immunocytochemistry was used to investigate the changes of PKC?.Results After 3 h of MCAO and 24 h of reperfusion, the weight of rats in group Ⅱ, Ⅲ, Ⅳ, Ⅴ decreased and their neurological deficits scores increased. Compared to the rats of sham group, the numbers of apoptosis neurons in striatum were marked-ly increased, and the expression of PKC? were significantly decreased in rats of injury group (P

6 h (n = 20). Swan-Ganz catheter was left in place after surgry for 40h. MAP, HR, ECG, cardiac output (CO), cardiac index (CI), PAP, PCWP, CVP, SVR, PVR and DO_2,VO_2, O_2-extraction rate (O_2 ER) were measured and/or calculated immediately after operation (T_1), 16 h (T_2 ),24 h (T_3 ) and 40 h (T_4 ) after operation. Results VAS scores were significantly lower in PCIA group than thosein IM group at T_(2, 3, 4) (P

Pulmonary function changes during and after cardiopulmonary bypass were studied using single breath test for CO_2 (SBT-CO_2) in 16 adult patients undergoing cardiac surgery. The results showed that P_(A-a)CO_2 and P_(A-a)O_2 increased significantly after bypass though PaCO_2 kept in normal range by adjusting ventilation volume. The CO_2 production increased as time passed after bypass, resulting in the increase of required minute volume and the rise of airway pressure. Compliance showed a tendency to decrease, while physologic dead space and alveolar dead space increased significantly. It is concluded that the causes of pulmonary dysfunction occurring in early stage of post-bypass are mainly due to the V/Q mismatch induced by low perfusion of the lung. To improve the pulmonary function at the early stage of post-bypass, the circulatory function should be improved accordingly.