Objective To evaluate the effect of edaravone on apoptosis in hippocampal cells in a rat model of endotoxic shock.Methods Thirty-six male Sprague-Dawley rats, weighing 200-250 g, aged 6 weeks, were randomly divided into 3 groups (n=12 each) using a random number table: control group (group C), endotoxic shock group (group ES), and edaravone group (group E).Lipopolysaccharide 10 mg/kg was injected via the femoral vein to establish the model of endotoxic shock in ES and E groups, while the equal volume of normal saline was given in group C.In group E, edaravone 3 mg/kg was intravenously injected immediately after establishment of the model once every 2 h until the animals were sacrificed.The equal volume of normal saline was given instead of edaravone in C and ES groups.At 6 and 12 h after administration of edaravone, 6 rats in each group were sacrificed, and the hippocampi were isolated for determination of malondialdehyde (MDA) content (using thiobarbituric acid method) , tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) contents (using enzyme-linked immunosorbent assay), and cell apoptosis in hippocampal CA1 region (by TUNEL assay).The apoptotic index was calculated.Results Compared with group C, the MDA, TNF-α and IL-6 contents were significantly increased at 6 and 12 h after administration of edaravone, and the apoptotic index was increased at 12 h after administration of edaravone in ES and E groups.Compared with group ES, the MDA, TNF-α and IL-6 contents were significantly decreased at 6 and 12 h after administration of edaravone, and the apoptotic index was decreased at 12 h after administration of edaravone in group E.Conclusion Edaravone can reduce apoptosis in hippocampal cells, and the mechanism is associated with the reduced oxidative stress and inflammatory responses in a rat model of endotoxic shock.

Objective To evaluate the effects of edaravone on the permeability of blood-brain barrier in septic rats.Methods Ninety male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 3 groups (n=30 each):control group (group C),sepsis group (group lipopolysaccharide (LPS)) and edaravone group (group E).Sepsis was induced by injection of LPS 10 mg/kg via the femoral vein in LPS and E groups.After LPS injection,edaravone 3.0 mg/kg was injected intravenously every 2h for 7 times in group E.The equal volume of normal saline was administered instead of edaravone in C and LPS groups.At 2,6 and 12h after LPS injection,5 rats were chosen and Evan's blue (EB) was injected via the femoral vein,and then the rats were sacrificed and brain tissues were removed for determination of EB and water contents.Another 5 rats were chosen and blood samples were taken from the femoral artery for measurement of serum MDA concentration,and then the rats were sacrificed and the brain tissue was harvested for microscopic examination.Results Compared with group C,brain water and EB contents were significantly increased at 6 and 12h after LPS injection,and the serum MDA concentration was increased at 2,6 and 12h after LPS injection in LPS and E groups (P ＜ 0.05).Compared with group LPS,brain water and EB contents were significantly decreased at 6 and 12h after LPS injection,and serum MDA concentrations were decreased at 2,6 and 12h after LPS injection in group E (P ＜ 0.05).Sepsis-induced pathological changes were significantly attenuated in group E.Conclusion Edaravone can decrease the permeability of blood-brain barrier,attenuate brain edema and brain injury in septic rats,and reduction of oxygen free radical production may be involved in the mechanism.

ObjectiveTo investigate the effect of preoperative sleep disturbance on the efficacy of flurbiprofen for postoperative analgesia in patients undergoing endoscopic nasal surgery.MethodsNinety-six ASA Ⅰ or Ⅱ patients of both sexes aged 20-60 yr weighing 50-80 kg undergoing endoscopic nasal surgery were enrolled in this study.Pittsburg sleep quality index was used to evaluate long-term sleep quality before hospitalization and Athens sleep quality index was used to evaluate short-term sleep quality in hospital.The patients were divided into 4 groups according to the types of preoperative sleep disturbance ( n =24 each):group Ⅰ no sleep disturbance;group Ⅱ long-term sleep disturbance; group Ⅲ acute short-term sleep disturbance; group Ⅳ long-term + acute short-term sleep disturbance.Anesthesia was induced with sufentanil,propofol and cis-atracurium and maintained with iv infusion of remifentanil and propofol.The patients were intubated and mechanically ventilated.PETCO2 was maintained at 30-35 nun Hg.Controlled hypoteasion was performed with nicardipine,MAP was maintained at 50-70 mm Hg and HR at 60-90 bpm during operation.The patients received iv flurbiprofen 50 mg at 15 min before the end of operation for postoperative analgesia.When VAS score was more than 3 during the fnrst 6 h after operation,flurbiprofen 50 mg was given iv as rescue analgesic.ResultsThe incidence of rescue analgesic administered after operation was significantly larger in groups Ⅱ,Ⅲ and Ⅳ than in group Ⅰ,and in group Ⅳ than in groups Ⅱ and Ⅲ.There was no significant difference in the incidence of rescue analgesic administered during the first 6 h after operation between groups Ⅱ and Ⅲ.ConclusionPreoperative sleep disturbance has adverse effect on the efficacy of flurbiprofen for postoperative analgesia in patients undergoing endoscopic nasal surgery.

Objective To investigate the effects of dexmedetomidine on lipopolysaccharide (LPS)-induced brain injury in rats.Methods Thirty-six pathogen-free Sprague-Dawley rats,aged 6 weeks,weighing 200-250 g,were randomly divided into 3 groups (n =12 each):control group (group C),LPS group (group L) and dexmedetomidine group (group D).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 350 mg/kg,tracheostomized and mechanically ventilated.Dexmedetomidine 100 μg/kg was injected intraperitoneally and LPS 7.5 mg/kg was injected via the femoral vein 15 min later in group D.Normal saline 2 ml was injected intraperitoneally and LPS 7.5 mg/kg was injected via the femoral vein 15 min later in group L.Normal saline 2 ml was injected intraperitoneally and then injected via the femoral vein 15 min later in group C.Blood samples were obtained from the femoral artery at 2 and 4 h after LPS administration for determination of serum TNF-α concentration by ELISA.Six rats were chosen at 12 h after LPS administration,Evan's blue (EB) was injected via the femoral vein,and then the rats were sacrificed and brains removed for determination of EB content.Another six rats were sacrificed and their brains were immediately removed for determination of brain water content and for microscopic examination.Results The brain water content,EB content and serum TNF-α concentration were significantly increased in groups L and D as compared with group C (P ＜ 0.05).The brain water content,EB content and serum TNF-α concentration were significantly lower in group D than in group L (P ＜ 0.05).The microscopic examination showed that brain injury was attenuated in group D compared with group L.Conclusion Dexmedetomidine can reduce LPS-induced brain injury and reduction of the inflammatory response in the brain tissues and improvement in the permeability of the blood-brain barrier may be involved in the mechanism.

Objective To evaluate the accuracy of bispectral index(BIS)and entropy index in monitoring the depth of anesthesia in patients during target-controlled infusion(TCI)of propofol on induction of anesthesia.Methods Fifty ASA grade Ⅰ-Ⅱ of chronic sinusitis patients who performed the surgery of nasal sinus patency were enrolled in this study.After into operation room(T0),anesthesia was induced with TCI of propofol,and it was added 0.3 μ g/ml after 30 seconds once the plasma drug level was 2.1 μ g/ml(T1)until loss of consciousness(T2),and added 0.5 μg/ml(T3).When tracheal intubation,the patients was injected 0.6 mg/kg rocuronium in their intravenous at the prospective plasma drug level(T4).Each case was monitored with BIS,state entropy index(SE)and response entropy index(RE).The data at following time were recorded:T0-T4,tracheal intubation(T5),1 minute and 3 minutes after tracheal intubation(T6,T7),skin incision(T8).Results The value of BIS,SE and RE were significantly decreased compared with T0 (P ＜0.05).Mean arterial pressure(MAP)and heart rate were in normal range.The value of RE was significantly higher than SE at all the time points(93 ± 9 vs.87 ± 5,88 ± 12 vs.82 ± 12,73 ± 25 vs.72 ± 21,57±21 vs.56±22,46± 16vs.43 ± 17,39± 14 vs.37± 12,36± 14vs.34± 11,35 ± 11 vs.32±9,39±15 vs.36 ± 12)(P ＜ 0.05),but there was no significantly difference between BIS and SE at all the time points(P ＞ 0.05).The value of BIS had significantly positive correlation with SE and RE(r =0.887,0.901 ;P ＜ 0.01).Conclusions During deep hypnosis,BIS,SE and RE all can provide information about the level of consciousness during TCI of propofol on induction of anesthesia.RE is more preponderant as a monitor than BIS and SE.

Objective To evaluate the effect of sleep deprivation on cognitive function in the rats undergoing propofol anesthesia.Methods Sixty healthy male Sprague Dawley rats,aged 14-18 weeks,weighing 200-250 g,were randomly assigned into 3 groups (n=20 each) using a random number table:control group (group C),propofol anesthesia group (group P),and sleep deprivation + propofol anesthesia group (group SDP).Propofol was given as a bolus of 15 mg/kg followed by an infusion of 40 mg · kg-1 · h-1 for 2 h in group P.After the rats were subjected to rapid eye movement sleep deprivation for 24 h,the rats received propofol anesthesia in group SDP.Before sleep deprivation,after sleep deprivation,and at 1,3 and 7 days after anesthesia,Morris water maze test was used to assess the learning and memory function,and the escape latency and frequency of crossing the original platform were recorded.Ten rats randomly selected from each group at 1 and 7 days after anesthesia were sacrificed,and brains were removed to observe the morphology of nerve cells in the hippocampal CA1 region (by Nissl's staining) and to detect the expression of phosphorylated Tau at Thr231 (Tau-pThr231) in the hippocampal CA1 region (by immunohistochemisty).Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform was decreased,the expression of Tau-pThr231 in the hippocampal CA1 region was up-regulated at 1 day after anesthesia in P and SDP groups (P＜0.05),especially in group SDP (P＜0.05),and there was no significant difference between the groups at the other time points (P＞0.05).The pathological changes were aggravated at 1 day after anesthesia in group SDP compared with group P,and there was no significant difference at 3 and 7 days after anesthesia between group SDP and group P.Conclusion Sleep deprivation can aggravate the transient cognitive dysfunction after propofol anesthesia,and the mechanism is related to promotion of Tau phosphorylation in the rats.

Objective To investigate the effects of sevoflurane anesthesia in diabetic pregnant rats on the cognitive function of the offspring rats. Methods Forty female Sprague?Dawley rats and 5 male rats, weighing 200-250 g, were used in the study. Twenty pregnant rats at 7 weeks of gestation were randomly selected, and diabetes mellitus was induced by intraperitoneal streptozotocin 45 mg∕kg and confirmed by blood glucose level>10.4 mmol∕L. Twenty pregnant rats at 20 days of gestation, in which diabetes mellitus was not induced, were selected and divided into 2 groups ( n=10 each) using a random number table:sevoflurane group (group S) and control group (group C). Twenty pregnant rats at 20 days of gestation with diabetes mellitus were selected and divided into 2 groups ( n=10 each) using a random number table:sevoflurane group (group DS) and control group ( group DC). In DS and S groups, the pregnant rats were placed in a self?made anesthetic box and inhaled 2% sevoflurane for 2 h. At 6 weeks after birth, the offspring rats were selected, and Morris water maze test was performed. The rats were sacrificed, brains were removed, and the hippocampi and cortex were removed for determination of phosphorylated cyclic a?denosine monophosphate response element?binding protein ( p?CREB) expression using immuno?histochem?istry. Results Compared with group C, the escape latency was significantly prolonged, and the frequency of crossing the original platform was significantly decreased in S and DC groups ( P<0.05) . Compared with group DC, the escape latency was significantly prolonged, and the frequency of crossing the original plat?form was significantly decreased in group DS (P<0.01). Compared with group S, the escape latency was significantly prolonged, the frequency of crossing the original platform was significantly decreased ( P<0.05) , and lighter staining for p?CREB was found, and the number of p?CREB positive cells was decreased in the hippocampus and cortex in group DS. Conclusion Sevoflurane anesthesia?induced cognitive dys?function is aggravated in the offspring rats of diabetic pregnant rats, and the mechanism is related to inhibi?tion of CREB phosphorylation.

To investigate the inhibiting effects of ketamine on arterial plasma TNF-? concentration and lung injury in septic shock rat. Method: 40 Wister rats were divided into five groups. 15mg?kg~(-1) endotoxin (LPS) was intravenously injected alone (group Ⅰ)or ip ketamine 50,100 and 200mg?kg~(-1) before LPS, then ketamine was infused at 10mg?kg~(-1)?min~(-1) (Ⅱ, Ⅲ and Ⅳgroup). TNF-? was assessed with ELISA, and at the same time the arterial blood oxygen tension and lung water content were measured. Result: In contrast to normal control level, arterial plasma TNF-? levels and lung water content increased and arterial oxygen tension decreased after LPS in group Ⅰ, but in the rats of giving ketamine, plasma TNF-? level decreased more than that in the rats of giving LPS alone (group Ⅰ), change of arterial blood oxygen tension and lung water content in former groups were better than that of later, in dosage-dependent way. Conclusion: Ketamine can dose-relatedly decrease TNF-? concentration and lung injury degree induced by endotoxin.

Objective To investigate the effects of pulmonary arterial endothelium cells(PAEC) injuryed by tumor necrosis factor ? (TNF-?) on the proliferation of pulmonary arterial smooth muscle cells (PASMC) and the influence of heat stress response (HSR) on it .Methods Normal PAEC or PAEC endured with HSR were incubated with TNF-? at the concentrations of 500, 1000 and 2000u/ml in 1 hour, then cultured in DMEM without serum in 24 hours, the upper liquid was collected to prepare the endothelial cell-conditioned medium liquid (EC-CMⅠ or EC-CMⅡ ), in which PASMC were incubated in 24 hours as group Ⅰ or group Ⅱ respectively. The normal endothelial cell-conditioned medium liquid was also prepared to incubate PASMC in 24 hours as group Ⅲ.The PASMC were incubated without the endothelial cell-conditioned medium liquid as group Ⅳ.Flow cytometry was applied to determining the intracellular DNA content of the incubated PASMC. The fractions of different cytocycle phases were calculated according to the areas under the curves of DNA content.Results Compared with those of group Ⅳ, the percentage of PASMC in G0-G1 phases increased markedly ,and in S and G2-M phases decreased significantly in group Ⅲ (P

0 05) The duration of T 1 recoving to 90% of baseline was 34 57min,and the recovery index was 24 29 min No any histamine related side effects were observed in all patients Conclusions Intravenous infusion of rapacuronium can produce safe and effective neuromuscular blockasde during desflurane, sevoflurane, isoflurane, or propofol anesthesia After the rapacuronium infusion of 45 60 min, the recovery from the neuromuscular blockasde is prolonged