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.

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 investigate the relationship between the plasma concentration of nitric oxide (NO) and prognosis of the hemorrhagic shock. Method:The blood levels of NO and Lactate (LA) were measured with fluorophotometry and colorimetry in 30 hemorrhagic shock patients,and another 30 patients for elective surgery served as a control. Result :Concentration of NO was significantly lower and that of LA was significantly higher in hemorrhagic shock group than that of control group. NO level had a negative correlation with LA level and injury index. NO level in the patients complicated by sepsis were still lower than the control. Conclusion:Decrease of NO level may result in disturbance of microcirculation and increase of LA. So nitroglycerin should be used as early as possible in the hemorrhagic shock patients.

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

Objective The purpose of this study was to assess the effects of heat stress response (HSR) on i of pulmonary arterial endothelium cells (PAEC)incubated with TNF-?. We tried to illustrate the mechanism of injury to PAEC caused by TNF-? and the effects of HSR.Methods The study consisted of four groups.In group Ⅰ confluent monolayer of calf PAEC were directly incubated with TNF-? at final concentrations of 500, 1 000 and 2 000 u/ml for 24 h.In group Ⅱ PAEC were first bathed in 42℃ water for 20 min and then allowed to recover for 24 h.In turn they were incubated with TNF-? at the same concentrations.In group Ⅲ PAEC were not heated and incubated with TNF-?.In group Ⅳ PAEC were heated but not incubated with TNF-?.i of PAEC was assayed by fluorospectrophotometry and i of four groups were compared.The change in i before and after incubation of PAEC with TNF-?(?i) was calculated.Results (1) i was considerably higher in group Ⅰ than that in group Ⅲ at different concentrations in dose-dependent way.(2) Although i was higher in group Ⅳ than that in group Ⅲ, HSR could inhibit the further increase in i of PAEC incubated with TNF-?.Conclusions HSR may decrease the i in PAEC incubated with TNF-?.It indicates that HSR can prevent PAEC from calcium overload and provide protection on PAEC against injuries.

Objective Desflurane is now well accepted by anesthesiologists because of its rapid induction and recovery but carboxyhemoglobin(CUHb) formation from interaction of desflurane with soda lime is a major concern. The purpose of this study was to investigate the effects of different fresh gas flow(FGF) rates on COHb formation during desflurane anesthesia. Methods Forty ASA Ⅰ-Ⅱ nonsmoking patients undergoing elective surgery were randomly divided into four groups with ten patients in each group according to FGF rate: group Ⅰ 0.5L/min; groupⅡ 1.0L/min; group Ⅲ 2.0L/min; group Ⅳ4.0L/min. The patients were premedicated with pethidine 1mg/kg and atropine 0.01mg/kg. Anesthesia was induced with midazolam 0.05mg/kg, propofol 2mg/kg and fentanyl 7pg/kg. Intubation was facilitated with succinylcholine. Anesthesia was maintained with desflurane( 1 .5 MAC), nitrous oxide( 50%) and intermittent vecuronim and fentanyl. PET CO2 was maintained between 35-40 mmHg. Venous blood samples were taken before and 2h, 4h and 6h after induction of anesthesia and at the end of operation for determination of COHb level. Results There was no significant difference among the four groups in age, gender and weight. COHb concentration was not significantly different before and 2h after induction of anesthesia among the four groups, but increased significantly at 4h and 6h after induction of anesthesia and at the end of surgery in groupⅣ, and tended to increase as the operation was prolonged. It was found that patients who developed postoperative headaehe and PONV were mostly from group IV, but no patients developed delayed neuropsychologic sequelae. Conclusions COHb level increases with high FGF rate but not with low FGF rate because of dryness and higher temperature of soda lime. Fresh soda lime should not be left in Canister too long and should be replaced shortly before anesthesia.

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.