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.

Adult ; Humans ; Male ; Middle Aged ; Phosphines ; poisoning ; Young Adult

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.

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 test whether sodium arsenite can induce in vitro reverse mutation of Salmonella typhimurium histamine-auxotroph mutant. Methods Ames test was carded out with Salmonella typhimurium strains TA97,TA98,TA100 and TA102 by standard method with or without the liver microsomal enzyme activation system (+S9,-S9). Results At concentrations of sodium arsenite from 500.00 to 5000.00 μg/plate, no colonies were seen on the plates of TA97,TA98,TA100 or TA102, with or without the presence of S9. At concentrations of sodium arsenite of 0.01,0.10,10.00 μg/plate and with the presence of S9, twice as many colonies grew on the plates of TA102 as the negative control(P<0.05). Without S9 activation,twice as many colonies grew on the plates of TA100 as the negative control(P<0.05)at concentrations of sodium arsenite of 1.00,10.00 μg/plate(P<0.05). The reverse mutation colonies induced by sodium arsenite in TA98 strain were twice as many as negative control group at concentrations of 0.01,0.10 μg/plate(P<0.05). There was no obvious increase of the strain clones in the other(P0.05). Conclusions With and without S9 activation, the doses of 500.00,5000.00 μg/plate sodium arsenite resulted in a toxic effect and a reduction of the revertants among the strain. At concentrations of 0.01～10.00 μg/plate, sodium arsenite exhibited mutngenesis effects.