Objective To evaluate the efficacy and the effects of sevoflurane induced hypotension on balance of cerebral oxygen supply and consumption and on cerebral energy metabolism. Methods Forty patients undergoing elective procedures were randomly divided into three groups. Group Ⅰ :sevoflurane induced hypotension ; group Ⅱ: sevoflurane maintained normal arterial tension ; group Ⅲ: nitroprusside induced hypotension . In groupⅠ and Ⅲ MAP was decreased to 50%-60% of baseline ,was kept for 40 min either by sevoflurane inhalation or by nitroprusside infusion. MAP ,HR,ECG were monitored continuously, and radial arterial blood samples and jugular blood samples were taken synchronously for measuring blood gas and blood lactate ,SOD and MAD levels. Results In group Ⅰ during induced hypotension Da jvO 2 showed reduction ,but in group Ⅲ Da jvO 2 increased significantly. There were no significant changes in blood lactate level and in the cerebral arteriovenous differences of MAD and SOD in three groups.Conclusions The sevoflurane induced hypotension has no adverse effect on cerebral oxygen balance and the cerebral perfusion . The cerebral energy metabolism is well maintained . Sevoflurane can safely applied to controlled hypotension during cerebral neurosystem.

OBJECTIVE: To establish a method for analysis of proteome of human peripheral leukocytes and to explore the difference between the healthy volunteers and patients with acute lymphocyte leukemia(ALL) in leukocyte proteomics and to study the ALL-related abnormal proteins.METHODS: Peripheral blood samples taken from 10 healthy volunteers and 10 ALL patients were separated for the extraction of leukocyte proteins.The leukocyte proteins were separated by two-dimensional electrophoresis(2-DE).2-DE patterns were analyzed by PDQuest 2D software and the differentially expressed proteins were identified by matrix assisted laser desorption ionization-time of flight-mass spectrometer(MALDITOF-MS) and bioinformatics.RESULTS: The 2-DE patterns of peripheral blood leucocytes from patients with ALL versus those from healthy volunteers were analyzed by PDQuest 2D software and the differentially expressed proteins identified by matrix assisted laser desorption ionization-time of flight-mass spectrometer(MALDI-TOF-MS) were confirmed to beALL-related proteins: AnnexinA5 and cytoskeleton 14 etc.CONCLUSION: Using MALDI-TOF-MS and bioinformatics,the AnnexinA5 and cytoskeleton 14 proteins had been proved to be of close relationship with ALL.The results provided a satisfactory basis for the searching for treatment targets and the molecular targets for the early diagnosis of ALL.

Objective To evaluate the effect of preconditioning with nimodipine on postoperative cognitive dys function of aged rats.Methods Ninety healthy male Sprague-Dawley rats,aged 18 months,weighing 400-500 g,were randomly divided into 3 groups (n =30 each) using a random number table:nimodipine control group (group N),surgery group (group S),and nimodipine + surgery group (N+ S group).In N and N + S groups,nimodipine 1 mg/kg was intraperitoneally injected,while the equal volume of normal saline was given instead in S group.30 min later,group N inhaled pure oxygen for 2 h,and S and N + S groups inhaled 1.8 ％ isoflourane for 2 h when splenectomy was performed.Morris water maze test was performed on 1 day before operation and 1st,3rd and 7th days after operation.After the end of Morris water maze test at 1 day before operation and 1st and 7th days after operation,10 rats were sacrificed and brains were removed and hippocampi were isolated for determination of apoptosis in hippocampal neurons,intracellular [Ca2+] i in cytoplasm,and hippocampal Bcl-2 and Bax mRNA expression and for examination of ultrastructure of hippocampal neurons.Results Compared with the value before administration,the escape latency was significantly prolonged,the frequency of crossing the original platform was decreased,apoptotic rate and [Ca2+]i were increased,Bcl-2 mRNA expression was down-regulated,and Bax mRNA expression and Bax/Bcl-2 mRNA ratio were up-regulated at each time point after operation in S and N + S groups,and no significant changes were found in the parameters mentioned above in N group.Compared with group S,the escape latency was significantly shortened,the frequency of crossing the original platform was inecreased,apoptotic rate and [Ca2+]i were decreased,Bcl-2 mRNA expression was up-regulated,and Bax mRNA expression was down-regulated at each time point after operation in group N + S.Pathological changes were found in S and N + S groups and the damage was severer in S group than in N + S group.Conclusion Nimodepine preconditioning can prevent postoperative cognitive dysfunction of aged rats,and inhibition of calcium overloadinduced apoptosis in hippocampal neurons may be involved in the mechanism.

Objective To evaluate the role of calpain in sevoflurane anesthesia-induced apoptosis in hippocampal neurons of aged rats.Methods Fifty-four healthy female Sprague-Dawley rats,aged 18 months,weighing 450-550 g,were randomly divided into 3 groups (n=12 each) using a random number table:control group (group C),sevoflurane group (Sev group) and calpain inhibitor M DL28170 group (group M).In group C,the rats inhaled 50％ O2-50％N2 for 3 h.In Sev group,the rats inhaled 3％ sevoflurane for 3 h.In group M,MDL28170 10 mg/kg was injected via the tail vein,30 min later 3％ sevoflurane was inhaled for 3 h,and MDL28170 was simultaneously infused at 3.33 mg · kg 1 · h-1 via the tail vein.Nine rats in each group were selected,and cognitive function was assessed by using Morris water maze test at 30 min before anesthesia and 1-5 days after anesthesia.The escape latency and frequency of crossing the original platform were recorded.After the end of Morris water maze test performed at 30 min before anesthesia and 1-5 days after anesthesia,3 rats in each group were sacrificed,and hippocampal tissues were obtained for detection of cell apoptosis (by flow cytometry) and intracellular [Ca2+] i.Apoptotic rate was calculated.Results Compared with group C,the escape latency was significantly prolonged,and the frequency of crossing the original platform was decreased,and the apoptotic rate and intracellular [Ca2+]i were increased at 1 day after anesthesia in Sev and M groups.Compared with group Sev,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,and the apoptotic rate was decreased at 1 day after anesthesia,and no significant change was found in intracellular [Ca2+]i in group M.Conclusion Calpain activation is involved in sevoflurane anesthesia-induced apoptosis in hippocampal neurons of aged rats.

Objective To evaluate the effects of the prone position on pulmonary gas exchange during mechanical ventilation under general anesthesia.Methods Thirty patients scheduled for elective spine surgery in the prone position under general anesthesia (group prone,n =30),30 patients scheduled for elective spine surgery in the supine position under general anesthesia (group supine,n=30),aged 30-64 yr,with body mass index of 19-30 kg/m2,of ASA physical status Ⅰ or Ⅱ,were enrolled in the study.After induction of general anesthesia,the patients were mechanically ventilated.Anesthesia was maintained with total intravenous anesthesia.At 10 min before pre-oxygenation (T0),10 min after intubation (immediately after the patients were moved from the supine to the prone position) (T1),45 and 90 min after intubation (T2,3),5 min before extubation (immediately before supine position to the prone position) (T4),and 15 min after extubation (T5),arterial blood samples were taken for blood gas analysis,and PaO2 and PaCO2 were recorded.Alveolar-arterial oxygen difference (A-aDO2) was calculated.Digital radiography was performed and the changes of the lung were observed.Results Compared with supine group,PaO2 was significantly increased and A-aDO2 was decreased at T1-4 in prone group.There was no significant difference in PaCO2,and PaO2 and A-aDO2 at T0 and T5 between the two groups.The results of digital radiography showed no atelectasis at different time points in either group.Conclusion Pulmonary gas exchange in the prone position is superior to that in the supine position during mechanical ventilationunder general anesthesia.

Objective To evaluate the role of mitochondria-mediated apoptosis in hippocampal neurons in sevoflurane anesthesia-induced cognitive dysfunction in aged rats.Methods Sixty healthy male Sprague-Dawley rats,aged 20 months,weighing 550-600 g,were randomly divided into 2 groups (n =30 each) using a random number table:control group (group C) and sevoflurane anesthesia group (group S).Animals inhaled pure oxygen and 3 ％ sevoflurane for 4 h in C and S groups,respectively.Ten rats were chosen at 1 and 6 days after anesthesia and hippocampal tissues were obtained for detection of cell apoptosis and mitochondrial membrane potential (MMP) (using flow cytometry) and expression of cytochrome c (Cyt c) in cytoplasm and activated caspase-3 in hippocampal neurons (by Western blot).The apoptotic rate was calculated.Results Compared with group C,the escape latency was significantly prolonged,the frequency of crossing the original platform,the percentage of time of staying at the original platform quadrant and MMP were decreased,the apoptotic rate was increased,and the expression of activated caspase-3 and Cyt c in cytoplasm was up-regulated in.group S.Conclusion The mechanism by which sevoflurane anesthesia induces cognitive dysfunction is related to the activation of mitochondria-mediated apoptosis in hippocampal neurons of aged rats.

BACKGROUND:Sleep deprivation, resulting in a series of physiological and psychological reactions, is a common phenomenon in our modem society. Recently, many physical and medical therapies are on their way to eliminate the negative influence the sleep deprivation exerted on our human beings, and a large number of cigarette smokers believe that cigarette smoke can obviously improve their abnormal behavioral performance and negative emotional fluctuation caused by sleep deprivation in short terms.However, there are few researches but many disputes when it comes to effect of passive smoking on the behavior and emotion of rats on the occasion of acute sleep deprivation.OBJECTIVE: To investigate the effect of passive smoking (PS) on the behavior and emotion of rats with acute sleep deprivation (SD).DESIGN: Completed randomized and controlled study.SETTING: Basic Medicine Experiment Center, School of Basic Medicine;Department of Radiation Medicine, School of Preventive Medicine, Fourth Military Medical University of Chinese PLA.MATERIALS: The experiment was carried out at Experiment Center of Basic Medicine, Fourth Military Medical University of Chinese PLA from April to June 2004. Totally 49 healthy adult male Sprague-Dawley rats,being 3 months old, weighting (180±15) g, were randomly divided into 5groups: sleep deprivation + 24-hour passive smoking group (n=8), 24-hour sleep deprivation group (n=8), sleep deprivation + 54-hour passive smoking group (n=8), 54-hour sleep deprivation group (n=8), and blank control group (n=7).METHODS: ① Rats in sleep deprivation + 24-hour passive smoking group, 24-hour sleep deprivation group, sleep deprivation + 54-hour passive smoking group and 54-hour sleep deprivation group were performed with sleep deprivation with flower pot method for 24 and 54 hours, and rats in sleep deprivation + 24-hour passive smoking group and sleep deprivation + 54-hour passive smoking group were treated with passive smoking at the same time at a frequency of 12 times/day, 120 minute/time, 3cigarettes were lighted at the same time and kept into ashes. ② Broad field test was conducted to determine the behavioral and emotional changes of the rats. We trailed their activities by video recorder for 5 minutes each time. Then we presented the image information to computer process and finally got the total distance and the average distance from the center of the broad field for each rat during the 5-minite test. Meanwhile, we also observed the emotional variety and excitability of the rats. The nearer the average distance from center was, the more the emotional behavior and the greater excitability were; and the longer the total distance was, the greater the excitability was. ③ All the data were expressed with Mean ± SD, the method of non-parametric rank sum test was adopte d for comparing among groups, P ＜ 0.05 was regarded as statistical significance.MAIN OUTCOME MEASURES: Comparisons between DC and TD of rats in each group, and changes of behavior and emotion of rats in each group.RESULTS: Data of all the 49 rats was entered the final data analysis without any loss. ① Observation of emotional stage: Compared with sleep deprivation + 54-hour passive smoking group, rats in sleep deprivation+24-hour passive smoking group appeared more quiet and indifferent, and presented lower excitability, less sensitivity to outside stimulus and less aggressive behaviors towards other rats, and the same as 24-hour sleep deprivation group, compared with 54-hour sleep deprivation group. ② Results from the open field test: DC of 24-hour sleep deprivation group was significantly smaller than that of blank control group and sleep deprivation + 24-hour passive smoking group [(53.93±1.83, 58.21±4.45, 58.11±1.62) cm, (P＜ 0.01-0.05)]. DC of 54-hour sleep deprivation group was significantly bigger than that of 24-hour sleep deprivation group [(61.53±3.02, 58.11±1.62) cm, (P＜ 0.01)]; TD of 24-hour sleep deprivation group was significantly bigger than that of sleep deprivation + 24-hour passive smoking group [(3310.45±1 445.97, 1 818.20±733.25, 2 338.15±694.70) cm, (P ＜ 0.01-0.05)], and that of 54-hour sleep deprivation group was bigger than that of sleep deprivation + 54-hour passive smoking group andsmaller than that of 24-hour sleep deprivation group [(2 410.70t548.64, 1 473.50±945.89, 3 310.45±1 445.97) cm, (P＜0.05)].CONCLUSION: With the prolongation of sleep deprivation time, behavior and emotional reaction of rats are shown from exciting to inhibiting, however, passive smoking can inhibit behavior and emotional state of rats during the whole sleep deprivation.

Objective To investigate the role of GABAB1 receptors in spinal dorsal horn neurons in the development of diabetic neuropathic pain (DNP). Methods Sixty pathogen free male SD rats aged 4 weeks weighing 150-170 g were randomly divided into 2 groups ( n = 30 each): control group and DNP group. Diabetes mellitus was induced by single intraperitoneal injection of streptozotocin 50 mg/kg. Blood glucose levels and paw withdrawal threshold to mechanical stimuli were measured at 3, 5 and 7 weeks (T1, T2, T3 ) after IP STZ/NS ( n = 10 each). The animals were sacrificed after PWL measurement. The lumbar segment of the spinal cord was removed for determination of the expression of GABAB1 receptors by immuno-histochemistry, RT-PCR and Western blot analysis. Results The blood glucose levels were significantly higher while the PWT was significantly lower at T1,T2 and T3 in group DNP than in control group. The expression of GABAB1 receptor mRNA and protein in spinal dorsal horn was significantly lower at T2 and T3 in DNP group than in control group. Conclusion The expression of GABAb1 receptors is down-regulated in spinal dorsal horn neurons in rats with DNP.

Objective To evaluate the role of M3 muscarinic acetylcholine receptor (M3 mAChR) in the release of glycinergic neurotransmitter by using oxotremorine-M (Oxo-M: a nonselective mAChR agonist) and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP: a highly selective M3mAChR antagonist). Methods Twenty male 3-4 weeks old SD rats weighing 160-180 g after successful intrathecal catheterization were randomized into 2 groups (n = 10 each): normal saline group (group NS) and pertussis toxin (group PTX).Pertussis toxin 1.5 μg/10 μl was injected IT in group PTX, while in group NS normal saline 10 μl was injected IT instead. The animals were killed at day 7 after injection. The spinal cords were removed and sliced and placed in artificial CSF. Glycinergic spontaneous inhibitory postsynaptic currents (sIPSCs) were measured in spinal lamina Ⅱneurons using whole-cell voltage-clamp technique. Five minutes after sealing, Oxo-M (final concentration 3 μ mol/L) was added. Oxo-M was then completely washed out 3 min later and 4-DAMP (final concentration 25 nmol/L) was added after 5 min of stabilization. In the presence of 4-DAMP, Oxo-M (final concentration 3 μmol/L) was added again 3 min later. sIPSCs were recorded before addition of Oxo-M (T1), 3 min after addition of Oxo-M (T2), 3 min after addition of 4-DAMP (T3), 3 min after the second addition of Oxo-M (T4). Results Compared with the baseline value at T1 , Oxo-M significantly increased the frequency of glycinergic sIPSCs at T2without changing the amplitude at T2-4 in both groups. The frequency of sIPSCs was significantly lower at T4 than at T2 in both groups (P ＜ 0.05 or 0.01). There was no significant difference in both frequency and amplitude of glycinergic sIPSCs between the two groups. Conclusion M3 mAChR plays a predominant role in the release of glycinergic transmitter in the spinal lamina Ⅱ neurons in rats.

Objective To investigate the effect and mechanism of sodium ferulate (SF) on injury of gastric mucosa after traumatic hemorrhage shock resuscitation in rabbits.Methods One hundred healthy rabbits were randomly ( random number) divided into 4 groups ( n =25 in each group):control group ( A),model group ( B),pre-resuscitation SF group (C) and post-resuscitation SF group (D).The gastric mucosa injury model was established by using a method of comminuted fracture of femur and blood depletion.SF 30 mg/kg was injected into vein of rabbits' ear 20 min before resuscitation in group C and 30 min after resuscitation in group D,while rabbits of remaining groups received equal volume of normal saline instead.The gastric mucosa was obtained 90 min after resuscitation.The damage index (DI) of gastric mucosa was observed with method of Guth and the ultra-structure of parietal cell of stomach was observed under electronic microscope and the contents of TXB2 and 6-Keto-PGF1α in gastric tissue homogenate were determined with radio-immunity methods,and the ratios of TXB2/6-Keto-PGF1α were calculated.Data were analyzed by ANOVA ( LSD-t test ),and P ＜ 0.05 was considered as statistical significance. Results Under the electronic microscope,the secreting tubules were observed to be closed tightly in the parietal cells of stomach in the group A,showing a static status.However,in the group B,the number of normal secreting tubules was increased and the lumens were enlarged obviously.Compared with the group B,the number of normal secreting tubules was decreased and the enlargement of secreting tubules was not obvious in group C.The degree of changes in secreting tubules in group D was that between group C and group B.Compared with group A,the DI,the content of TXB2 and ratio of TXB2 to 6-Keto-PGF1α in other three groups were higher [DI: (81.5+13.6), (61.3+18.2), (70.5+17.2) vs.(4.2+2.7); the contents of TXB2:(4.95 +0.51),(3.75+0.64),(4.39±0.69) vs.(2.76±0.44); and the ratios of TXB2 to 6-KetoPGF1α:(0.064±0.002),(0.037±0.005), (0.049±0.002) vs.(0.027±0.002)] (P＜0.01),but the contents of 6-Keto-PGF1α in other 3 groups were lower [ (77.9±8.9),(96.4±11.2),(89.2+11.4) vs. (109.3±7.6)] (P＜0.05orP＜0.01).Compared with group B,theDI [ (61.3±18.2),(70.5±17.2) vs.(81.5±13.6)] and the contents of TXB2 [ (3.75±0.64), (4.39±0.69) vs.(4.95±0.51)] and the ratios ofTXB2 to6-Keto-PGF1α [ (0.037±0.005), (0.049±0.002) vs.(0.064 ±0.002)] in groups C and D were lower (P ＜ 0.05 or P ＜ 0.01 ),but the contents of 6-KetoPGF1α in groups C and D [ (96.4 ± 11.2),( 89.2 ± 11.4) vs.(77.9 ± 8.9) ] were higher ( P ＜ 0.05 or P ＜ 0.01 ).Compared with group C,the DI [ ( 70.5 ± 17.2) vs.61.3 ± 18.2) ] and the contents of TXB2 [ (4.39 ± 0.69) vs.(3.75 ± 0.64) ] and the ratios of TXB2 to 6-Keto-PGF1α [ (0.049 ± 0.002 ) vs.(0.037 +0.005) ] in group D were higher ( P ＜ 0.05 or P ＜ 0.01 ),but the content of 6-Keto-PGF1α in group D [ ( 89.2 ± 11.4 ) vs.(96.4 ± 11.2) ] was lower ( P ＜ 0.05 ).Conclusions SF can attenuate the injury of gastric mucosa after traumatic hemorrhage shock resuscitation in rabbits,and its therapeutic effects is better when it is administered before resuscitation than those as it is administered after resuscitation.The possible mechanism is associated with the effects of improving balance between TXB2 and 6-Keto-PGF1α and inhibiting the secreting function of parietal cell of stomach.