BACKGROUND: Pyramidal cells in hippocampal CA1 region are neurons most susceptible to ischemia-hypoxia damage. Their membrane potential is shown as hyperpolarization of cell membrane during early hypoxia. With the progress of hypoxia time, cell membrane has slow and rapid hyperpolarization, which causes irreversible damage to neurons.OBJECTIVE: To investigate the effects of the blocker of N-methyl-D-aspartate receptor MK801 on the electrophysiological changes of CA1 neurons during hypoxia in isolated hippocampal slices of rats with intracellular recording technique.DESIGN: Observational and controlled study.SETTING: The 97th Hospital of the Chinese PLA, Provincial Key Anesthesiology Laboratory of Xuzhou Medical College; Center of Health Science, State University of New York.MATERIALS: The experiment was conducted from September 2002 to March 2003 in the State University of New York. Five adult male SD rats were anesthetized with 0.02 volume of isoflurane after 3 minutes' pre-oxygenation with oxygen.METHODS: The hippocampal slices from the rats were randomly divided into simple anoxia group (n=10) and MK801 group (n=10). The slices in simple anoxia group were only subjected to 10-minute hypoxia with the artificial cerebrospinal fluid (ACSF), and the slices in MK801 group were treated with 100 μmol/L MK801 for 10 minutes before and during 10 minutes of hypoxia. The neuronal membrane potential before hypoxia, the rate of slow depolarization, the amplitude of and time to rapid depolarization were recorded with intracellular recording technique described in the literature. Meanwhile, the neuronal response to the intracellular current injection and Schaffer collateral stimulation were observed respectively at the end of 60 minutes' re-oxygenation.gion of hippocampal slices: It was significantly higher in simple anoxia group than in MK801 group [(0.20±0.05) mV/s, (0.08±0.03) mV/s, P ＜ 0.05].hippocampal slices: It was significantly higher in MK801 group than in of rapid depolarization of pyramidal cells in CA1 region of hippocampal slices: It was significantly lower in MK801 group than in simple anoxia sponse to stimuli was recovered in 9 out of 10 neurons.CONCLUSION: MK801 blocker of N-methyl-D-aspartate receptor can decrease the rate of slow depolarization of neurons induced by hypoxia, postpone the onset of rapid depolarization of neurons, and decrease the amplitude of rapid depolarization of neurons. This suggests that the blocker of N-methyl-D-aspartate receptor can relieve the hypoxic damage to neurons and promote the functional recovery of neurons.

Medical students' English autonomy learning is different from other students,basing on some relevant autonomy learning theories,the authors investigated such aspects as learning motivation,achievement,length of time-spending,choice of learning strategy,major,gender,learning phase and family background of medical students'English autonomy learning.And at the same time,the authors analyzed its current situation and put forward some solutions to the existing problems.

Objective To analyze the relative factors of functional recovery after upper limbs replantation. Methods From September, 2009 to March, 2014, 24 consecutive patients after upper limb replantation for amputation were retrospectively analyzed. The Disability of Arm Shoulder and Hand (DASH) was used to assess the functional recovery of the upper limbs at the last follow-up. The non-conditional Logistic regression was used to analyze the correlation of gender, age, time from injury to surgery, amputated level, amputated method, isch-emia hours, dominant hand or not, rehabilitation treatment, rehabilitation duration, and the DASH scores. Results The DASH score was>28.50 in 15 patients, while ≤28.50 in 9 patients. The Logistic regression analysis demonstrated that amputated method and rehabilitation treatment correlated with the functional recovery of upper limbs (χ2>7.360, P<0.05), and no correlation was found in the other factors (χ2<3.789, t=1.515, P>0.05). Conclusion The amputated method and rehabilitation treatment after operation are the factors related to the func-tional recovery after upper limb replantation.

To investigate the effects of ketamine on nitric oxide synathase(NOS)activity, nitrc oxide (NO) output and cyclic guanosine 3', 5'-monophosphate(cGMP)content in the rat brain. Method: Thirty two SD rats were divided randomly into control group and ketamine group. The aminals were administred intraperitoneally(ip)normal saline 10mg?kg~(-1) or ketamine 100mg?kg~(-1), respectively. NOS activity and NO output were assassed with spectrophotometric analysis, cGMP content was measured with radioimmunoassay, Result: Ketamine 100mg?kg~(-1) ip significantly inhibited NOS activity(P

Tn investigate the effects of propofol on Ca~(2+) ATPase activity in rat cerebral synaptic membrane. Method: Thirty SD rats were divided randomly into three groups. The aminals were administtered introperi toneally(ip) propofol 50mg?kg~(-1), 100mg?kg~(-1) or normal saline 10mg?kg~(-1)(control group), respectively. These rats were immediately decapitated after having disappeared righting reflex. In oredr to prepare synaptosomes, brain tissues were dissected on ice, then homogenized and centrifuged. Ca~(2+)-ATPase activity was assaed with spcetrophotometric analysis. Result: Propofol 100mg?kg~(-1) ip significantly inhibited Ca~(2+)-ATPase activity of cerebrocortical, brain stems and hippocampal synaptic membrane as compared with that of normal saline group(P

Objective:To investigate effects of propofol on nitric oxide synthase (NOS) activity and nitric oxide (NO)output of rat brain. Method: Sixteen SD rats were divided randomly into two groups. The animals were administered introperitoneally(ip) normal saline 10 ml?kg~(-1)(control group)or propofol 100mg?kg~(-1)(propofolgroup),respectively. These rats were decapitated immediately after having disappeared righting reflex. After rapid removal of cerebellum, brain stem,hippocampus and cerebral cortex,tissues were homogenized and centrifuged. NOS activity and NO output were assayed with spectrophotometric analysis. Result: In propofol group,NOS activity was significantly inhibited, NO outpul was significantly reduced in cerebellum, brain stem,hippoeampus and cerebral cortex as compared with those of control group(P

Objective:To investigate the effects of enflurane on antioxidant ability in ischemic preconditioned rat hearts in vitro. Method:Ninety-six SD rat hearts were perfused with Langendorff device. All hearts were randomly allocated to four groups:Control, enflurane group receiving 40 min of enflurane (1.5MAC),ischemic preconditioning group undergoing two 5-min ischemia and 10-min reperfusion, enflurane + ischemia group receiving enflurane (1.5MAC) for 10 min before ischemia preconditioning procedures. All groups underwent 25-min ischemia and 30-min reperfusion. Left ventricular pressure (LVP), heart rats (HR)and ischemic contracture pressure (ICP) were monitored. Myocardial superoxide dismutase(SOD)and malodialdehyde(MDA)were measured before ischemia, 15min following ischemia and 30 min following reperfusion. Result: Treated groups had better myocardial functional recovery of contractility compared to control groups,with preconditioning being better than enflurane (P

Objective: To study the effects of halothane and sevoflurane on myocardial function and energy metabolism. Method:The model of Langendorff perfused isolated rat heart was used to investigate the effects of halothane and sevoflurane on HR,LVEDP,LVDP,+dp/dt,-dp/dt and coronary flow(CF)before and after ischemia. and the myocardial ATP content were measured with HPLC before ischemia and 10 min after ischemia and at the end of reperfusion. Result: 1.5 MAC sevoflurane significantly increased CF in normal isolated rat hearts. Both halothane and sevoflurane differently depressed myocardial contratile function,increased normal myocardial energy storage. At 10th min of ischemia the decrease of myocardial ATP content was delayed by halothane and sevoflurane. At the end of reperfusion,the both anesthetics improved the recovery of myocardial function and matebolism,especially sevoflurane. Conclusion: Both anesthetics can protect myocardium from ischemic reperfusion injury through improving post-ischemic myocardial energy recovery.

Objective To study the therapeutical effect of glutathione(GL),a powerful antioxidant on the symptoms and ECG in patients with coronary heart disease and its mechanisms.Methods Eighty-five subjects with coronary heart disease were recruited(45 male and 40 female).The patients were randomized to receive GL (240 mg,ivgtt,qd,for 14 days,n=44)on the top of conventional treatment(aspirin+?-blocks+ACEI)or conven- tional treatement alone(control,n=41).The serum MDA,SOD,NO levels were determined.Electrocardio- graphy(ST stage,T wave)was examined.Results GL significantly improved clinical symptoms scores(2.0+0.5 vs control:1.5+0.5,P

OBJECTIVE: To explore the effects of Gymnadenia conopsea alcohol extract (GcAE) on the collagen synthesis in rat lungs exposed to silica and the influence on antioxidase activities, level of lipid peroxidation (LPO). METHODS: One hundred and twenty rats were randomly divided into control group, silica group, and GcAE-treated group. Silicotic animal models were established by direct tracheal instillation of silica into rat lungs surgically. From the second day of model establishment, rats in GcAE-treated group were orally given GcAE [8 g/(kg x d) corresponding to raw herb]. At 7, 14, 21, 28 and 60 days after establishment of the animal model, eight rats in each group were sacrificed, and samples were collected. The malondialdehyde (MDA) content, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities in plasma were assayed by a spectrophotometer. Types I and III collagen were detected by Sirius red polarization and microscopy, and measuered by Image-Pro Plus Version 4.5 for Windows software. RESULTS: GcAE could reduce the lung/body weight ratio of rats exposed to silica, the synthesis of types I and III collagen of the lungs and the level of lipid peroxidation, increase the activities of SOD and GPx. CONCLUSION: GcAE can ameliorate the silica-induced pulmonary fibrosis by increasing the activities of antioxidase and alleviating the damage of lipid peroxidation to the lungs.