BACKGROUND: The disorder of energy metabolism and cerebral edema after cerebral ischemia-reperfusion are the important factors to inducecerebral ischemia-reperfusion injury. The Chinese herb, breviscapine, whose effective component is scutellarin, can prevent the activation of protein kinase C evoked by ischemia-reperfusion, relieve calcic overload and reduce the volume of ischemia infarcted focus volume, and then alleviate cerebral ischemia-reperfusion injury. But what are the influences of breviscapine on energy metabolism and cerebral edema after cerebral ischemia-reperfusion?OBJECTIVE: To observe the effects of breviscapine parenteral solution on energy metabolism and cerebral edema after cerebral ischemia-reperfusion in gerbils.DESIGN: A randomized control trial.SETTING: Affiliated Hospital of Jining Medical College, Jiangsu Provincial Key Laboratory of Anesthesiology, Affiliated Hospital of Xuzhou Medical College.MATERIALS: The experiment was carried out in the Jiangsu Provincial Key Laboratory of Anesthesiology Between February and August 1999. Seventy-two male gerbils were used.METHODS: The gerbils were randomly divided into sham-operated group (n=8), normothermia control group (n=32) and breviscapine group (n=32).According to the reperfused time, the normothermia control group and breviscapine group were divided into 4 subgroups with 8 gerbils in each subgroup: 0, 10, 30 and 60-minute reperfusion groups. The gerbils in the normothermia control group and breviscapine group were made into models of forebrain ischemia reperfusion, treated with ischemia for 10 minutes. In the sham-operated group, only bilateral common carotid arteries were freed but not occluded. In the breviscapine group, the gerbils were given intraperitoneal injection of breviscapine psrenteral solution (90 mg/kg) at 15 minutes before ischemia. The gerbils in the sham-operated group and normothermia control group were treated with saline of the same volume. The brain water was determined by drying electrothermostat. The contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP) and adenosine phosphate (AMP) in hippocampus were determined with high performance liquid chromatography and ultraviolet detector.MAIN OUTCOME MEASURES: ① ATP, ADP and AMP contents in hippocampus; ② Water contents in cerebral cortex.RESULTS: All the 72 gerbils were involved in the analysis of results without deletion. ① ATP, ADP and AMP contents in hippocampus: At 0, 10, 30 and 60 minutes after reperfusion, ATP and adenine nucleotide pool contents in hippocampal tissue in the normothermia control group were obviously decreased, the ATP contents were 68%, 56%, 49% and 50% of those in the sham-operated group respectively (P ＜ 0.01), and adenine nucleotide pool contents were 62%, 50%, 51% and 52% of those in the sham-operated group respectively (P ＜ 0.01). The ATP contents at each time point in the breviscapine group were 84%, 69%, 64% and 63% of those in the sham-operated group respectively, and the adenine nucleotide pool contents were 86%, 72%, 68% and 69% of those in the sham-operated group respectively, which were all obviously higher than those in the normothermia control group (P ＜ 0.05). ②Water contents in cerebral cortex: The water content after cerebral ischemia-reperfusion in the normothermia control group was obviously higher than that in the sham-operated group, and gradually aggravated with the prolongation of reperfusion. The water content in the breviscapine group was obviously higher than that in the sham-operated group, but markedly lower than that in the normothermia control group (P ＜ 0.05).CONCLUSION: Breviscapine can play a role in protecting brain through inhibiting disorder of energy metabolism and relieving cerebral edema.

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.

Objective To investigate the changes of platelet-leukocyte aggregations(PLA) in patients with acute cerebral infarction and its relationship with C-reactive protein(CRP) and platelet aggregation rate(PAgT).Methods The PLA,CRP and PAgT were measured in 46 patients with acute cerebral infarction(CI group) and in 24 patients without cerebral vascular diseases(control group).Results The platelet-monocyte aggregations(PMA),PAgT and CRP in CI group were((13.00?0.76)%,(59.46?3.07)%,(9.39?1.28) mg/L,respectively,however,there were(6.55?0.29)%,(39.38?5.42)%,(2.37?0.46)mg/L respectively in control group.There were significant differences between the two groups(all(P

Aim To investigate the role of peripheral benzodiazepine receptor in rat cardiac mitochondrial permeability transition.Methods The isolated rat cardiac mitochondria were incubated with different doses(50,100,200 ?mol?L-1) of PBR antagonist 1-(2-chlorophenyl-N-methyl-1-methylpropyl)-3-isoquinolinecarboxamide (PK 11195). In additional group(CsA group), 5 ?mol?L-1 cyclosporine A (CsA), an inhibitor of MPT was added 5 minutes before the addition of 100 ?mol?L-1 PK 11195. Negative control group(Con group) was given none treatment. Positive control group(Ca2+ group) was given 150 ?mol?L-1 CaCl2. The absorbanceat 520 nm(Abs 520 nm) was monitored with a split-beam spectrophotometer at 30℃ for 10 min. The mitochondrial ultrastructure was assessed by transmission electron microscopy. Mitochondrial cytochrome C release was demonstrated by Western Blotting.Results PK11195 triggered large-amplitude mitochondrial swelling in a dose dependent manner(vs Con group,P

Aim To explore the effect of propofol preconditioning on cardiocyte apoptosis and cytochrome C release from mitochondria during hypoxia/reoxygenation in isolated rat hearts.Methods Fifty male Sprague-Dawley rats weighing 250～300 g were randomly divided into 5 groups(n=10 each):control group(C);Dimethyl sulfoxide(DMSO)preconditioning group(D);3 propofol preconditioning groups with 25 ?mol?L-1(P1)、50 ?mol?L-1(P2)、100 ?mol?L-1(P3)propofol respectively.The isolated rat hearts were retrogradely perfused via aorta with K-H solution on Langendorff apparatus.The isolated hearts were made hypoxia for 30 minutes followed by 60 minutes reoxygenation in each group.The D,P1,P2,P3 groups were preconditioned by perfusing 10 min K-H solution containing 20 ?mol?L-1 DMSO and 25,50,100 ?mol?L-1 propofol respectively and then followed by 5 min K-H solution reperfusion before hypoxia.The preconditioning procedure was repeated twice.The cardiac functional variables were recorded after equilibration(baseline values),immediately before hypoxia,at the end of 30 min and 60 min reoxygenation.Apoptotic myocardial cells were detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling(TUNEL)and the level of cytochrome C expression in myocardial cytosol and mitochondria was measured by Western blot at the end of reoxygenation.Results At the end of 30 min and 60 min reoxygenation,LVEDP was significantly lower and LVDP was significantly higher in P1,P2,P3 groups than in D group(P

Currently hypothermia neuroprotection is one of the study topics of general interest. The studies of therapeutic hypothermia for acute stroke are increasingly arousing general concern. This article reviews the mechanism of therapeutic hypothermia for acute stroke, the effect of increased body temperature on acute stroke, and the clinical application of therapeutic hypothermia for acute stroke.

0.05).Inside experimental area,pain scores were decreased in both intradermal 0.25% lidocaine and saline injection group(P

Objective To compare the effects of combined general-epidural anesthesia (CGEA) and general anesthesia (GA) on energy metabolism and oxygen cost of breathing.Methods Forty patients (25 male, 15 female) aged 42-61 yr weighing 42-75 kg scheduled for elective upper abdominal surgery were randomly divided into 2 groups : group CGEA (Ⅰ, n = 20) and group GA (Ⅱ, n = 20) . The patients were premedicated with midazolam 0.05 mg?kg-1 and scopolamine 0.3 mg i.m. . In groupⅠepidural catheter was placed at T9-10 A. test dose of 4ml of 2 % lidocaine was given. When the height of block was confirmed general anesthesia was started. In both groups anesthesia was induced with etomidate 0.3 mg?kg-1 , fentanyl 8 ?g?kg-1 and tracheal intubation was facilitated with atracurium 0.8 mg?kg-1 . Anesthesia was maintained with propofol in both group and intermittent epidural lidocaine in CGEA group and intermittent i. v. boluses of fentanyl in GA group. Muscle relaxation was maintained with atracurium infusion at 8 ?g?kg-1 ? min-1 during operation. Oxygen consumption ( VO2 ), CO2 production (VCO2 ) , energy expenditure ( EE) and respiratory quotient (RQ) were measured before anesthesia, during and after operation using indirect calorimetry (Datex, Deltatrac MBM-200) . Postoperative oxygen cost of breathing (OCB) was calculated during spontaneous breathing and controlled ventilation. Results VO2 , VCO2 , EE were significantly lower and RQ was significantly higher during operation than those before anesthesia in both groups (P

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