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 role of microglial activation in spinal cord in a rat model of persistent postoperative pain evoked by skin/muscle incision and retraction (SMIR) .Methods Seventy-two male SD rats weighing 200-250 g in which intrathecal (IT) catheter was successfully inserted were randomly divided into 3 groups ( n = 24 each) : group sham operation; group SMIR and group SMIR + FT minocycline (a specific microglia inhibitor) . The rat model of persistent postoperative pain evoked by SMIR was established according to the method described by Flatters. Pain behavior was assessed by paw mechanical withdrawal threshold ( MWT) to von Frey filament stimulation at 1 day before (T0,baseline) and 3, 7, 12, 22 and 32 days after operation (T1-5,) . Four animals were sacrificed at each time point in each group for detection of the expression of Iba-1 (a specific marker of microglia) in the spinal dorsal horn by immunofluorescence and the microglia was counted. Results MWT was significantly decreasedat T1-4, while the expression of Iba-1 and microglia counts in the spinal dorsal horn were significantly increased at T1, 2 by SMIR in group Ⅱ. IT minocycline significantly attenuated the hyperalgesia induced by SMIR at T1-4 and decreased Iba-1 expression and microglia counts at T1,2 in group Ⅲ. Conclusion Microglial activation in the spinal cord plays an important role in the development and maintenance of SMIR-evoked persistent postoperative pain in rats.

Objective To investigate the role of gamma-aminobutyric acid transporter-1 (GAT-1) in the spinal cord in a rat model of bone cancer pain.Methods Eighty female SD rats weighing 150-180 g were randomly divided into 5 groups (n =16 each): sham operation group(group Ⅰ ),bone cancer pain group(group Ⅲ ),sham operation+ NO-711 group(group Ⅲ ),Ⅳ group BCP + NO-711 group(group Ⅳ ) and BCP + vehicle group (group Ⅴ ).Bone cancer pain was induced by inoculating Walker-256 mammary gland carcinoma cells into medullary cavity of tibia.NO-711 (20 μg,10 μl) was administered intrathecally once a day for 3 consecutive days from the 14th day after operation.Mechanical withdrawl threshold (MWT) of mechanical stimulus was determined the day before operation and at days 3,5,7,10,14 and 16 after operation.The animals were sacrificed on the 16th day after operation,and then the spinal cords were removed for determination of the expression of GAT-1 and double immunostaining of GAT-1 and glial fibrillary acidic protein (GFAP,astrocyte marker).Results MWT were significantly decreased in groups Ⅱ,Ⅳ and Ⅴ as compared with groups.Ⅰ and Ⅲ.The expression of GAT-1 significantly up-regulated in groups Ⅱ,Ⅴ as compared with groups Ⅰ and Ⅲ.NO-711 significantly increased MWT,while decreased the expression of GAT-1 in group Ⅳ compared with groups Ⅱ and Ⅴ.The expression of GAT-1 up-regulation appeared colocalizes with in astrocytes activation in spinal dorsal horn.Conclusion The up-regulation of expression of GAT-1 in spinal cord is involued in the development and maintenance of bone cancer pain,which may be related to the astrocytes activation.

Aim To investigate the relationship between spinal cord noradrenergic neurons ? 1 adrenoceptors and the spinal analgesia of ketamine. Methods Kunming mice were used. Analgesia tests were investigated with warm water tail flick test. The effects of intrathecal injection (ith) of ketamine (50,100,200 ?g)on tail flick latency of animals were observed. And the effect of pretreatment with intrathecal 6 hydrodoapa(6 OHDA, 6?g ) and ? 1 adrenoceptor antagonist prazosin (5, 15 ?g) or terazosin (5, 15 ?g) , respectively on the spinal analgesia of ketamine (100 ?g,ith) was studied. Results Dose dependent analgesia was observed following ith ketamine (100,200 ?g, 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

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.