ABSTRACT
Objective To investigate the protective effect and its mechanism of metabotropic glutamate receptor 1 ( mGluR1) negative allosteric modulator JNJ16259685 on neuron after subarachnoid hemorrhage (SAH) in rats. Methods Ninety SPF-grade SD male rats were selected. They were randomly divided into 3 groups:sham operation group (n=18),SAH+placebo group (n=36),and SAH+JNJ16259685(JNJ) group (n=36). A SAH model was induced by intravascular puncture. SAH +placebo group received intraperitoneal injection of aseptic water containing 5% dimethyl sulfoxide (DMSO) at 2,24 and 48 h after operation. The SAH+JNJ group was intraperitoneally injected with 1 mg/kg JNJ16259685 ( dissolved in sterile water in 5% DMSO). Garcia scoring criteria were used to assess neurological deficits at 72 h after SAH. Dry and wet weight method was used to detect brain edema. Evans Blue method was used to assess blood-brain barrier permeability. A calcium assay kit was used to detect the mitochondrial calcium ion concentration. Immunofluorescence staining was used to observe neuronal apoptosis. GraphPad 7. 0 software was used to conduct one-way analysis of variance in all indicators among the 3 groups. Results Compared with the sham operation group,the Garcia score (11. 0 ± 0. 4) decreased in the SAH+placebo group. The water content in left and right hemispheres was 80. 5 ± 0. 1% and 80. 3 ± 0. 2% respectively,the Evans blue dye extravasation (2. 8 ± 0. 2),basal cortical mitochondrial calcium ion concentration (2. 5 ± 0. 3),and neuronal apoptosis in basal cortex and hippocampus CA1 region (the number of active caspase-3/NeuN positive cells was 300 ±30/mm2and 20 ± 2/mm respectively) increased (all P<0. 05);and the Garcia score (13. 0 ± 0. 5) was significantly higher in the SAH+JNJ group than in the SAH+placebo group. Water content in left and right hemispheres was 79. 8 ± 0. 2% and 79. 3 ± 0. 1% respectively,Evans blue dye extravasation (1. 8 ±0. 2),basal cortex mitochondrial calcium ion concentration (1. 7 ± 0. 1),basal cortex and the number of neuronal apoptosis in hippocampal CA1 region (the number of active caspase-3/NeuN positive cells were 180 ± 10/mm2,12 ±2/mm) reduced compared with the SAH+placebo group (all P<0. 05). Conclusion After SAH,JNJ16259685 relieves cerebral edema and reduces blood-brain barrier permeability,inhibits the increase of cortical mitochondrial calcium ion concentration,and reduces neuronal apoptosis,thereby exerting neuroprotective effects.
ABSTRACT
Objective To explore the protective effect of erythropoietin(EPO) administrated by intranasal on cerebral ischemia reperfusion in rats with acute cerebral infarction reperfusion.Methods Total of 100 SD rats were divided into model control group,sham operation group,intraperitoneal administration group ([PEPO group),nasal saline group (INNS group) group,and nasal drug delivery group (INEPO group) with 20 in each group.The middle cerebral artery occlusion model of rat was established by thread embolism method and the NSS method was used to evaluate the neural behavior of rats.The expression of EPO in peripheral blood,cerebrospinal fluid and brain regions of rats were detected by Elisa.The vascular endothelial growth factor(VEGF) in brain was detected by immunofluorescence and then the density of newborn blood vessels in the brain was measured.Results Fifteen days after the operation,the NSS score of INEPO group(3.80± 1.61) was significantly lower than that of IPEPO group (11.53±2.11),and the difference was statistically significant(P＜0.01).And the levels of EPO in blood,cerebrospinal fluid and different brain regions of rats in INEPO group were higher than that of INNS group(all P＜0.01).Compared with IPE-PO group,the level of EPO cerebrospinal fluid and different brain regions of rats in INEPO group increased obviously,the difference was statistically significant (all P＜0.01),and the EPO concentration of the olfactory bulb was the most obvious (INEPO group:(1 456.90 ± 128.22) pg/ml,IPEPO group:(426.11 ± 36.68)pg/ml,P＜0.01).Seventy-two hours after operation,the expression of CD31 in ischemic penumbra of rats of model control group (18.21 ± 3.45),INNS group (18.54 ± 2.58),IPEPO group (27.01 ± 2.13) and INEPO group(35.52±2.79)was increased compared with sham operation group (5.14± 1.28),and the difference was statistically significant (all P＜0.05).The expression of CD31 in IPEPO group and INEPO group was significantly higher than that in INNS group (P＜0.05).In INEPO group,the expression of CD31 increased significantly compared with that of IPEPO group (P＜0.05).Conclusion Nasal administration of EPO can effectively improve the neurological function of rats with ischemia-reperfusion,and increase the expression of CD31 in the brain tissue of rats.The effect of nasal administration is better than that of intraperitoneal administration.
ABSTRACT
Objective To explore the effects of application calcitonin gene related peptide(CGRP) in cisterna magna on cerebral vasospasm after experimental subarachnoid hemorrhage (subarachnoid hemorrhage,SAH) in rat models.Methods 64 male Wistar rats were randomly divided into 4 groups.Group A was normal control group.After the subarachnoid hemorrhage models were established,group B,C,D were given normal saline,CGRP and adenovirus CGRP through cisterna magna respectively.White blood cells in cerebrospinal fluid were detected by automatic blood analyzer,CGRP activity was detected by enzyme linked immunosorbent assay,circulating endothelial cells were observed through laser scanning confocal microscope and parietal cortex regional cerebral blood flow were observed by laser doppler flowmeter.Basilar artery vasospasm and arterial blood gas analysis were detected by digital subtraction angiography and blood gas analyzer respectively.Results Before and after administration,there were no statistical differences in white blood cells and artery blood gas among the 4 groups (both P＞ 0.05).After administration 48 h,compared with group A,concentrations of CGRP in cerebrospinal fluid group B (0.006±0.002) did not increase (P＞0.05),but increased 200 times in Group C ((1.160±0.170) nmol/L,P＜0.05)and nearly 400 times in group D ((2.071±0.412) nmol/L,P＜0.05).Peripheral blood circulating endothelial cells count:after administration 48 h,group C((5.56±0.61) ind/0.9 μL) was less than in group B((9.94± 0.73) ind/0.9 μL).Group D((5.16±0.61) ind/0.9 μL) was less than group C(P＜0.01).Regional cerebral blood flow:after administration,compared with group B,cerebral blood flow of group C and group D increased,and the differences were both statistically significant (P＜0.01).Basilar artery diameter was detected after administration 12 h,group D ((1.000±0.025) mm) was 13％ bigger than group B ((0.670±0.028)mm,P＜0.05),3％ bigger than group C ((0.900±0.023) mm) (P＞0.05).Conclusion Cerebral vasospasm after SAH can be effectively improved by administration CGRP in cisterna magna.Adenovirus CGRP effect is better than CGRP.
ABSTRACT
Objective To explore the effect of protein kinase C inhibitor on the level of phosphralated extracellular regulated protein kinases in the spinal trigeminal nucleus of migraine model rats.Methods Healthy adult male SD rats were randomly divided into four groups:normal group (group C),sham operation group (group C),migraine model group(group M),and H-7group(H-7group),with 18 rats in each group.Dural blood flow and the extracellular discharge frequency in the spinal trigeminal nucleus was recorded.ERK1/2 phosphorylation was tested.Results (1) Dural blood flow:compared with group C((3.8± 1.0)％),the dural blood flow in M group ((78.0±4.2) ％)increased obviously(P＜0.01) ; compared with M group((78.0±4.2)％),the dural blood flow in H-7 group((-24.8±4.9) ％) decreased obviously(P＜0.01).(2) The percentage of extracellular discharge frequency change:two hours after treatment,the percentage of extracellula discharge frequency change in group M ((325.9 ±47.3)％)was higher than that in group C((107.3±16.4)％).The percentage of discharge frequency change in group H-7((136.0±26.5)％) was lower than that in group M((325.9±47.3)％).There was no significant difference in the percentage of discharge frequency change between group H-7((136.0±26.5) ％) and group C((107.3 ± 16.4)％).(2) ERK1/2 phosphorylation:the ERK1/2 phosphorylation in group M was higher than that in group C.The ERK1/2 phosphorylation in group H-7 was lower than than that in group C and group M.Conclusion ERK1/2 is a downstream PKC signal path and PKC may have indirect activation of ERK1/2.
ABSTRACT
Objective To study the promotive effect of neovascularization on rats with cerebral infarction by nasal administration of granulocyte colony-stimulating factor.Methods A blinded,vehicle-controlled study of ING-CSF and IHG-CSF administration was performed by intraluminal middle cerebral artery occlusion (MCAO) model.All Sprague-Dawley rats were randomly divided into sham-operation group,model group,INNS group,IHGCSF group and ING-CSF group.The neurologic behavioral tests were assessed after reperfusion 72 h.Mter 72 h of MCAO,the brains of rats were stainned with TTC and the infarcted volume was calculated by computer image analysis.The expression of vascular endothelial growth factor (VEGF) in the brain was determined by immune-histochemistry.The density of angiogenesis in the brain was counted under fluorescence microscope.Results The score of neurological function of ING-CSF group(3.90± 1.65)was improved significantly compared with the IHG-CSF group (10.55±2.19) at the point of 72 h after cerebral infarction (P＜0.01).The cerebral infarct volume of ING-CSF group((20.01±3.29) ％) was reduced evidently compared with the IHG-CSF group((33.48±4.49) ％) at 72 h (P＜ 0.01);while the cerebral infarct volume of INNS group ((60.20±7.72) ％)was not markedly different compared with the model group((61.49±6.41)％) at 72 h (P＞0.05).The expression of VEGF in the brains of ING-CSF group was significantly higher than other groups at 72 h.Conclusion Intranasal administration G-CSF can improve neurological function and vascular angiogenesis in rats following MCAO.
ABSTRACT
Objective To observe the effects of CoC12 treatment on the expression of Hypoxia-inducible factor-1(HIF-1α) in mice hippocampus at different time point.Methods Balb/c mice were injected with CoCl2 and the change of HIF-1 α was detected by western blot and immunofluorescence and confocal laser scanning microscope at different time point(0h,1h,2h,3h,4h,5h and 6h) after injection.Results The relative protein level of HIF-1α was 0.135 ±0.01,0.572 ±0.01,0.595 ±0.03,1.09 ±0.03,1.30 +0.04,1.275 ±0.03,0.947 ±0.03respectively at different time point after the injection.The HIF-1α protein level reached its peak value at 4 h and decreased at 5h and 6h.Fluorescence intensity of HIF-1α was 13.33 ± 3.42,30.95 ± 7.86,46.50 ± 9.65,61.50± 10.02,88.30 + 15.69,71.39 ± 11.28,67.41 ± 10.78 respectively at different time point after the injection.The HIF-1α fluorescence intensity also reached its peak value at 4 h and decreased at 5h and 6h.Conclusion Time dependent HIF-1α accumulation was in close correlation with the CoCl2.
ABSTRACT
Aim To establish a method to evaluate lymphatic drainage of macromolecular tracer in cerebrospinal fluid in rats.Methods Rat cervical lymphatic blockade(CLB)models were established by occlusion of cervical lymphatic tubes and removal of cervical lymphatic nodes.The rats were divided into non CLB(normal controls) and CLB groups.~(125)I-labeled human serum albumin(~(125)I-HSA)was injected into the left lateral cerebral ventricle,and blood samples were collected and ~(125)I-HSA concentrations were detected continually within 24 hours.Concentration-time curve was drawn according to the single compartment model in pharmacokinetics.Parameters of pharmacokinetics such as area under curve(AUC),maximum concentration(C_(max)),transfer rate constant K_a and peak time(T_(max))were derived.The AUC,C_(max),K_a,and T_(max) regarding the lymphatic drainage of ~(125)I-HSA were calculated based on the differences between the two groups.Results AUC,C_(max),K_a of ~(125)I-HSA by lymphatic drainage were 51.97 mg·L~(-1)·h~(-1),2.91 mg·L~(-1),and 0.64 h~(-1),respectively.The proportion of AUC,C_(max),K_a of ~(125)I-HSA by lymphatic drainage to those of drained by both arachnoid granulations and lymphatics was 71.53%,44.02%,58.18%,respectively.T_(max) in CLB group(8.36±0.82 h)was much longer than that in non CLB group(3.57±0.54 h).Conclusions A method to evaluate lymphatic drainage of macromolecular tracer in cerebrospinal fluid in rats is successfully established.The lymphatic drainage pathway plays an important role in eliminating macromolecular substances in cerebrospinal fluid.
ABSTRACT
AIM:To determine the injured effect of cerebrospinal fluid(CSF) from subarachnoid hemorrhage(SAH) after cerebral lymphatic blockage(CLB) on PC12 cells. METHODS:SAH and CLB models of adult New Zealand rabbits were used. CSF was obtained from experimental animals after 5 d of modeling and was added into cultured PC12 cells. The cells were randomly divided into blank control(F12 Ham's),normal CSF,SAH CSF,and SAH+CLB CSF groups. At different time points,the survival rate of PC12 cells was measured by MTT assay. LDH leakage was detected. Expression of Bax and heat-shock protein 70(HSP70) was determined by immunohistochemical staining. RESULTS:MTT assay and detection of LDH leakage revealed that the survival rate of PC12 cells was obviously inhibited and the leakage of LDH increased in SAH CSF group and SAH+CLB CSF group. CSF from normal rabbit did not damage the PC12,as compared to blank controls. Above effects were more obvious in SAH+CLB CSF group than those in SAH CSF group. Bax and HSP70 protein expression was found in both SAH CSF group and SAH+CLB CSF group. Expression of Bax protein in SAH+CLB CSF group was stronger than that in SAH CSF group in a time dependent manner. At 0.5 h and 1 h,the expression of HSP70 protein in SAH+CLB CSF group was stronger than that in SAH CSF group,whereas the expression became weaker at 2 h and 4 h in that group. CONCLUSION:Blockage of cerebral lymphatic drainage pathway deteriorates the damage of CSF from SAH on PC12 cells,indicating this pathway may acts as an endogenous protective mechanism in SAH.
ABSTRACT
Pathological pain or clinical pain is caused by tissue and nerve injuries, and is usually chronic and mainly divided into inflammatory pain and neuropathic pain. Pathological pain is typically characterized by hyperalgesia (increased responsiveness to noxious stimuli) and allodynia (painful responses to normally innocuous stimuli). The mitogen-activated proteins kinases (MAPKs) are a family of evolutionally conserved molecules that play a critical role in cell signaling, consisting of extracellular signal regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), which play an important role in neural plasticity of pathological pain. Inhibition of MAPKs alleviates inflammatory pain and neuropathic pain in different animal models. It is very important to study the inhibition of MAPKs as a therapeutic approach to treat pathological pain.
ABSTRACT
The MAPKs activation pathway consists of three protein kinases in activation sequence:MAPKs kinase kinases (MKKKs)→,MAPKs kinases (MKKs)→MAPKs and four pathways:extracellular signal-regulated kinase (MAPK~(ERK)),C-JUN N-terminal kinase (MAPK~(JNK)),MAPK~(P38) and MKKS/MAPK~(ERK5) activation pathways.It has been proved that MAPKs(ERK,JNK and P38) are acvtivated in the progress of morphine tolerance.Inhibitors of any element of MAPKs activation pathway may function as a potential clinical medicine for morphine tolerance.
ABSTRACT
Objective To investigate the influence of cerebral lymphatic blockade (CLB) on apoptosis of hippocampal neurons after subarachnoid hemorrhage (SAH) in rats. Methods Healthy adult Wistar rats were randomly assigned to normal control group,SAH group and SAH + CLB group. SAH model was induced by double injection of autologous blood into the cistema magna. On day 3 after second injection, hippocampal cell shape structure of each group were determined by hematoxylin-eosin staining (HE) and propidium iodide (PI) staining. Terminal-deoxynucleotidy transferase mediated nick end labeling (TUNEL) fluorescent was used to determine the situ apoptosis. Immunohistochemistry was conducted to study the expression of caspase-3 and Bcl-2 in hippocampal neurons. Results (1) HE staining and PI staining showed the hippocampal neurons of SAH rats were partly shrink,and nuclei showed wavy or folded seam-like,some crescent-shaped; the hippocampal neurons in SAH + CLB group distributed sparsely,nuclear fragmentation,apoptotic bodies could be seen,surrounded by vacuole formation, Compared with the SAH group, the number of apoptotic cells in SAH + CLB group was significantly increased(the number of apoptotic cells: 0.71 ±0.05,25.36 ±4. 02,37. 82 ±5.93, P<0.01). (2) The fluorescence intensity of positive cells by TUNEL stain in SAH group and SAH + CLB group was higher than in normal control group,while the SAH + CLB group was significantly higher than the SAH group (the fluorescence intensity: 0.19 ±0.03,1.70 ±0.37,2.54±0.53, P<0.01). (3) The fluorescence intensity of caspase-3 in SAH group and SAH + CLB group was higher than the normal control group, while the SAH + CLB group was significantly higher than the SAH group (the fluorescence intensity: 0.14 ±0.03,2.45 ±0.49,2.96 ±0.44, P<0.01). (4) The fluorescence intensity of Bcl-2 in SAH group and SAH + CLB group was higher than the normal control group, while the SAH + CLB group was significantly lower than the SAH group(the fluorescence intensity: 0.58 ±0.08, 3.40 ±0.61,2.67 ±0.44, P<0.01). Conclusion Cerebral lymphatic blockade induce the apoptosis of hipp-ocampal neurons in rats after SAH,which mechanism may be related to high expression of caspase-3 and low ex-pression of Bcl-2.
ABSTRACT
Objective To investigate the pathway of lymphatic drainage of proteins from cerebral parenchyma in subarachnoid hemorrhage rat models. Methods Healthy adult male Wistar rats were divided into Saline group, Evans blue-labeled albumin (EBA) group, and SAH + EBA group. SAH models were produced by double injection of autologous arterial blood into cisterna magna. Using a modified microinjection method, EBA was injected into left candate-putamen of the EBA group and EBA + SAH group rats. In Saline control group, saline was injected. After injection, at 12 hours, 1 day, 2 days, 3 days and 5 days, the animals were sacrificed and the fluorescence signals of EBA were imagined and analyzed along the possible lymphatic drainage pathway, e.g. the brain tissue, the wall of common carotid artery, and cervical lymphatic nodes. Results One day after injection, in EBA group, the fluorescence of EBA initially appeared on the left of the brain, the wall of common carotid artery, left lateral cerebral ventricle, and the perivascular spaces of cerebral vessels. The fluorescence signals gradually expanded to the opposite side.Large amount of fluorescence granules accumulated in the outer layer of common carotid artery. Fluorescence was also found in cervical lymphatic nodes. Two days after injection in this group, the density of fluorescencein the brain became weaker while the density of fluorescence in rhinencephalon became stronger. The fluorescence of EBA was found in lymphatic nodes adjacent to abdominal aorta. In SAH + EBA group,reduced amount and velocity of the drainage of EBA from left caudate-putamen to rhinencephalon, cervical lymphatic nodes, and lymphatic nodes adjacent to abdominal aorta were observed. From 12 hours to 5 days after injection, fluorescence intensity of EBA in deep cervical lymphatic nodes in SAH + EBA group(8.9 ±2. 0, 11.9 ± 2. 5, 17.4 ± 3.7, 26.7 ± 4. 5 and 59.0 ± 8. 1 ) were lower than those in EBA group ( 14. 5 ±3.2, 27.5 ±7.4, 60.3 ±12.3, 138.0±12.0 and 108. 1 ±13.4, F=13. 17, 24.04, 66.81, 302.77 and 59.36, P ＜ 0. 01 ). From 2 to 5 days, fluorescence intensity of EBA in lymphatic nodes adjacent to abdominal aorta was also lower in SAH + EBA group( 11.0 ± 1.5, 12. 5 ±2. 8, 23.6 ±3. 2) than those in EBA group(26. 3 ±5.9, 47.5 ±9.6, 41.0 ±9.3; F =38. 17, 72.52, 19.01, P ＜0.01). Conclusion SAH can result in reduced drainage of macromolecular substances, e.g. protein, from the brain via lymphatic pathway.
ABSTRACT
Aim To investigate the influence of intranasal delivery of calcitonin gene-related peptide(CGRP)on cerebral blood supply and expression of vascular endothelial growth factor(VEGF)following experimental subarachnoid hemorrhage(SAH).Methods Wistar rats were divided into normal control group,SAH group,intranasal normal saline(NS)+SAH group and intranasal CGRP+SAH group.SAH models were produced by double injection of autologous arterial blood into cisterna magna.CGRP and NS were given by intranasal perfusion.Dynamic observations of regional cerebral blood flow(rCBF)of cerebral cortex were made using a laser Doppler flowmeter probe.On the third day after the second cisternal injection,the expression of VEGF protein in cerebral cortex was observed by immunofluorescence method combined with laser confocal microscopic observation.Results Anatomic observation revealed that SAH models were successfully manufactured.In SAH and intranasal NS+SAH groups,a drastic and persistent drop in rCBF was noted during the observed periods.The decrease of rCBF in intranasal CGRP+SAH group was slighter as compared with that in SAH and intranasal NS+SAH groups.In SAH and intranasal NS+SAH groups,increased expression of VEGF protein in cerebral cortex was observed on the third day after second cisternal injection as compared with that in normal control group.The expression of VEGF in intranasal CGRP+SAH group was more obvious than that in intranasal NS+SAH group.Conclusion Intranasal delivery of CGRP improves cerebral blood supply and promotes angiogenesis by enhancing the expression of VEGF after SAH.
ABSTRACT
Objective To explore the protective effect of rhG-CSF given intranasally on cerebral infarct rats by observing the neurological dysfunction and the expression of Fas ligand (FasL) in hippocampus of cerebral infarct rats.Methods Middle cerebral artery occlusion(MCAO) model rats were established by nylon strand,reperfuse 2 hours later,and give rhG-CSF through subcutaneous and intranasal way.The rats were divided into the nermal group,the sham-operated control group(sham),MCAO group,MCAO+NS given intranasally group(NS),MCAO + rhG-CSF given subcutaneously group,and MCAO + rhG-CSF given intranasally group each group had 6 rats. At the time of 3d after reperfusion,neurological severity scores (NSS) test was performed and the expression of FasL was detected via immunohistochemical staining in collateral hippocampus. Results Neurological dysfunction appeared in all groups except for the normal and the sham group. The dysfunction of the MCAO and the NS group was the most serious,the NSS was the highest(10.20±1.85,10.30±1.76),the number of FasL positive cells was the most(41.17±3.25,41.00±2.76),and there was no obvious difference between the two groups ( P ＞0.05);the NSS and FasL positive cells decreased in the subcutaneous group(5.67±1.32,P ＜0.01;32.67±1.97,P ＜0.01) and decreased further more in the intranasal group(4.00±0.93,P ＜0.05;19.50±1.05,P ＜0.01).Conclusions rhG-CSF given intranasally can relieve the neurological dysfunction of cerebral infarct rats,and brain cells are thereby protected by resisting the expression of FasL.
ABSTRACT
AIM To determine the effect of L-arginin e on cerebral blood perfusion following subarachnoid hemorrhage(SAH) in rats. METHODS Endovascular perforating SAH models were replicated in Wista r rats, and animals were divided into sham-operated group, SAH group and SAH+ L-arginine group. Dynamic changes of regional cerebral blood flow (rCBF) with in 24 hours were measured and serum nitric oxide(NO, NO - 2/NO - 3)levels at different time points within 24 hours were detected. Mean arterial blood pre ssure and blood gas were monitored during the experiment. RESULTS No obvious change in physiological parameters in the three groups was observed . rCBF and serum nitric oxide level at every time point after operation in SAH g roup were lower than those in sham-operated group. Pathological alterations abo ve in SAH+L-arginine group were less obvious than those in SAH group. CONCLUSION L-arginine, by antagonizing the decrease of nitric oxi de, exerts protective effect on secondary cerebral ischemia following SAH.
ABSTRACT
AIM: To investigate the changes of somatosensory evoked potential(SEP), nitric oxide (NO) levels both in serum and in brain tissue after subarachnoid hemorrhage(SAH) and the influence of Ginkgo biloba extract(GBE) on them. METHODS: Wistar rats were divided into sham-operated group, pure SAH group and GBE-treated group. Dynamic changes of regional cerebral blood flow( rCBF),SEP, and NO levels both in serum and in brain tissue were detected within 24 hours after operation. RESULTS: In pure SAH group, rCBF decreased immediately after operation, with no tendency to recover within 24 hours. Latency of SEP delayed progressively from 1 hour to 24 hours after SAH.NO levels in serum and in brain tissue decreased and increased respectively from 1 hour to 24 hours after SAH. GBE effectively antagonized the changes of above parameters. CONCLUSION: SEP is useful in the judgement of cerebral ischemic damage after SAH. Decrease of serum NO and increase of brain NO are important factors leading to cerebral vasospasm and neural damage respectively after SAH. GBE relieves cerebral ischemic damage by reversing the pathological alterations of NO.
ABSTRACT
[A Review] Many clinical and basic researches have revealed that brain damage can be deteriorated by diabetes significantly. However, its pathogenesis remains unclear. Recently, apoptosis have become the focus of research on brain damage. This article introduces the related investigations.
ABSTRACT
The medical care insurance system has been gradually adopted in Chinese society,whose steady movement is dependent of the benefit balance among all stakeholders of the medical insurance system.Based on Rolles's social justice theory,this article analyzed the equality in the medical insurance payment approaches of prospective payment system and post payment system,pointing out their respective influences on each stakeholder in the medical insurance system.
ABSTRACT
OBJECTIVE To find out the prevalent distribution and multidrug resistance trend of meticillin-resistant Staphylococcus(MRS) and to prevent fulminant prevalence of MRS and opt for effective therapeutic means.METHODS The bacterium was(identified) by the way of API Staph and the TH-16S′s coding tube.The(antimicrobial) susceptibility testing was adoped by ATB-STAPH5 and MRS was examined by dilution and K-B.All statistical analyses were performed using SPLM 3.0 software.RESULTS The isolation rate of meticillin-resistant S.aureus(MRSA) and meticillin-resistant coagulase negative Staphylococcus(MRCNS) was 38.09%,20.00%and 87.65%,89.00%,(respectively) in 2 years.Along with the age of patients,the infection from MRS was(increasing).The isolation rate of MRSA was 28-26%,but that of MRCNS was more than 80% from S.epidermidis,S.haemolyticus,S.hominis,and S.saprophyticus subsp saprophyticus.All parts of our body can be(infected) by MRS.The more than 30% MRSA were multidrug resistant and the approximately 11.87-13.75% MRCNS were also multidrug(resistant).(CONCLUSIONS) The isolation rate of MRSA from national surveillance(network) is not(different) with that of MRCNS.
ABSTRACT
AIM: To investigate the role of nitric oxide in the development of brain edema after subarachnoid hemorrhage(SAH), and the influence of L-arginine on them. METHODS: Noncraniotomy models of SAH in Wistar rats were used and animals were divided into sham-operated group, SAH group and SAH plus L-arginine group. Dynamic changes of regional cerebral blood flow within 24 hours were measured. Serum nitric oxide level, brain water and sodium content at different time points within 24 hours were also detected. RESULTS: Regional cerebral blood flow and serum nitric oxide level at every time point after operation in SAH group were lower than those in sham-operated group, while brain water content and sodium content in the former group were higher than those in the latter group. Above pathological alterations in SAH plus L-arginine group were not so obvious as in SAH group. CONCLUSION: Decrease in serum nitric oxide plays a role in the development of brain edema after SAH, which may be partly reversed by administration of L-arginine.