NO与脑胶质瘤瘤周水肿的相关研究

一氧化氮（ＮＯ）在多种信号传递过程中发挥重要作用。最近有研究发现ＮＯ在肿瘤血管生成、微循环和通透性改变中起一定作用。本实验旨在探讨ＮＯ在胶质瘤中的含量及其与瘤周血管源性脑水肿间的关系。一、材料与方法１．选择２０例患者,术后病理证实为恶性星形细胞瘤,按ＷＨＯ１９９３年分类标准,Ⅲ级１１例、Ⅳ级９例,手术和影像学资料（ＣＴ）证实为幕上肿瘤,且位于大脑半球实质内。对照组为８例胶质增生患者。２．新鲜标本切除后立即在３个不同点取材,洗净血迹,置于冰上送往实验室,准确称取３００ｍｇ,制成组织匀浆,加去蛋白试…     

脑膜瘤血管内皮细胞生长因子与瘤周脑水肿关系的研究

目的 了解血管内皮细胞生长因子（ＶＥＧＦ）在脑膜瘤中的表达,探讨ＶＥＧＦ与瘤周脑水肿和微血管形成的关系。方法 应用免疫组化和免疫印迹技术,检测３３例脑膜瘤组织中ＶＥＧＦ蛋白表达与瘤周脑水肿和微血管形成的关系。结果 脑膜瘤ＶＥＧＦ表达率７５％,４例可疑表达。ＶＥＧＦ蛋白表达与ＰＶＢＥ和微血管形成存在肯定的相关产地脑膜瘤组织中,在瘤周脑水肿和微血管形成方面发挥重要作用。     

烫伤大鼠肠粘膜前列腺素水平与前列腺素转移因子mRNA表达的变化

目的　探讨烫伤大鼠肠粘膜前列腺素E2 (PGE2 )、前列腺素I2 (PGI2 )、血栓素A2 (TXA2 )水平和前列腺素转移因子 (PGT)mRNA表达变化及其意义。　方法　以 30 %TBSAⅢ度烫伤大鼠为模型 ,以放射免疫法测定肠粘膜中PGE2 、PGI2 、TXA2 的含量 ,用原位杂交检测PGTmRNA表达。　结果　大鼠肠粘膜PGE2 、PGI2 水平在伤后 12h升高 ,随后明显降低 (P <0.0 5～ 0.0 1);TXA2 水平在伤后 2 4、4 8h明显高于正常水平 (P <0.0 5 );PGTmRNA表达在伤后有增加的趋势。　 结论　烫伤后肠粘膜PGE2 水平降低及TXA2 水平升高 ,可能是肠粘膜损伤的机制之一 ;PGT对伤后PGs水平具有调节作用     

人脑胶质瘤血管生成素-2表达及其与管生成和脑水肿的关系

目的 研究血管生成素.2(Ang-2)基因在人脑胶质瘤表达及其与胶质瘤血管生成及瘤周水肿的关系。方法 用半定量逆转录-聚合酶链反应(RT-PCR)、免疫组织化学方法测定42例人脑胶质瘤和8例正常脑组织中Ang-2 mRNA及其蛋白表达情况。用免疫组织化学方法检测肿瘤微血管密度(MVD)。结果 正常脑组织中无或弱表达Ang-2。42例胶质瘤组织中均有Ang-2 mRNA表达,不同级别间Ang-2 mRNA的表达差异有显著性(P<0.05)。随着脑胶质瘤恶性程度的增加,Ang-2 mRNA的表达增高(r=0.894,P<0.01)。免疫组织化学结果显示,胶质瘤细胞及肿瘤血管内皮细胞中均有Ang-2蛋白表达。Ang-2 mRNA表达与MVD、脑水肿指数(EI)显著相关(分别为r=0.853,P<0.01;r=0.784,P<0.01)。结论 Ang-2可能参与胶质瘤血管生成,对胶质瘤瘤周脑水肿及恶性进展有促进作用。     

水通道1在胶质瘤性脑水肿发生中的意义

胶质瘤性脑水肿所导致的颅内压升高是造成胶质瘤患者预后不良的重要原因。为了探讨这一问题,我们进行以下研究。 一、材料与方法 1.星形胶质细胞的体外培养与细胞系:取10只新生1～2 d的SD大鼠,参照McCarthy等的方法,进行体外培养。实验全部采用2～3代胶质细胞。ECV304人脐静脉内皮细胞系由ECACC提供,培养条件同星形胶质细胞。U251人胶质瘤细胞由本实验室保存,培养条件同前。     

大鼠脑胶质瘤伽玛刀治疗后水肿与C-myc蛋白表达的关系

本研究旨在观察γ-刀治疗胶质瘤的水肿变化与C-myc蛋白表达之间的关系。进一步探讨其作用机制。     

绝育术后盆腔痛与前列腺素关系

<正> 绝育术后少数患者长期盆腔疼痛,但经各种检查未能发现异常。为探讨疼痛原因是否与前列腺素(PG)有关,我们对10例绝育术后盆腔无病变但长期疼痛的患者和15名正常盆腔妇女腹腔液中 PG 水平进行了测定,报告如下。一.对象和方法疼痛组10例,经腹腔镜检查未发现病变;正常组15名,因要求绝育施腹腔镜 Falope 环套扎术。盆腔正常。两组受检对象均无高血压、糖尿病、肾炎等疾病。月经规则,未服用过影响前列腺素族代谢的药物。标本采集:于月经周期第9～13天施腹腔镜检查术。直视下从子宫直肠陷凹抽吸腹腔液,记录液量。将     

甲基强的松龙与地塞米松对C6胶质瘤大鼠放射性脑水肿的治疗效果差异

目的 观察甲基强的松龙与地塞米松对C6胶质瘤大鼠放射性脑损伤后脑水肿程度的影响以及对血液中性粒细胞CDl8 mRNA表达水平的改变.方法 雄性Wistar大鼠100只,体质量250～300 g,随机分成5组,每组20只,分别为接受照射同时30 ms/kg体重甲基强的松龙或10 ms/ks体重甲基强的松龙或5 ms/kg体重地塞米松治疗组(A、B、C组),接受照射但未接受激素治疗的实验对照组(D),未接受照射和激素治疗的正常对照组(E).各组均颅内种植肿瘤,ABCD组于种植15 d后予60Co照射,同时自照射前3 d开始静脉注射激素或生理盐水,直至照射后6 d,照射后第7天取大鼠脑组织测含水量,颈总动脉取血,离心取中性粒细胞层,逆转录.聚合酶链反应(RlT-PCR)分析测定血液中性粒细胞CDl8 mRNA表达水平.结果 脑组织含水量与血液中性粒细胞CDl8 mRNA表达水平:D组、E组分别与ABC组比较差异均有统计学意义(P<0.05);D E组两组间比较,差异有统计学意义(P<0.05);c组分别与A B组比较,差异均有统计学意义(P<0.05);A、B两组间比较,差异无统计学意义(P>0.05).结论 甲基强的松龙与地塞米松均可通过抑制CD18表达的方式减轻放射性脑水肿,但甲基强的松龙效果较好.     

Serum progesterone levels correlate with decreased cerebral edema after traumatic brain injury in male rats

Previous animal research suggests that progesterone may have powerful neuroprotective effects in traumatic brain injury (TBI). This experiment tested the hypothesis that progesterone levels correlate with decreased cerebral edema in male rats with bilateral medial frontal cortex injuries. Three groups of male Sprague-Dawley rats were used: injured given progesterone (4 mg/kg), injured given vehicle (oil), and uninjured controls given vehicle. Progesterone or vehicle was administered intraperitoneally at 1, 6, and 24 h postinjury. At 48 h postinjury, the rats were killed, brains extracted, and assayed for edema. Percent difference in water content of the area surrounding the lesion was compared to posterior cortex. A strong inverse relationship was found between serum progesterone levels and percent cerebral edema; the higher the progesterone levels, the lower the percent edema. Both progesterone and oil-treated animals had some edema compared to sham-operated controls. The brains of the injured animals given control solution were higher in water content than either the uninjured group or injured progesterone-treated rats 48 h postinjury. These findings confirm that progesterone significantly decreases cerebral edema after TBI in adult male subjects.     

Effect of AVP on brain edema following traumatic brain injury

Objective: To evaluate plasma arginine vasopressin (AVP) level in patients with traumatic brain injury and investigate the role of AVP in the process of brain edema. Methods: A total of 30 patients with traumatic brain injury were involved in our study. They were divided into two groups by Glasgow Coma Scale: severe traumatic brain injury group (STBI, GCS≤8) and moderate traumatic brain injury group ( MTBI, GCS >8). Samples of venous blood were collected in the morning at rest from 15 healthy volunteers (control group) and within 24 h after traumatic brain injury from these patients for AVP determinations by radioimmunoassay. The severity and duration of the brain edema were estimated by head CT scan. Results: plasma AVP levels (ng/L) were (mean±SD): control, 3. 06±1. 49; MTBI, 38. 12±7. 25; and STBI, 66. 61±17. 10. The plasma level of AVP was significantly increased within 24 h after traumatic brain injury and followed by the reduction of GCS, suggesting the deterioration of cerebral injury (P<0. 01). And the AVP level was correlated with the severity (STBI r =0.919, P < 0.01; MTBI r = 0.724, P < 0.01) and the duration of brain edema (STBI r = 0. 790, P < 0. 01; MTBI r = 0. 712, P<0.01). Conclusions: The plasma AVP level is closely associated with the severity of traumatic brain injury. AVP may play an important role in pathogenesis of brain edema after traumatic brain injury.     

Correlation of cell apoptosis with brain edema and elevated intracranial pressure in traumatic brain injury

Traumaticbraininjury(TBI) isamongthemostseriousinjuries, frequentlycausingdeathorpermanentdisability. ItiscloselyrelatedwiththehottesttopicsabouthowtoreducetheneurologicalimpairmentwhichmayresultfromTBI.Necrosisinthedamagedregionhadbeenconventionallythoughttobetheonlydeathmodeoftheinjuredneuronsuntilrecently. Atpresent, alotofevidencehasindicatedthatapoptosismightbeanothermainmodeofcelldeathafteraheadtrauma.1 Inthisresearch, animalmodelofTBIwasmadewithadultrabbit, apoptoticcellsweredetecte…     

Aquaporin-4 and brain edema

Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid (CSF) and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. Experiments using AQP4-null mice provide strong evidence for AQP4 involvement in cerebral water balance. AQP4-null mice are protected from cellular (cytotoxic) brain edema produced by water intoxication, brain ischemia, or meningitis. However, AQP4 deletion aggravates vasogenic (fluid leak) brain edema produced by tumor, cortical freeze, intraparenchymal fluid infusion, or brain abscess. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 deletion also worsens obstructive hydrocephalus. Recently, AQP4 was also found to play a major role in processes unrelated to brain edema, including astrocyte migration and neuronal excitability. These findings suggest that modulation of AQP4 expression or function may be beneficial in several cerebral disorders, including hyponatremic brain edema, hydrocephalus, stroke, tumor, infection, epilepsy, and traumatic brain injury.     

Effects of magnesium sulfate on traumatic brain edema in rats

svarietyofneuroprotectiveagentshavebeensynthesized .However ,besidessomeagentspresentlybeingevaluatedinclinicaltrails ,mostofthesecompoundshavelimitedclinicalusebecauseofneurotoxicityandbehavioralsideeffects .Recently ,severalstudiesdemonstratedthattraumaticinjurytothebraincausesadecreaseinmagnesiumconcentrationcorrelatedwithinjuryseverity .1Sincethen ,moreandmoreattentionhasbeen paidtoMgSO4 foritsneuroprotectiveeffects .Magnesiumsulfatehasbeenwidelyusedinclinicalpracticeforalmost 10 0 years.…     

Aquaporin-4 and traumatic brain edema

Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist： ＂vasogenic＂ and ＂cytotoxic/cellular＂. However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 （AQP4） is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments,including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.     

Relationship between changes of N-methyl-D-aspartate receptor activity and brain edema after brain injury in rats

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允许性高碳酸血症对大鼠脑缺血再灌注时脑水肿的影响

目的 探讨允许性高碳酸血症对大鼠脑缺血再灌注时脑水肿的影响.方法 健康雄性Wistar大鼠40只,随机分为5组(n=8):假手术组(SH组)、脑缺血再灌注组(IR组)、PaCO2 60～80 mm Hg组(P1组)、PaCO2 81～100 mm Hg组(P2组)和PaCO2101～120 mm Hg组(P3组).采用双侧颈总动脉夹闭并发低血压法建立脑缺血再灌注损伤模型.P1组、P1组和P3组于再灌注同时吸入CO22 h,使PaCO2分别维持在各组相应PaCO2允许范围内.再灌注24 h时处死大鼠,测定脑水含量和海马水通道蛋白(AQP)-4表达.结果 与SH组比较,其余4组脑水含量及AQP-4表达升高(P<0.01);与IR组、P1组和P2组比较,P1组脑水含量及AQP-4表达升高(P<0.01);与IR组比较,P1组和P2组AQP-4表达下调(P<0.05).结论 允许性高碳酸血症PaCO2101～120 mm Hg可加重大鼠脑缺血再灌注时脑水肿的程度,可能与其上调AQP-4表达有关;而PaCO2 60～100 mm Hg时不加重脑水肿的程度.