血管内皮生长因子在高原脑水肿形成中作用的实验研究

目的:探讨血管内皮生长因子(VEGF)在高原脑水肿形成中的作用。方法:建立大鼠模拟高原模型,应用脑干湿重比率法定量脑水肿情况、应用荧光素钠透过率测定BBB通透性、应用实时荧光定量RT-PCR法检测脑组织VEGF mRNA含量以及应用蛋白印迹法半定量脑组织VEGF含量。结果:大鼠在高原24 h后脑组织含水率明显增高(P<0.05),荧光素钠透过率显著增加(P<0.01);VEGF mRNA转录及其表达显著增高(P<0.001)。结论:VEGF表达在高原脑水肿形成中起重要作用。     

Deep Brain Stimulation——A new treatment for tinnitus

Intractable tinnitus can lead to serious consequences. Study evidence indicates that the central nervous system is involved in generation and maintenance of chronic tinnitus and that tinnitus and other neurologic symptoms such as chronic pain may share similar mechanisms. Brain ablation and stimulation are used to treat chronic pain with success. Recent studies showed that ablation and stimulation in non-auditory areas resulted in tinnitus improvement. Deep brain stimulation (DBS) may be an alternative treatment for intractable tinnitus and deserves further study.     

早期脑室置管行颅内压监护对中型颅脑损伤患者的预后影响

目的　探讨早期脑室置管行颅内压 (ICP)和脑灌注压 (CPP)监护在中型颅脑损伤中的临床应用价值。方法　将 12 5例伤后 2 4h入院无手术指征的中型颅脑损伤 (GCS 9～ 12分 )患者 ,随机分为ICP监护组 :入院后即经恻脑室内穿刺置管行ICP与CPP连续监测 ,根据颅内压变化调整治疗方案 ;对照组 :入院后不做ICP监测 ,依据临床观察的意识及生命体征变化 ,进行治疗。结果　颅内压监护组脱水剂剂量、应用时间均低于对照组 ,疗效优于对照组 ,两组差异有显著意义 (P <0 0 5 )。结论　中型颅脑损伤病情极不稳定 ,早期行ICP监护能及早发现病情变化 ,对及时采取有效治疗措施 ,降低死残率 ,改善预后有重要意义。     

益气复智颗粒对多发脑梗死性痴呆模型大鼠脑组织细胞凋亡的影响

目的 观察益气复智颗粒对多发脑梗死性痴呆模型大鼠脑皮质形态学、细胞凋亡的影响。方法 采用颈内动脉注射血栓的方法，复制多发梗死性痴呆大鼠模型，观察益气复智颗粒12．42g/kg分别于手术前、手术前后、手术后灌胃对实验动物脑皮质形态学、细胞凋亡的影响。结果 益气复智颗粒能使脑缺血后脑内神经细胞凋亡数目下降。结论 益气复智颗粒具有较好的保护脑神经元，阻断脑缺血致神经细胞死亡病理过程的作用。     

梗阻性脑积水侧脑室及室周脑组织生物力学响应的有限元分析

目的运用有限元方法对梗阻性脑积水进行计算机模拟,研究分析侧脑室及室周脑组织的生物力学响应及其所产生的病理生理影响。方法依据正常国人颅脑MRI轴位T2加权图像获取解剖信息,在有限元软件ANSYS中生成包含侧脑室前、后角和体部的半侧脑层面的二维有限元模型。模拟脑组织为固、液两相物质组成的线性多孔弹性材料,设定生物力学特性参数及边界条件和初始条件,施加载荷,运用有限元软件ABAQUS进行计算求解,以云图形式输出结果。结果有限元模型动态模拟了梗阻性脑积水侧脑室各部的扩张过程,直观显示出各个时间步室周脑组织内的应力类型及分布、各部的应变和位移。结论膨胀性应力集中引起角部脑水肿;梗阻性脑积水早期侧脑室角部形态变化最明显;体部附近脑组织结构容易受压移位。这些生物力学响应是室内压增高的结果,也与侧脑室的解剖形态密切相关。     

Exo-focal postischemic neuronal damage in the rat brain: alteration of [H]forskolin binding using in vitro autoradiography

We studied the alteration of intracellular signal transduction using quantitative autoradiography of the second messenger system in order to clarify the mechanisms of delayed neuronal damage in the remote areas of rat brain after transient focal ischemia. Chronological changes of [³H]forskolin binding sites were measured to demonstrate the striatal-nigral pathway after 90 min of right middle cerebral artery (MCA) occlusion and after such occlusion followed by 3 h, 6 h, 1 day, 3 days, 1 week, 2 weeks and 4 weeks of recirculation. [³H]Forskolin binding sites were found to be markedly decreased in the lateral segment of the caudate putamen supplied by the occluded MCA after 90 min of ischemia with no recirculation. On the contrary, there was no alteration on day 1, but 3 days after ischemic insult, marked reduction of [³H]forskolin binding sites was observed in the ipsilateral substantia nigra which lay outside the ischemic areas. This postischemic delayed phenomenon observed in the substantia nigra developed concurrently with ⁴⁵Ca accumulation, which was detected there in our previous study. The delayed reduction of [³H]forskolin binding sites in the substantia nigra observed in the present study indicates that striatonigral terminal degeneration at presynaptic sites is caused by precedent ischemic damage of the ipsilateral caudate putamen and that exo-focal postischemic neuronal death is caused by a transsynaptic process associated with the ischemic foci.