36例脑干出血临床分析

随着医学影像学的发展,近年来对于脑干出血的诊断和预后有了更进一步的认识,本文对本院收治的36例经头部CT或MRI确诊的脑干出血患者的临床与预后因素进行分析,总结脑干出血救治经验,减少并发症及病死率,提高临床治愈率.     

脑缺血后钠通道Na(v)1.6的表达变化

目的 观察大鼠缺血脑组织中Na(v)1.6的表达变化及钠通道阻滞剂Riluzole对其表达的影响,探讨Na (v)1.6与脑缺血的关系.方法 105只SD大鼠按随机数字表法分假手术组(n=15)、脑缺血组(n=45)和Riluzole治疗组(n=45),后2组应用线栓法制作成大鼠右侧大脑中动脉永久性闭塞模型,Riluzole治疗组在造模后30 min按8 mg/kg静脉注射给药,1次/d.缺血后6 h、1 d、2 d、3 d、7 d时观察大鼠神经功能缺损情况,应用免疫荧光染色和实时定量PCR方法检测纹状体区Na(v)1.6的表达,TTC染色检测脑梗死体积的变化.结果 缺血组和Riluzole治疗组大鼠神经功能缺损在缺血后2 d表现最严重,相同时间点缺血组较Riluzole治疗组神经功能评分增高,比较差异有统计学意义(P＜0.05).免疫荧光染色显示缺血组和Riluzole治疗组Na(v)1.6表达均在缺血后1 d达高峰,随后下调.实时定量PCR显示缺血组Na(v)1.6 mRNA在缺血后6 h、1 d表达上调,2 d、3 d、7 d表达下调;Riluzole治疗组Na(v)1.6 mRNA缺血后6 h～7 d表达均呈下调趋势;相同时间点Riluzole治疗组Na(v)1.6 mRNA较缺血组表达下调,比较差异有统计学意义(P＜0.05).缺血组和Riluzole治疗组脑梗死体积均在缺血后3 d时最大,相同时间点Riluzole治疗组脑梗死体积比缺血组小,比较差异有统计学意义(P＜0.05).结论 Riluzole可以下调Na(v)1.6表达,减轻缺血性脑损伤,Na(v)1.6可能参与缺血性脑损伤的发病过程.

Abstract：

Objective To observe the changes of Na(v)1.6 expression in rats after acute cerebral ischemia and the effect of Riluzole (the sodium channel blocker) on these changes, and discuss the relationship between level of Na(v)l.6 and cerebral ischemia. Methods One hundred and five healthy SD rats were randomly divided into sham-operated group (n=15), ischemia control group (IC, n=45) and Riluzole therapy group (RT, n=45). Rat models of focal acute cerebral ischemia in the later 2 groups were established by permanent occlusion of right middle cerebral artery. Riluzole at a dosage of 8 mg/kg was given once daily to the rats of the RT group 30 min after ischemia. Tissues from the striatum were collected at different time points (6 h, and 1, 2, 3 and 7 d after ischemia); the expressions of Na(v)1.6 in the striatum were detected by immunofluorescence staining and real-time quantitative PCR at each time point; and the infarct volume was observed by triphenyltetrazolium chloride staining at each time point.Results The rats in the IC group and RT group showed neurologic impairment, especially 2 d after ischemia; rats of the IC group presented significantly higher scores of neurological function scale than those of the RT group at the same time point (P＜0.05). Immunofluorescence staining showed that the expression of Na (v)1.6 was up-regulated, and reached its peak level 1 d after ischemia but then, was down-regulated both in the IC group and RT group. Real-time quantitative PCR showed that the expression of Na(v)1.6 in the IC group was up-regulated 1 d after ischemia, and then down-regulated 2, 3 and 7 d after ischemia, however, that in the RT group was down-regulated 6 h after ischemia; the mRNA expression of Na (v)1.6 in the RT group was obviously down-regulated as compared with that in the IC group at the same time point (P＜0.05). The infarction volume became the largest 3 daRer ischemia both in the IC group and RT group; the infarction volume in RT group was smaller than that in IC group at the same time point (P＜0.05). Conclusion The expression of Na(v)1.6 is down-regulated after cerebral ischemic injury to mitigate acute cerebral ischemic injury, indicating that Na (v)1.6 might involve in the development of cerebral ischemic injury.     

纳洛酮治疗急性脑出血的临床研究

本文观察了本院神经内科2003年9月至2004年2月住院治疗的68例急性脑出血患者的临床特点,并分组对照,分析纳洛酮治疗的疗效和副作用。     

电针治疗大鼠急性缺血性脑损伤的作用机制

目的观察急性脑缺血后及电针治疗后大鼠脑组织中电压门控型钠通道亚型Nav1.6表达,探讨电针治疗急性缺血性脑损伤的作用机制。 方法选取144只健康SD大鼠用线栓法制作大鼠脑缺血模型,按随机数字表法分为脑缺血组、电针治疗组和药物治疗组,每组48只大鼠,另取24只健康SD大鼠作为假手术组,分别于脑缺血后6h、1d、2d、3d四个不同观察时间点取材后,应用实时定量荧光聚合酶链反应（PCR）检测Nav1.6表达,荧光法检测钙离子浓度,氯化三苯四唑染色检测脑梗死体积。 结果假手术组大鼠神经功能缺损Joshua评分均为0分,余3组缺血后6h、1d和2d时的Joshua评分均呈逐渐增高趋势,但在缺血3d时的Joshua评分与组内缺血2d时比较均有所降低,且各组组内差异均有统计学意义(P<0.05)。在大鼠脑缺血后不同时间点,电针治疗组Nav1.6表达先上调然后逐渐下调,组内比较,差异有统计学意义(P<0.05);钙离子浓度亦是早期升高,后期降低,且差异均有统计学意义(P<0.05);脑梗死体积百分比增大明显,组内差异有统计学意义(P<0.05)。以大鼠脑缺血3d时为例,在大鼠脑缺血后相同时间点与假手术组、脑缺血组和药物治疗组相比,电针治疗组的Joshua评分［（2.55±0.42）分］最低,Nav1.6表达［光密度值（0.387±0.023）］下调最明显,钙离子浓度［（448.4±12.4）nmol/L］最低,脑梗死体积百分比［（22.27±1.34）%］最小,且组间差异均有统计学意义(P<0.05)。 结论电针治疗脑缺血后大鼠可抑制缺血脑组织Nav1.6的表达,减少细胞Na+内流,减少细胞内Ca2+浓度,减轻缺血脑损伤;电针治疗对急性缺血性脑损伤的保护作用可能是通过抑制Nav1.6的表达来实现。     

新型隐球菌脑膜炎临床分析

目的:探讨新型隐球菌脑膜炎(CM)的临床特点、诊断、治疗方法。方法:对12例病原学检查证实的CM的临床资料进行分析。结果:(1)临床主要特点:颅内高压和脑膜刺激症;(2)首诊误诊率高,12例中仅2例首诊正确;(3)CM确诊有赖于C.S.F墨汁染色(离心沉淀后)或隐球菌培养;(4)联合用药(包括鞘内给药)及侧脑室引流疗效较单一用药高。结论:CM是以颅高压和脑膜刺激症为特点的亚急性脑膜炎,误诊率高,多次C.S.F离心沉淀有助于提高确诊率,合理用药及有效控制颅高压是治疗成败的关键。     

钠通道Na(v)1.6与缺血性脑损伤

目的 通过观察大鼠缺血脑组织中Na(v)1.6表达探讨Na(v)1.6与缺血性脑损伤的关系.方法 线栓法制作大鼠脑缺血模型,168只SD大鼠分为假手术组、脑缺血组和钠通道阻滞剂-riluzole、钙通道阻滞剂-nimodipine治疗组.大鼠脑缺血后6h、1d、2d、3d取材,应用免疫组化检测Na(v)1.6表达,荧光法检测钙离子浓度,氯化三苯四唑染色检测脑梗死体积.结果 Na(v)1.6在脑缺血后6h～1d表达上调,2～3d表达下调；相同时间点nimodipine治疗组与缺血组相比较,Na(v)1.6表达变化不明显；riluzol治疗组Na(v)1.6表达变化明显,差异具有显著性(P＜0.05).riluzol治疗组和nimodipine治疗组钙离子浓度、脑梗死体积均比缺血组降低,riluzol治疗组降低最明显,差异具有显著性(P＜0.05).结论 钠离子内流发生在脑缺血的早期阶段；脑缺血后Na(v)1.6表达上调,抑制Na(v)1.6表达可以减轻脑缺血损伤,Na(v)1.6参与了缺血性脑损伤.