拉莫三嗪对大鼠MCAO/IR模型脂质过氧化产物含量的影响

应用插线法大鼠大脑中动脉缺血再灌注（MCAO／IR）模型，检测皮层和基底节内脂质过氧化产物在缺血再灌流时的变化，研究拉莫三嗪对脂质过氧化产物的影响。讨论了具有抑制突触前膜谷氨酸释放的拉莫三嗪在脑缺血再灌流中的保护机制以及兴奋毒性氨基酸与自由基在脑缺血再灌流中作用和相互关系。     

黄芪皂甙对大鼠MCAO／IR模型氨基酸含量的影响——活体微透析研究

采用大鼠插线法缺血１小时再灌流２小时模型，比较对照组和黄芪皂甙（ＡＳＳ）组在缺血／再灌流时氨基酸和含水量的变化。结果：（１）脑缺血６０分钟时上升到峰值浓度，随后很快下降，再灌流２小时内未见回升；（２）ＡＳＳ组谷氨酸（Ｇｌｕ）峰值浓度下降了１３．２％，但未见统计学差异；（３）黄芪皂甙显著降低了梗塞灶内脑组织含水量。认为尽管ＡＳＳ未能使Ｇｌｕ产生明显下降，但能降低梗塞灶含水量，说明ＡＳＳ的脑保护作用可能是通过其它途径实现的。     

实验性脑缺血再灌流体感诱发电位变经的研究

研究大鼠脑缺血再灌流体感诱发电位变化。方法建立脑缺血再灌流动物模型，随机分成正常对照组９只，缺血和再灌流组２９只，在缺血１ｈ、２ｈ和再灌流１ｈ分别进行神经功能损评分，于缺血２ｈ再灌流１ｈ进行ＳＥＰ观察。结果大鼠脑缺血时，神经功能缺损以轻，中度局灶性损害为主要表现，再灌流后变化不明显，只有１只体征加重。     

黄芪对大鼠脑缺血血脑屏障及脑血流的影响

利用大鼠局灶性脑缺血再灌流和全脑缺血再灌流损伤两种动物模型，观察黄芪注射液对脑缺血后再灌注期间血脑屏蔽及脑血流的保护作用。结果显示，与相庆对照组比较，不论是全脑缺血还是局灶性脑缺血１ｈ后再灌流３ｄ，应用黄芪的各组动物脑水肿明显减轻，血脑屏障通透性改善，大脑局部血流量显著增加。     

阿魏酸钠对大鼠脑缺血—再灌流后氧化性DNA损伤的保护作用

为研究脑缺血 再灌流后氧化性DNA损伤及阿魏酸钠的保护作用 ,采用线栓法制成大鼠大脑中动脉阻塞及再通模型。大脑中动脉再通时静脉注射阿魏酸钠 (15mg/kg) ,用免疫组织化学方法检测脑缺血 2h ,再灌流 4 8h后缺血再灌流组、阿魏酸钠组及对照组脑组织再灌流后氧化性DNA损伤产物 8 羟基脱氧鸟苷(8 OHdG)的表达。结果发现对照组脑区仅见少数散在微弱的 8 OHdG阳性表达 ;缺血再灌流组大脑中动脉阻塞侧额顶叶上部皮质和内侧尾壳核脑区有大量的 8 OHdG阳性表达 ,较对照组显著增加 (P <0 .0 1) ;阿魏酸钠组 8 OHdG阳性表达在脑区分布与缺血再灌流组相似 ,但较缺血再灌流组显著减少 (P <0 .0 1)。上述结果表明脑缺血—再灌流所致的氧化性DNA损伤主要存在于缺血半暗带 ,阿魏酸钠对氧化性DNA损伤具有保护作用。     

中性粘多糖对缺血再灌流脑组织ATP含量的影响

为观察中性粘多糖对缺血再灌流脑组织损伤的作用。我们应用沙土鼠制成的全脑缺血模型，测定缺血组织中的三磷酸腺苷、超氧化物歧化酶及脂质过氧化物。结果显示，提前服用ＮＭ，在缺血时可使脑组织ＡＴＰ含量恢复到正常水平，也可提高再灌流时脑组织ＡＴＰ水平，且后者随着ＳＯＤ活力升高，ＬＰＯ的含量降低，其含量有所恢复。     

高血压大鼠局部脑缺血再灌流边缘区超微结构改变

用透射电镜观察了肾血管性高血压大鼠局部脑缺血早期再灌流及持续缺血９个实验组和假手术组缺血边缘区超微结构改变。结果发现：局部脑缺血０．５至３小时再灌流均较相应持续缺血神经元损害轻；缺血６小时再灌流，神经元细胞器固缩，并有暗黑颗粒沉积。表明在高血压鼠局部脑缺血早期，恢复血流有利于边缘区神经元恢复。     

氧自由基在家兔不完全性脑缺血再灌流损伤中的作用

本文应用电子自旋共振技术,用直接冷冻样品方法,动态观测家免不完全性缺血再灌流脑组织中的氧自由基信号,同时用TBA比色法检测脑组织中的脂质过氧化水平。结果表明,脑缺血再灌流后,早期即可产生大量的氧自由基,而且在再灌流相当时间内仍可持续大量产生,由它引发的脂质过氧化是导致脑损伤的主要原因之一。     

大鼠脑缺血再灌流脑区一氧化氮变化的研究

目的研究大鼠脑缺血及再灌流后脑部一氧化氮的变化。方法采用荧光法和放射免疫法测定４个脑区一氧化氮（ＮＯ）代谢产物ＮＯ２和环磷酸鸟苷（ｃＧＭＰ）。结果脑缺血１０ｍｉｎ,各脑区ＮＯ２和ｃＧＭＰ含量明显增高;脑缺血３０ｍｉｎ,各脑区ＮＯ２和ｃＧＭＰ含量开始下降。缺血１０ｍｉｎ再灌流１５ｍｉｎ以及缺血３０ｍｉｎ再灌流１５ｍｉｎ,各脑区ＮＯ２和ｃＧＭＰ含量再次增加,与单纯脑缺血组相比,有显著差异性（Ｐ＜０．０５或Ｐ＜０．０１）。结论ＮＯ参与了脑缺血再灌流的损伤过程     

新西兰白兔实验性栓塞性脑梗塞模型中缺血后再灌流的作用

早期及时地获得再灌流可能中止缺血性脑损伤进一步恶化的进程，以致恢复受累组织的代谢功能［‘］。然而一旦过了一定时限则缺血性损害可能成为不可逆的，此时获得的再灌流可能进一步损伤缺血组织，导致致命的缺血和破坏，最终细胞死亡［’］。再设流损伤是一系列的损伤机制最终导致自由基（超氧离子）释放的结果u’‘］——脂质过氧化，细胞膜自我消化，细胞死亡。以往的一些研究未能很明确地建立起对脑缺血病灶是有害的，而非有益的再灌流时间窗口。采用溶栓治疗（介人性或非介人性）时最需要决定这种再灌流逆转成缺血损伤反应的“安全区…     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.