蛛网膜下腔血性与非血性刺激物对脑血管影响的组织学比较

目的通过对蛛网膜下腔血性、非血性刺激物对脑血管影响的比较,探讨蛛网膜下腔出血(SAH)后迟发性脑血管痉挛(DCVS)的发病机制。方法将40只新西兰白兔随机分为5组:假手术组、非抗凝自体动脉血组、抗凝自体动脉血组、Kaoline(高岭土)组和失活细菌组,每组8只。假手术组动物仅做枕大池假穿刺;非抗凝血组动物采用经枕大池二次注血法制作DCVS模型;抗凝自体动脉血组用肝素处理后的自体动脉血代替非抗凝血行枕大池二次注血;Kaoline组和失活细菌组经枕大池穿刺分别注入15%Kaoline悬浊液(0.25ml/kg)、失活细菌悬浊液(3×1010个/ml;0.25ml/kg)。各组受试动物在7d时用4%多聚甲醛灌注处死,将脑组织连同基底动脉及其分支取出行HE染色、免疫组化检测TNF-α供组织学研究。结果与假手术组基底动脉血管形态相比,非抗凝血组、Kaoline组和失活细菌组均有不同程度的血管痉挛,抗凝血组无明显血管痉挛。TNF-α表达随血管痉挛程度加重而增加。结论蛛网膜下腔内不同刺激物导致与SAH后DCVS相同的病理改变提示:蛛网膜下腔内刺激物所致血管局部的过度炎症反应可能是导致血管痉挛发生的重要原因。     

CCK-8对家兔SAH后迟发性脑血管痉挛病理变化的影响

目的:利用胆囊收缩素-8(CCK-8)的抗炎作用,观察其对自发性蛛网膜下腔出血后迟发性脑血管痉挛病理改变的影响。方法:雄性新西兰白兔60只随机分为四组(n=15)。①假手术组:仅进行枕大池穿刺和假注血;②SAH组:经家兔枕大池二次注射自体动脉血(0．8ml／kg)制作SAH模型;③SAH+CCK-8组:对SAH模型自day 0开始经枕大池注入 CCK-8(8μg／kg,0．5ml),每日一次直到动物处死;④SAH+生理盐水组:对SAH模型自day 0开始经枕大池注入等量37℃生理盐水,每日一次直到动物处死。各组分别在day 4、day 7和day 14分三批处死动物,每批5只。结果:假手术组动物基底动脉组织结构正常。SAH组动物基底动脉在day4、day7时出现血管痉挛,以day 7时最为显著,day 14血管痉挛得到缓解。CCK-8治疗组动物的血管痉挛程度有不同程度缓解,血管壁NF-κB、TNF-a表达明显减弱,与同时段SAH组和SAH+ 生理盐水组比较以day7时最为显著(P<0．05)。结论:CCK-8对SAH后迟发性脑血管痉挛具有一定的预防作用。     

经颅多普勒超声诊断自发性蛛网膜下腔出血后脑血管痉挛

<正>自发性蛛网膜下腔出血(subarachnoid hemorrhage,SAH)常由脑动脉瘤破裂导致,出血引致颅底脑池内颈内动脉、椎基底动脉及其分支为主的脑血管痉挛(cerebral vasospasm,CVS),并因此出现迟发性缺血性脑损伤。上述血管痉挛常常在发病后就开始存在,于发病后1 w达高峰期,是SAH致残和死亡的重要原因。CT动脉成像(computer tomography     

辛伐他汀对兔蛛网膜下腔出血后迟发性脑血管痉挛中血管壁增殖的影响

目的 探讨辛伐他汀对兔蛛网膜下腔出血(SAH)后迟发性脑血管痉挛(CVS)中血管壁增殖的影响.方法 36只新西兰大白兔随机分为3组:①对照组,常规饲养并枕大池二次注入0.9%生理盐水;②SAH组,通过二次枕大池注血建立SAH模型;③辛伐他汀+SAH组,每日胃灌辛伐他汀5 ms/kg,连续7 d后建立SAH模型.各组兔模型前后行两次脑血管造影.灌注后取基底动脉组织制作病理切片,分别于光镜和透射电镜下观察其显微以及超微结构.采用免疫组化及免疫荧光方法检测基底动脉组织中增殖细胞核抗原(PCNA)及α-平滑肌肌动蛋白(α-SMA)表达量的变化,同时采用Real-Time PCR检测其血小板源性生长因子-B(PDGF-B)基因表达量的变化.采用SPSS10.0软件进行统计分析.结果 通过脑血管造影可以观察到二次注血后兔基底动脉出现明显的痉挛,管径变细;而给予辛伐他汀后,痉挛减轻.SAH组兔基底动脉壁略有增厚,电镜显示平滑肌细胞内合成旺盛;而给予辛伐他汀预处理后这些变化明显减轻.SAH组兔基底动脉管壁平滑肌细胞内α-SMA、PCNA、PDGF-B表达明显高于对照组(P＜0.05),而给予辛伐他汀后三者表达量明显降低(P＜0.05).结论 辛伐他汀可能通过抑制迟发性CVS中血管壁平滑肌细胞的增殖来缓解SAH后迟发性CVS.     

兔脑基底动脉痉挛的实验研究

目的：探讨脑动脉壁局部性反应,免疫反应在蛛网膜下腔出血后迟发性血管痉挛发病机制中的作用及脑池局部应用尼莫地平对迟发性血管痉挛发生的预防作用,方法：在经斜坡暴露并穿刺兔基底动脉制备蛛网膜下腔出血模型基础上,测量各组动物血管痉挛前,后基底动脉直径并观察血管病理变化及动脉壁免疫球蛋白IgG沉积情况,结果：存在迟发性脑血痉挛的脑动脉壁渐次出现动脉中膜平滑肌变性,坏死,内皮细胞脱落及外膜炎症细胞浸润等现理改变,免疫球蛋白IgG在血管壁上表现为“一过性沉积”,与血管痉挛程度无明显关联,及池局部应用尼莫地平在蛛网膜下腔出血后早期,虽然可以明显缓解脑动脉痉挛,但并不能完全阻止迟发性脑血后迟发性血管痉挛的实质是以脑动脉壁的炎性反应为主,为临床超早期手术清除蛛网膜下腔出血提供了理论基础。     

盐酸法舒地尔对蛛网膜下腔出血后血管痉挛的实验研究

目的通过建立大鼠蛛网膜下腔出血（SAH）模型,探讨盐酸法舒地尔对蛛网膜下腔出血后血管痉挛的缓解作用和神经保护作用,并与尼莫地平对比,观察疗效。方法通过枕大池二次注血法建立大鼠SAH模型,观察基底动脉和海马神经元形态变化,测量基底动脉管径和管壁厚度,计算海马CA1区神经元密度,检测基底动脉内皮型一氧化氮合成酶（eNOS）的表达。结果各组模型大鼠的基底动脉均出现血管痉挛,海马CA1区正常神经元数目明显减少,多数神经元发生变性,基底动脉的eNOS表达明显减弱。但注射法舒地尔组与其他模型组相比能较大程度的缓解以上变化,具有统计学差异（P〈0.05）,且优于尼莫地平。结论法舒地尔可以有效缓解SAH后的迟发性脑血管痉挛,具有神经保护作用,其缓解迟发性脑血管痉挛作用和神经保护作用与动脉壁产生的一氧化氮（NO）有关。     

实验性蛛网膜下腔出血后兔脑血管病理结构的动态变化

目的观察蛛网膜下腔出血后脑血管病理结构的动态变化,以建立可靠的脑血管痉挛模型。方法实验分正常组、对照组(枕大池注入等量生理盐水)、SAH3d组、SAH5d组、SAH7d组、SAH10d组和SAH14d组,枕大池二次注血法建立兔蛛网膜下腔出血模型,应用脑血管造影、光镜和透射电镜检查等方法观察SAH后基底动脉形态改变。结果脑血管造影发现SAH后第3d基底动脉狭窄,第7d达高峰。光镜和透射电镜检查显示出血后第3d开始出现血管管腔狭窄、管壁增厚、内皮细胞和平滑肌细胞变性,并随时间推移加重,第5d和第7d病理改变更明显,尤以第7d为著,10d后缓解。结论兔枕大池二次注血法是可靠的SAH后脑血管痉挛模型制作方法。     

两种蛛网膜下腔出血动物模型的CTA比较

目的探讨多排螺旋cT血管造影对兔蛛网膜下腔出血（SAH）诱发迟发性脑血管痉挛（DCVS）两种动物模型的效果。方法兔枕大池二次注血蛛网膜下腔出血模型（A组）与症状性蛛网膜下腔出血模型（B组）各20只,分别于1d、4d、7d、11d、14d行CTA检查,测量其血管痉挛程度。结果枕大池二次注血模型血管痉挛在注血后4d达到高峰,14d开始缓解,通过CTA测量血管直径了解痉挛程度。结论两种模型比较,CTA测量枕大池二次注血模型中血管痉挛的变化可靠、微创,为研究蛛网膜下腔出血后迟发性脑血管痉挛提供了确实可靠的动物模型和观察手段。     

血管内一氧化氮合酶基因转染预防脑血管痉挛的实验研究

目的采用血管内基因转染的方法,将重组内皮型一氧化氮合酶(eNOS)基因转染入蛛网膜下腔出血(SAH)后迟发性脑血管痉挛大鼠脑动脉,探讨防治SAH后迟发性脑血管痉挛的新方法。方法首先构建携带eNOS基因的重组腺病毒。采用小脑延髓池二次注血法建立大鼠SAH后迟发性脑血管痉挛模型。通过颈动脉微泵持续滴注方法进行基因转染,并设置对照组。结果第7天采用免疫组化证实重组eNOS基因表达,重组eNOS主要表达于内皮层。第7天显微镜下测定血管内eNOS转染组脑动脉环平均直径较单纯SAH组增大,电镜观察血管痉挛较单纯SAH组减轻。结论通过本研究证实采用颈动脉微泵持续滴注方法可在大鼠脑动脉表达重组eNOS,重组基因主要表达于动脉内皮细胞,可达到缓解SAH后迟发性脑血管痉挛的目的。     

DSA和TCD对兔蛛网膜下腔出血脑血管痉挛的评价

目的 探讨在小动物如兔蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)模型上经股动脉入路行选择性椎-基底动脉造影的可行性;探讨TCD对兔SAH后CVS状况的评价效度.方法 采用枕大池2次注血法建立兔迟发性CVS的动物模型.术前1 d和术后3、5 d行选择性脑血管造影,判断CVS的程度;术前1 d及术后1、3、 5、 7 d行TCD连续检测基底动脉血流速度,从而判断CVS的变化及程度.结果 在家兔CVS动物模型上成功完成左侧椎动脉选择性插管和造影,可有效地判断CVS的严重程度;采用TCD连续监测基底动脉血流速度可获得稳定图谱,能观察到制模后血流速度的变化情况.结论 经兔股动脉入路行选择性椎-基底动脉造影是完全可行的,TCD可连续监测兔基底动脉血流速度,对兔SAH后CVS状况的评价稳定可靠,TCD与脑血管造影在检测SAH后CVS方面具有良好相关性.     

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.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -