免疫抑制剂硫唑嘌呤对慢性脑血管痉挛的防治作用

目的观察免疫抑制药物对慢性脑血管痉挛的预防作用。方法采用本单位以往建立的犬“二次蛛网膜下腔出血”模型，观察硫唑嘌呤对慢性脑血管痉挛的预防作用。结果在蛛网膜下腔出血第７天，硫唑嘌呤组的基底动脉口径为（８７.１±２５．９）％，管壁ＭＤＡ含量为０．０３±０．０１ｎｍｏｌ／ｍｇ；而安慰剂组的血管口径为（５２．７±１７．１）％，ＭＤＡ含量为０．１０７±０．０５ｎｍｏｌ／ｍｇ。组织学检查发现硫唑嘌呤组的血管壁结构破坏明显较安慰剂组轻。结论蛛网膜下腔出血后慢性脑血管痉挛主要是免疫系统参与的炎症反应的结果，抗炎抗免疫疗法能有效预防慢性脑血管痉挛。     

764－3对脑血管痉挛防治的研究

本实验在狗“二次蛛网膜下腔出血”模型上分别观察了７６４－３对血管痉挛的直接作用和对慢性脑血管痉挛的预防作用。结果表明：推荐剂量（２ｍｇ／ｋｇ，静注）的７６４－３对动脉血管无直接扩张作用。通过７６４－３的连续预防用药（４０ｍｇ／ｋｇ·日，肌注）能减轻慢性脑血管痉挛的程度（Ｐ值＜０．０５），降低动脉壁的过氧化脂质（Ｐ值＜０．０５），同时对全身血压、心率及白细胞数无不良影响。本文对上述结果进行了讨论。     

中药川芎嗪对蛛网膜下腔出血后脑血管痉挛的实验研究

目的观察川芎嗪（TMP）对蛛网膜下腔出血后脑血管痉挛（CVS）的治疗效果。方法制备能够连续造影的兔CVS动物模型，将其随机分为TMP组、尼莫地平组和对照组，每组13只，各组分别注入TMP 60mg／kg、尼莫地平0．1mg／kg及等量生理盐水，观察各组动物的神经功能状态变化，并应用脑血管造影、经颅多普勒（TCD）及电镜技术，了解药物对急、慢性CVS的治疗效果。结果CVS急性期静脉注射TMP、尼莫地平30min后，基底动脉口径分别由（57．17±11．40）％、（58．0±10．90）％扩大到（80.16±14.22）％、（90．0±11.38）％（均P〈0．01）。在CVS慢性期，动脉口径扩张不明显（P〉0．05），但TCD检测基底动脉的平均血流速度则分别由（57.92±10．54）cm／s、（61.61±11.49）cm／s下降到（36．58±10.39）cm／s、（33.67±7.57）cm／s（均P〈0.01）；形态学研究显示：对照组基底动脉内皮细胞、平滑肌细胞及神经细胞的损害程度明显重于实验组。结论①TMP能够缓解CVS，明显改善CVS后的神经系统功能损害症状。②TMP与尼莫地平对CVS同样具有良好的治疗效果，但TMP60mg／kg对脑组织、血管组织的保护作用优于尼莫地平0.1mg／kg。     

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。     

764—3对脑血管痉挛防治的研究

本实验在锆“二次蛛网膜下腔出血”模型上分别观察了７６４－３对血管痉挛的直接作用和对慢性脑血管痉挛的预防作用。结果表明，推荐剂量的７６４－３对动脉血管无直接扩张作用。通过７６４－３的连续预防用药减轻慢性脑血管痉挛的程度，降低动脉壁的过氧化脂质，同时对全身血压，心率及白细胞数无不良影响。     

蛛网膜下腔出血后脑血管痉挛与脑脊液免疫球蛋白的关系

检测４１例蛛网膜下腔出血病人脑脊液中免疫球蛋白Ｇ的含量，其中２２例为蛛网膜下腔出血后伴脑血管痉挛患者，其脑脊液中免疫球蛋白Ｇ含量为８３．０４±３１．７８ｍｇ／Ｌ，１９例不伴脑血管痉挛病人，脑脊液中免疫球蛋白Ｇ含最为：３０．７９±２２．１３ｍｇ／Ｌ；脑血管痉挛组脑脊液中免疫球蛋白Ｇ含量明显高于非脑血管痉挛组（Ｐ＜０．０１）。结果表明蛛网膜下腔出血后脑血管痉挛有免疫反应的存在。     

实验性迟发性脑血管痉挛时痉挛动脉的自由基代谢

为探讨蛛网膜下腔出血（ＳＡＨ）后迟发性脑血管痉挛（ＤＣＶＳ）时痉挛动脉的自由基代谢变化。通过了对ＤＣＶＳ时痉挛动脉的自由基含量、自由基清除酶超氧化物岐化酶（Ｃｕ－ＺｎＳＯＤ）与过氧化氢酶（Ｃａｔ）活性以及自由基代谢产物脂质过氧化物（ＬＰＯ）含量的测定。结果显示：（１）痉挛动脉的自由基含量比对照组明显升高（Ｐ＜０．０１）；（２）Ｃｕ－ＺｎＳＯＤ活性明显降低（Ｐ＜０．０５），Ｃａｔ活性明显升高（Ｐ＜０．０１）；（３）ＬＰＯ含量明显升高（Ｐ＜０．０１）。本实验结果证实ＳＡＨ后ＤＣＶＳ时痉挛动脉存在自由基的代谢紊乱，自由基介导的病理作用可能在ＤＣＶＳ发病机理中起重要作用。     

腰大池持续引流配合尼莫地平治疗蛛网膜下腔出血后脑血管痉挛的研究

目的：探讨腰大池引流配合尼莫地平能否降低蛛网膜下腔出血后脑血管痉挛的发生。方法。通过对近3年来64例蛛网膜下腔出血患进行随机分组，治疗组32例行腰大池引流配合应用尼莫地平。对照组32例给予常规治疗，对结果进行对比分析。结果：治疗组中仅有2例发生脑血管痉挛，对照组有8例发生脑血管痉挛。结论：腰大池持续引流配合静点尼莫地平能显降低蛛网膜下腔出血后脑血管痉挛的发生。     

西比灵预防蛛网膜下腔出血后脑血管痉挛的疗效观察

目的：观察西比灵预防蛛网膜下腔出血后脑血管痉挛的疗效。方法：84例发病24h内入院的蛛网膜下腔出血患者随机分为治疗组和对照组。治疗组予西比灵5mg，口服2/d，同时予止血、镇静、止痛、脱水等常规治疗。对照组予尼莫地平60mg口服，4/d，止血、镇静、止痛、脱水等治疗同治疗组。结果：治疗组4例出现脑血管痉挛，占9．5％；对照组3例出现脑血管痉挛，占7．1％。两组脑血管痉挛发生率无显著差异（P＞0．05）。结论：口服西比灵预防蛛网膜下腔出血后脑血管痉挛有效。     

蛛网膜下腔出血后脑血管痉挛及再出血临床分析

目的通过分析蛛网膜下腔出血后脑血管痉挛及再出血的临床诊治、总结经验以提高对这两个合并症的诊治水平。方法对１２５例蛛网膜下腔出血患者的临床表现,诊治情况进行总结分析。结果１２５例蛛网膜下腔出血中３０例出现脑血管痉挛,占总数的２４％,其中２例死亡。应用钙拮抗剂组脑血管痉挛发生率明显低于未应用钙拮抗剂组,两组相比有显著性差异,再出血２２例,占总数１７．６％,１２例死亡。此两种并发症占总死亡率的８２．４％。结论早期应用钙拮抗剂可预防或降低脑血管痉挛发生率,从而减少蛛网膜下腔出血严重并发症。再出血是蛛网膜下腔出血死亡的主要原因之一。     

Clinical and experimental studies on the action of ethamsylate on haemostasis and on platelet functions

In a series of tests,the action of ethamsylate on haemostasis and on platelet functions was examined. After oral administration of the drug,a highly significant diminution of the bleeding time and of the blood loss from a standard wound was observed. This effect was demonstrated in healthy individuals and in patients suffering from platelet dysfunctions,and there was a distinct dose relation. There was also an increase of platelet adhesion,of PF 3 availability and of PF 4 release. The action of prostacyclin on the epinephrine induced platelet aggregation could be inhibited by ethamsylate. This offers a possible explanation for some of the effects on hemostasis. In addition,an action of ethamsylate on the platelet membrane was assumed since an in vitro increase of functions of the platelet membrane like PF 3 availability would not be explainable by a possible inhibition of prostacyclin.     

Reflections and Comments on Research on Memory and Conversation From an Ethnographic Perspective

Reflecting on three papers included in this issue, we suggest that research on memory and conversation could benefit by making more use of analyzing real‐life situations or close to real‐life scenarios, full speech and body interactions, and the interaction with the physical environment. We also suggest that the process of remembering during conversation is investigated on a level of detail and sequence that allow for locating actual functions of different actions. Finally, we suggest that a life‐span perspective on transactive memory systems must also model the development, maintenance, breakdown, and reestablishment of such systems.     

Growth and degeneration of axons on astrocyte surfaces: Effects on extracellular matrix and on later axonal growth

Cultured astrocytes deposit an extracellular matrix which has been shown by immunocytochemistry to react with antibodies to tenascin, laminin, and fibronectin. Neuronal-glial interaction down-regulates these components of the matrix, causing a reduction in extracellular matrix localized to areas of contact with axons. Axons used for these experiments were from embryonic rat retinal explants. In some experiments explants were removed from the co-cultures and their axons allowed to degenerate. Degeneration of axons did not reverse the local reduction of extracellular matrix brought about by axon outgrowth. The period of axon outgrowth studied was 4-5 days; the period of degeneration was 2-3 days. Astrocytes alone, astrocytes with intact retinal explants, and astrocytes with 2-day degenerated retinal axons were tested for their ability to support neurite outgrowth from embryonic rat cortical neurons. Neurite outgrowth occurred on all astrocyte cultures. Cortical neurite lengths, measured 2 days after plating, were not significantly different between astrocytes alone and astrocytes with degenerated retinal axons. However, there was a tendency for neurites to be shorter on astrocytes with intact retinal axons present. Two conclusions may be drawn from these results. First, the state of differentiation of astrocytes, as marked by their assembly of extracellular matrix, is altered by contact with axons. Second, degeneration of axons alone, in the absence of other cell types, is not a sufficient signal to reestablish assembly of extracellular matrix. However, neither is it a sufficient signal to render astrocytes inhospitable to further axonal outgrowth or regeneration. © 1993 Wiley-Liss, Inc.     

Drug effects on REM sleep and on endogenous depression

In earlier work REM sleep deprivation (RSD) by arousals improved endogenous depression. This suggested that drugs producing a similar RSD would have antidepressant activity. The arousal RSD was large, persisted for weeks, and was followed by a REM rebound. We call RSD with these properties arousal-type RSD. The present study reviewed literature from 1962 to 1989 on drug REM sleep effects to examine the hypothesis that drugs producing arousal-type RSD improve endogenous depression. The literature reviewed concerned the REM sleep effects of amine precursors, antidepressants, antihistamines, antipsychotics, barbiturates, benzodiazepines, other hypnotics, drugs affecting cholinergic and noradrenergic neurotransmission, ethanol, lithium and narcotics. Four hundred and sixty-eight relevant papers were read and 215 contributed information that could be used in the review. The findings indicated that all drugs producing arousal-type RSD improved endogenous depression. Four drugs that improved endogenous depression did not produce arousal-type RSD.     

Effect of calcium phosphate on thrombin and on its sensitivity to heparin and antithrombin-III

Thrombin was inactivated by antithrombin-III and the rate of inactivation was accelerated by heparin either in 0.04 M sodium phosphate buffer or in 0.04 M Tris-HCl buffer, at pH 7.4. Calcium chloride, at a final concentration of 1 mM, influenced slightly thrombin inactivation by both antithrombin and antithrombin plus heparin in Tris-HCl buffer, whereas in phosphate buffer the sensitivity of enzyme to antithrombin and heparin decreased.Thrombin showed also increased stability against the inactivating effect of heat at 54°C in sodium phosphate buffer containing calcium chloride.These findings suggest that thrombin bound to calcium phosphate is extremely stable against inactivation by antithrombin and heparin, while its clotting activity does not change. This nature of enzyme may play a role in predisposition for thrombosis during arteriosclerosis.     

Influence of vestibular input on spatial and nonspatial memory and on hippocampal NMDA receptors

It has recently been shown that a lack of vestibular sensory information decreases spatial memory performance and induces biochemical changes in the hippocampus in rodents. After vestibular neurectomy, patients display spatial memory deficit and hippocampal atrophy. Our objectives were to explore: (a) spatial (Y maze, radial-arm maze), and non-spatial (object recognition) memory performance, (b) modulation of NMDA receptors within the hippocampus using radioligand binding, and (c) hippocampal atrophy, using MRI, in a rat model of bilateral labyrinthectomy realized in two operations. Chemical vestibular lesions (VLs) were induced in 24 animals by transtympanic injections of sodium arsanilate (30 mg/0.1 ml/ear), one side being lesioned 3 weeks after the other. The control group received transtympanic saline solution (0.1 ml/ear) (n = 24). Spatial memory performance (Y maze and radial maze) decreased after VL. Conversely, non-spatial memory performance (object recognition) was not affected by VL. No hippocampal atrophy was observed with MRI, but density of NMDA receptors were increased in the hippocampus after VL. These findings show that the lack of vestibular information induced specific deficits in spatial memory. Additionally, quantitative autoradiographic data suggest the involvement of the glutamatergic system in spatial memory processes related to vestibular information. When studying spatial memory performances in the presence of vestibular syndrome, two-step labyrinthectomy is a suitable procedure for distinguishing between the roles of the specific components of vestibular input loss and those of impaired locomotor activity.