Loss of long-term potentiation in the hippocampus after experimental subarachnoid hemorrhage in rats

Survivors of aneurysmal subarachnoid hemorrhage (SAH) often suffer from cognitive impairment such as memory loss. However, the underlying mechanisms of these impairments are not known. Long-term potentiation (LTP) of synapses in the hippocampus is generally regarded as a molecular substrate of memory. The purpose of this study was to examine the effect of SAH on LTP in the hippocampal Schaffer collateral (CA3–CA1) pathway in a rat model of SAH. We found SAH caused significant vasospasm of the middle cerebral artery (MCA) compared to saline injected or sham controls (P<0.001). Basic neurotransmission quantified as excitatory post synaptic and spike response from animals with SAH were significantly decreased as compared to naive controls (P<0.05). However, sham operated and saline injected controls showed similar amplitude as naive controls. This suggests that reduction in basic neurotransmission is due to blood in the subarachnoid space. Similarly, analysis of LTP demonstrated that naive, sham and saline controls have a 92±16%, 69±27% and 71±14% increase over the baseline in the average spike amplitude following high frequency stimulation (HFS), respectively. This indicates the presence of LTP (P<0.05). In contrast, the spike amplitude in animals of SAH returned to baseline level within 60 min post HFS indicating the absence of LTP. We conclude that SAH caused vasospasm of the MCA that was associated with disrupted basic neurotransmission and plasticity at CA3–CA1 synapses. These changes might be accountable for the memory loss in humans with SAH.     

腰大池持续外引流合并鞘内注射尿激酶治疗脑血管痉挛的临床效果

目的探讨鞘内局部注射尿激酶治疗蛛网膜下腔出血后脑血管痉挛的疗效。方法将动脉瘤性蛛网膜下腔出血患者随机分为对照组和实验组,对照组采用常规综合治疗加静脉泵入尼莫地平治疗,实验组在对照组的基础上放置腰大池引流管并脑池内注射尿激酶治疗,通过观察病情变化评价两组的治疗疗效。结果实验组剧烈头痛、恶心呕吐、意识障碍及脑膜刺激征等主要症状及体征的缓解率明显高于对照组（P〈0.05）,实验组（5/26）脑血管痉挛发生率明显低于对照组（10/24,P〈0.05）。结论早期鞘内注射尿激酶并持续外引流防治脑血管痉挛的效果良好,且术后脑积水的并发症少。     

枕大池注入硫酸镁对兔蛛网膜下腔出血后脑血管痉挛的逆转及脑保护作用

目的:研究枕大池注入硫酸镁注射液是否能逆转兔蛛网膜下腔出血后脑血管痉挛以及脑组织损伤。方法:采用兔一次性注血的方法建立蛛网膜下腔出血模型。将30只新西兰大白兔随机分为3组:假手术组、模型组和MgSO4组。前二组于术后24h枕大池注入0.1mL.kg-1生理盐水,后一组注入0.1mL.kg-14%MgSO4。48h后处死兔取基底动脉以及海马组织行病理检查,测定基底动脉管腔横切面积和海马CA1区正常神经元密度。结果:以基底动脉管腔横切面积及海马CA1区正常神经元密度为指标,模型组低于假手术组和MgSO4组(P<0.01),而后二组比较无明显差异(P>0.05)。结论:枕大池注入硫酸镁注射液可能具有逆转兔蛛网膜下腔出血后脑血管痉挛以及脑血管痉挛所致海马神经元损伤作用。     

兔症状性脑血管痉挛细胞凋亡的电镜研究

目的研究兔症状性脑血管痉挛的细胞凋亡情况。方法建立兔症状性脑血管痉挛模型,然后采用透射电镜观察兔基底动脉细胞的形态变化。结果电镜下见基底动脉的内皮细胞、平滑肌细胞胞核固缩,胞浆空泡化,类似细胞早期凋亡改变。结论凋亡可能参与脑血管痉挛,为研究和治疗脑血管痉挛提供一种新的思路。     

硫酸镁防治蛛网膜下腔出血后脑血管痉挛的疗效观察

目的:观察硫酸镁防治蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的疗效。方法:将SAH患者54例,随机分为治疗组(28例)和对照组(26例)。对照组采用脱水、止血等常规疗法;治疗组在常规疗法基础上加用25%硫酸镁15ml加生理盐水250ml,静脉滴注,2次/天;10天后改为1次/天,再用10天停用。采用经颅多普勒(TCD)检测SAH患者脑动脉的收缩峰速度,观察各组CVS发生的情况。结果:治疗组继发CVS 4例(14.3%),对照组13例(50%)。治疗组患者脑动脉的收缩率流速(Vp)较对照组差异极有显著性(P<0.01);且治疗后与治疗前Vp相经差异极有显著性(P<0.01);对照组患者治疗前后的Vp相比差异无显著性(P>0.05)。结论:硫酸镁防治SAH后CVS疗效确切。     

外伤性蛛网膜下腔出血致脑血管痉挛机制的研究进展

外伤性蛛网膜下腔出血后脑血管痉挛是一种严重的并发症,其发病机制目前尚不明确。虽然新的治疗方法如经皮血管介入成形术及使用罂粟碱应用较普遍,但临床治疗仍局限于三高治疗及使用钙离子拮抗剂治疗。本文将就目前外伤性蛛网膜下腔出血后脑血管痉挛的发病机制加以综述,并提出今后研究的方向。     

Imaging findings in rabies

A 10 year old Vietnamese girl presented with clinical features of an acute encephalitic process. A cerebral angiogram performed to rule out vasculitis showed narrowing at the supraclinoid internal carotid and terminal basilar arteries. A diagnosis of rabies was established at autopsy. Although the major blood vessels and basal meninges were normal it was possible that transient arterial spasm induced by the viral infection was responsible for the angiographic appearance. Other imaging findings in our patient are described with a brief review of the literature. This is only the second case of rabies reported in Australia.^1,2 Rabies is a rare disease in the Australian community. Recently one patient with atypical clinical presentation was confirmed to have the disease only at autopsy. In the clinical work-up, various radiological examinations were performed and a range of interesting features were encountered including an abnormal cerebral angiogram. The purpose of this paper is to report on these unusual features and to review those documented in the literature.     

Hypersensitivity of prediabetic JCR:LA-cp rats to fine airborne combustion particle-induced direct and noradrenergic-mediated vascular contraction.

Particulate matter with mean aerodynamic diameter < or =2.5 microm (PM(2.5)), from diesel exhaust, coal or residual oil burning, and from industrial plants, is a significant component of airborne pollution. Type 2 diabetes is associated with enhanced risk of adverse cardiovascular events following exposure to PM(2.5). Particle properties, sources, and pathophysiological mechanisms responsible are unknown. We studied effects of residual oil fly ash (ROFA) from a large U.S. powerplant on vascular function in a prediabetic, hyperinsulinemic model, the JCR:LA-cp rat. Residual oil fly ash leachate (ROFA-L) was studied using aortic rings from young-adult, obese, insulin-resistant rats and lean normal rats in vitro. Contractile response to phenylephrine and relaxant response to acetylcholine were determined in the presence and absence of L-NAME (N(G)-nitro-L-arginine methyl ester). In a separate series of studies, the direct contractile effects of ROFA-L on repeated exposure were determined. ROFA-L (12.5 microg ml(-1)) increased phenylephrine-mediated contraction in obese (p < 0.05), but not in lean rat aortae, with the effect being exacerbated by L-NAME, and it reduced acetylcholine-mediated relaxation of both obese and lean aortae (p < 0.0001). Initial exposure of aortae to ROFA-L caused a small contractile response (<0.05 g), which was markedly greater on second exposure in the obese (approximately 0.6 g, p < 0.0001) aortae but marginal in lean (approximately 0.1 g) aortae. Our data demonstrate that bioavailable constituents of oil combustion particles enhance noradrenergic-mediated vascular contraction, impair endothelium-mediated relaxation, and induce direct vasocontraction in prediabetic rats. These observations provide the first direct evidence of the causal properties of PM(2.5) and identify the pathophysiological role of the early prediabetic state in susceptibility to environmentally induced cardiovascular disease. These are important implications for public health and public policy.     

蛛网膜下腔出血后血浆和脑脊液ET、CGRP变化与脑血管痉挛的关系

目的：观察伴和不伴脑血管痉挛蛛网膜下腔出血患者血浆与脑脊液中ET和CGRP浓度的变化。方法：根据是否合并脑血管痉挛，将53例蛛网膜下腔出血患者分为有症状脑血管痉挛组、无症状脑血管痉挛组和非痉挛组。72h、1W、2W、3W和4W时分别抽血和采取脑脊液，对照组为无神经系统疾病、免疫系统疾病与免疫相关疾病的外科手术病人，分别测定血浆和脑脊液中ET和CGRP含量。结果：出血后。3组患者血浆和脑脊液ET逐渐增加，1-2W时达最高，随后含量又逐步降低，而血浆和脑脊液CGRP逐渐降低，1-2W时降到最低，随后含量又逐步升高：1W、2W、3W时痉挛组血浆和脑脊液中CGRP含量较非痉挛组明显降低，而ET含量较非痉挛组明显增高。结论：蛛网膜下腔出血后血浆和脑脊液ET升高与CGRP含量降低可能是引起脑血管痉挛的重要因素。     

实验性蛛网膜下腔出血基底动脉的形态学研究

【目的】应用蛛网膜下腔出血（SAH）的大鼠模型，对基底动脉进行形态学测定和组织病理学检查，动态观察SAH的病理演变过程，进一步探讨脑血管痉挛（CVS）的发生机制。【方法】50只SD大鼠随机分为对照组和SAH第1、3、5、7天组，改良枕大池2次注血法，建立SAH的模型。在相应时段处死取基底动脉，应用光学显微镜进行形态学测定，应用透射电子显微镜观察基底动脉超微结构变化。【结果】（1）光学显微镜检查：与对照组相比，SAH组发生了明显的血管痉挛，表现为血管直径减小、管壁增厚、管腔周长减少、内弹力膜皱褶，同时可见痉挛血管细胞增殖现象明显。尤以第5天组最显著（P〈0．05）。出血第1、3、5、7天组基底动脉直径分别减少了46．34％、33．95％、50．59％、17．21％；管壁厚度分别增加了98．55％、75．58％、159．27％、19．21％；管腔内周长分别减少了56．30％、45．97％、62．50％、25．77％。（2）透射电子显微镜观察：与对照组比较，SAH组内皮细胞出现类凋亡样变化，包括内皮细胞膜起泡，胞质凝聚，胞浆空泡变，核染色质凝聚、趋边。以第5天组最显著，伴有大量内皮细胞的剥离导致内弹力膜的裸露，平滑肌细胞的坏死。至第7天组，血管痉挛有所缓解，内皮细胞凋亡、坏死减轻。【结论】SAH后CVS的发生与血管周围细胞的增殖以及基底动脉内皮细胞类凋亡样变化相一致，表明凋亡和血管细胞增殖可能是CVS发生机制中非常重要的因素。同时该大鼠模型可以很好地模拟人类SAH的病理演变过程。