内质网应激在蛛网膜下腔出血后早期脑损伤中的作用

自发性蛛网膜下腔出血(subarachnoid hemorrhage,SAH)是临床上的一种急性脑血管病,致残率和病死率均很高.最近的研究显示,SAH发病后72 h内即会出现早期脑损伤(early braininjury,EBI),并与SAH患者转归不良密切相关.导致EBI的可能机制有许多,例如炎症、自噬、细胞凋亡等,这些损伤机制均与内质网应激有关.文章就内质网应激在SAH后EBI中的作用进行了综述.     

自噬在蛛网膜下腔出血后早期脑损伤中作用的研究进展

近几年研究发现,蛛网膜下腔出血（SAH）后72 h内即出现的早期脑损伤（early brain injury,EBI）与SAH的不良预后密切相关,成为研究关注的热点.自噬（autophagy）很早就被发现存在于多种组织细胞中,参与降解和回收受损细胞器和大分子物质,出现于多种生理过程和疾病的病理过程中.Lee 等[1]研究发现,SAH后立即可检测到皮质内自噬活性的增强.但自噬在SAH后EBI中的作用及具体机制尚不明确.我们就自噬与EBI的关系综述如下.     

动脉瘤性蛛网膜下腔出血患者急性期外周血中高迁移率族蛋白1水平的变化

颅内动脉瘤破裂导致的自发性蛛网膜下腔出血(SAH)发生后的最初72h内,机体会发生多种病理改变。近年来,这些早期出现的急性病理改变逐渐被学者们所重视,并被认为可能是影响预后的重要因素[1]。在SAH引起的早期脑损伤中,神经炎性反应被视为引起早期病理变化的因素之一。高迁移率族蛋白1(high-mobility group box protein-1,HMGB-1)是一种普遍存在于哺乳动物细胞中的核蛋白,能调     

蛛网膜下腔出血后早期脑损伤

蛛网膜下腔出血(subarachnoid hemorrhage,SAH)是一种致残率和病死率很高的疾病,临床仍缺乏有效的治疗手段.近年来的研究发现,早期脑损伤可能是导致SAH患者病死率较高和决定预后的首要原因.文章主要对SAH早期脑损伤的动物模型和发病机制做了综述.     

CTA在自发性蛛网膜下腔出血早期病因诊断学中的应用

自发性蛛网膜下腔出血（SAH）年发病率为6／10万。再出血是自发性蛛网膜下腔出血患者致死、致残的主要原因,要杜绝再出血,关键是早期明确SAH的病因并针对病因进行治疗。随着CT技术的不断成熟,CT血管造影（CTA）在SAH早期病因诊断上逐渐体现出其准确率高、安全性好的优势。2007年-2009年我院对32例早期SAH患者进行了CTA检查,同时进行了数字减影血管造影（DSA）检查作为对比。     

自发性蛛网膜下腔出血患者心电图异常的影响因素及其与预后的关系

目的：探讨自发性蛛网膜下腔出血（SAH）患者早期心电图异常的影响因素及其与预后的关系。方法：收集上海华山医院2000年1月至2006年6月收治的800例SAH患者年龄、发病时的意识水平、血压、Fisher分级及合并脑疝、脑积水、脑血管痉挛、脑室出血、肺部感染、上消化道出血等资料，分析其与心电图异常的相关性以及心电图异常与预后的相关性。结果：患者年龄、发病时意识障碍、Fisher分级以及合并脑疝、脑积水、脑血管痉挛等因素均与心电图异常相关，心电图异常与预后显著相关。结论：对于急性SAH患者，应重视心电图监护，采取积极的预防措施，严格防治并发症，保护心功能，改善患者的预后。     

动脉瘤性蛛网膜下腔出血后发热控制的研究进展

发热是动脉瘤性蛛网膜下腔出血（SAH）后最常见的系统性并发症,约41%～72%的SAH患者出现发热[1-3]。通常发热被定义为核心温度〉38.3℃。SAH后的发热,可以加重脑水肿,加重颅内压,增加缺血性脑损伤,影响意识状态,对患者的神经功能及预后有不利影响。     

动脉瘤性蛛网膜下腔出血后亚细胞器结构及功能的研究进展

<正>动脉瘤性蛛网下腔出血(aneurysm subarachnoid hemorrhage,a SAH)预后差主要与早期脑损害(early brain injury,EBI)和随后出现的脑血管痉挛(cerebral vasospasm,CVS)密切相关[1]。最新研究显示,尽管内皮血管收缩肽受体拮抗剂能够显著改善实验动物及患者的CVS程度,但不能改善预后[2];此外,70%的a SAH患者影像学可见CVS改变,但仅1/3的患     

蛛网膜下腔出血继发迟发性脑缺血的发病机制研究进展

蛛网膜下腔出血(SAH)是神经科常见的脑血管危重症疾病之一。迟发性脑缺血(DCI)是SAH常见的并发症,也是公认的患者预后不良的重要原因之一。目前SAH患者继发DCI尚无法预测,其发病机制极为复杂。脑血管痉挛、血脑屏障破坏、早期脑损伤、细胞凋亡、微循环障碍、炎症性反应、氧化应激等众多因素均可参与DCI的发生。本文就SAH患者继发DCI的机制的研究进展进行综述。     

中脑周围非动脉瘤性蛛网膜下腔出血9例临床分析

中脑周围非动脉瘤性蛛网膜下腔出血（PNSH）是一种特殊类型的蛛网膜下腔出血（SAH），其临床症状较轻，很少发生再出血、继发性脑血管痉挛及脑积水，患者预后较好。1998年1月-2004年12月。我院收治自发性SAH患者102例，其中PNSH9例。现将其临床特点分析如下。     

Melatonin attenuates inflammatory response‐induced brain edema in early brain injury following a subarachnoid hemorrhage: a possible role for the regulation of pro‐inflammatory cytokines

Melatonin is a strong anti‐oxidant that has beneficial effects against early brain injury (EBI) following a subarachnoid hemorrhage (SAH) in rats; protection includes the reduction of both mortality and neurological deficits. The molecular mechanisms underlying these clinical effects in the SAH model have not been clearly identified. This study examined the influence of melatonin on brain edema secondary to disruption of the blood–brain barrier (BBB) and the relationship between these effects and pro‐inflammatory cytokines in EBI following SAH using the filament perforation model of SAH in male Sprague–Dawley rats. Melatonin (150 mg/kg) or vehicle was given via an intraperitoneal injection 2 hr after SAH induction. Brain samples were extracted 24 hr after SAH. Melatonin treatment markedly attenuated brain edema secondary to BBB dysfunctions by preventing the disruption of tight junction protein expression (ZO‐1, occludin, and claudin‐5). Melatonin treatment also repressed cortical levels of pro‐inflammatory cytokines (IL‐1β, IL‐6, and TNF‐α), which were increased in EBI 24 hr after SAH. To further identify the mechanism of this protection, we demonstrated that administration of melatonin attenuated matrix metallopeptidase 9 expression/activity and vascular endothelial growth factor expression, which are related to the inflammatory response and BBB disruption in EBI after SAH. Taken together, this report shows that melatonin prevents disruption of tight junction proteins which might play a role in attenuating brain edema secondary to BBB dysfunctions by repressing the inflammatory response in EBI after SAH, possibly associated with regulation of pro‐inflammatory cytokines.     

Melatonin‐enhanced autophagy protects against neural apoptosis via a mitochondrial pathway in early brain injury following a subarachnoid hemorrhage

Melatonin is a strong antioxidant that has beneficial effects against early brain injury (EBI) following a subarachnoid hemorrhage (SAH) in rats; protection includes reduced mortality and brain water content. The molecular mechanisms underlying these clinical effects in the SAH model, however, have not been clearly identified. This study was undertaken to determine the influence of melatonin on neural apoptosis and the potential mechanism of these effects in EBI following SAH using the filament perforation model of SAH in male Sprague Dawley rats. Melatonin (150 mg/kg) or vehicle was given via an intraperitoneal injection 2 hr after SAH induction. Brain samples were extracted 24 hr after SAH. The results show that melatonin treatment markedly reduced caspase‐3 activity and the number of TUNEL‐positive cells, while the treatment increased the LC3‐II/LC3‐I, an autophagy marker, which indicated that melatonin‐enhanced autophagy ameliorated apoptotic cell death in rats subjected to SAH. To further identify the mechanism of autophagy protection, we demonstrated that melatonin administration reduced Bax translocation to the mitochondria and the release of cytochrome c into the cytosol. Taken together, this report demonstrates that melatonin improved the neurological outcome in rats by protecting against neural apoptosis after the induction of filament perforation SAH; moreover, the mechanism of these antiapoptosis effects was related to the enhancement of autophagy, which ameliorated cell apoptosis via a mitochondrial pathway.     

蛛网膜下腔出血后铁代谢机制的研究进展

脑血管痉挛(CVS)是蛛网膜下腔出血(SAH)的常见并发症,是SAH患者致死、致残的主要原因之一.近年来对其发病机制及治疗方法进行了深入的研究,发现铁代谢在SAH后脑血管痉挛中有着重要作用.本文就近年来国内外学者在SAH后铁代谢病理生理机制的研究进展作一综述.     

Melatonin activates the Nrf2-ARE pathway when it protects against early brain injury in a subarachnoid hemorrhage model

Melatonin has beneficial effects against early brain injury (EBI) by modulating cerebral oxidative stress after experimental subarachnoid hemorrhage (SAH); however, few investigations relate to the precise underlying molecular mechanisms. To date, the relation between melatonin and nuclear factor erythroid 2-related factor 2 and antioxidant responsive element (Nrf2-ARE) pathway has not been studied in SAH models. This study was undertaken to evaluate the influence of melatonin on Nrf2-ARE pathway in rats after SAH. Adult male SD rats were divided into four groups: (i) control group (n=18); (ii) SAH group (n=18); (iii) SAH+vehicle group (n=18); and (iv) SAH+melatonin group (n=18). The rat SAH model was induced by injection of 0.3mL fresh arterial, nonheparinized blood into the prechiasmatic cistern in 20s. In SAH+melatonin group, melatonin was administered i.p. at 150mg/kg at 2 and 24hr after the induction of SAH. Brain samples were extracted at 48hr after SAH. Treatment with melatonin markedly increased the expressions of Nrf2-ARE pathway-related agents, such as Nrf2, heme oxygenase-1, NAD(P)H:quinone oxidoreductase 1, and glutathione S-transferase α-1. Administration of melatonin following SAH significantly ameliorated EBI, including brain edema, blood-brain barrier (BBB) impairment, cortical apoptosis, and neurological deficits. In conclusion, post-SAH melatonin administration may attenuate EBI in this SAH model, possibly through activating Nrf2-ARE pathway and modulating cerebral oxidative stress by inducing antioxidant and detoxifying enzymes.     

Epidemiology of Traumatic Brain Injury and Subarachnoid Hemorrhage

Incidence rates of traumatic brain injury are high in both industrialized and non-industrialized countries and have been estimated variously to be between 150–250 cases per 100,000 population per year. The estimated incidence rates for subarachnoid hemorrhage (SAH) are between 10 to 25 cases per 100,000 population per year. Seasonal variation in the occurrence of subarachnoid hemorrhage has been reported in studies from different countries, with significant seasonal variations and peak periods for aneurysmal SAH differing widely. A differential racial distribution for SAH has been found as well as a higher mortality rate for women than for men. The cognitive and behavioral consequences of TBI and SAH are significant and affect the quality of life of patients and their families. Recent publications have informed of hypopituitary deficits in patients sustaining TBI or SAH. It is not clear whether the cognitive deficits found in these patients are due to the consequences of the brain injury itself or are related to the hypopituitary deficits. There is a need for research distinguishing the differential cognitive and behavioral effects of the brain injury and the endocrinological deficits in these patients, and for developing adequate treatment.     

磁共振梯度回波T2*加权像对蛛网膜下腔出血合并侧脑室后角内积血的诊断及其临床意义

目的探讨磁共振梯度回波T2*加权成像(GRE-T2*WI)序列对蛛网膜下腔出血(SAH)合并侧脑室后角内积血的诊断及其临床意义。方法对50例临床上经症状、体征、CT或腰椎穿刺确诊为SAH的患者进行研究,将50例SAH患者根据头颅MRI检查距发病的时间分为急性期SAH组(≤4 d),亚急性、慢性期SAH组(4 d),分析急性期和亚急性、慢性期SAH组患者合并侧脑室后角内积血的比例,探讨磁共振GRE-T2*WI序列对SAH合并侧脑室后角内积血的诊断价值及其临床意义。结果 (1)急性期SAH组:26例急性期SAH患者磁共振GRE-T2*WI序列均发现侧脑室后角内积血,比例为100%;(2)亚急性、慢性期SAH组:24例亚急性、慢性期SAH患者磁共振GRET2*WI序列发现侧脑室后角内积血21例,比例达87.5%;(3)磁共振GRE-T2*WI序列上侧脑室后角内积血表现为侧脑室后角内环行低信号影伴液平,与侧脑室内脑脊液高信号影形成鲜明对比,显示清晰,易于辨认,且极少量侧脑室后角内积血也能清晰显影。因蛛网膜下腔狭小,分布范围广,脑脊液循环流动,有血管影干扰等特点,在MRI诊断SAH阅片过程中存在一定难度,发现GRE-T2*WI序列侧脑室后角内积血,除外脑室出血破入蛛网膜下腔和原发脑室出血,提示SAH。结论 (1)SAH合并侧脑室后角内积血在SAH的急性期、亚急性慢性期均有很高的比例;(2)磁共振GRE-T2*WI序列上对侧脑室后角内积血显示清晰、易于辨认,磁共振GRE-T2*WI序列诊断侧脑室后角内积血除外脑出血破入蛛网膜下腔、原发脑室出血提示有SAH。     

Churg-Strauss syndrome presenting as spontaneous subarachnoid haemorrhage

Churg–Strauss syndrome (CSS) is a systemic small-vessel vasculitis characterised by the presence of asthma and eosinophilia. Central nervous system involvement (cerebral infarctions or intracerebral haemorrhage) is rare in CSS. Spontaneous subarachnoid hemorrhage (SAH) has been described in other systemic vasculitides. SAH is exceptional in CSS. We present a 47-year-old woman with CSS presenting as a spontaneous SAH with cerebral angiography findings consistent with vasculitis of the basilar artery and without aneurysms or arteriovenous malformations. She received treatment with prednisone and cyclophosphamide, and 2 months later the basilar artery was normal on magnetic resonance angiography. Received: 27 May 2001 / Accepted: 17 November 2001     

非动脉瘤性蛛网膜下腔出血的临床分析

目的 提高对非动脉瘤性蛛网膜下腔出血临床和影像特征、预后的认识水平,指导临床诊治.方法 首次3维脑血管造影阴性的自发性蛛网膜下腔出血患者2～3周后复查造影,两次均阴性定义为非动脉瘤性蛛网膜下腔出血.分2个亚组:中脑周围和非中脑周围非动脉瘤性蛛网膜下腔出血.结果 49例造影阴性.中脑周围者24例预后良好(格拉斯哥昏迷评分...     

蛛网膜下腔出血后脑血管痉挛的危险因素

脑血管痉挛(CVS)是蛛网膜下腔出血(SAH)患者死亡和残疾的主要原因。CVS的发生率约为30%-60%,一般于SAH后3-4d开始出现症状,第2周达高峰,需3周左右恢复。早期评价病情和预测CVS的发生,有利于预防和恰当的治疗,降低病死率和致残率。文章对SAH后CVS的危险因素做了综述。