白细胞、血小板动态变化与蛛网膜下腔出血后脑血管痉挛的关系

目的研究蛛网膜下腔出血患者外周血白细胞及血小板动态变化,探讨其对蛛网膜下腔出血后脑血管痉挛的预测价值。方法 发病24h内的蛛网膜下腔出血病人共60例,其中男34例,女26例,平均56.1±12.8岁。根据是否发生脑血管痉挛患者分为两组:脑血管痉挛组74例,无脑血管痉挛组36例。Hunt-Hess临床分级:脑血管痉挛组Ⅱ级8例,Ⅲ级11例,Ⅳ级5例;无脑血管痉挛组Ⅰ级9例,Ⅱ级24例,Ⅲ级3例。采用全自动血细胞分析仪,对患者发病后ld及3d、7d、14d晨肘静脉血白细胞及血小板数量动态观察比较。结果 脑血管痉挛组患者发病后3d、7d、14d白细胞计数明显高于无脑血管痉挛组患者(P<0.01),两组发病后24h、3d、7d、14d血小板计数无统计学差异(P>0.05)。结论 蛛网膜下腔出血后脑血管痉挛患者外周血白细胞增加、外周血白细胞动态变化可作为预测脑血管痉挛发生的指征之一。     

iFlow成像技术对中脑周围非动脉瘤性蛛网膜下腔出血后脑血管痉挛的评估

目的 探讨iFlow成像技术在中脑周围非动脉瘤性蛛网膜下腔出血（PNSAH）后脑血管痉挛评估中的价值。方法 收集经CT及两次血管造影明确诊断为PNSAH 60例为观察组,收集我院同期颅内动脉瘤单纯弹簧圈栓塞治疗后半年以上随访复查造影时未见复发60例为对照组。利用西门子公司iFlow软件测量首次造影和复查造影时双侧颈内动脉分叉部、双侧大脑中动脉分叉部、双侧椎动脉造影基底动脉末端相同部位的造影剂达峰时间（TTP）。结果 与对照组相比,观察组首次造影中双侧椎-基底动脉末端造影剂TTP明显增高（P<0.05）,观察组复查造影中双侧椎-基底动脉末端、右侧颈内分叉部、右侧大脑中分叉部造影剂TTP均明显增高（P<0.05）。与首次造影相比,观察组复查造影双侧椎-基底动脉末端造影剂TTP明显增高（P<0.05）。结论 PNSAH后存在血管痉挛,且以基底动脉最明显,应用iFlow技术评估脑血管痉挛的具有可行性。     

蛛网膜下腔出血后迟发性脑血管痉挛的临床研究

为了探讨蛛网膜下腔出血（ＳＡＨ）后迟发性脑血管痉挛（ＤＣＶＳ）的临床规律，本文对６１例ＳＡＨ住院病人的脑动脉造影（ＣＡＧ）、ＣＴ及临床资料进行了回顾研究，结果如下：１、ＳＡＨ并ＤＣＶＳ的主要病因为颅内动脉瘤破裂，ＤＣＶＳ发生与颅内动脉瘤所在的部位及大小无明显关系．ＤＣＶＳ时轻度痉挛略多于重度痉挛．２、ＣＴ见基底池存在明显的高密度影时，能预示ＤＣＶＳ的发生。３、ＤＣＶＳ常与脑内血肿、脑室出血、脑积水或脑梗塞同时存在。４、ＳＡＨ再发出血，尤其是近期再发出血，可能产生或加重ＤＣＶＳ．５、ＤＣＶＳ的发生及程度与临床病情严重程度有关，ＤＣＶＳ的程度越重，临床病情也越重。６、ＤＣＶＳ的主要体征为意识障碍，近半数的病人有神经示位体征。     

中脑周围池非动脉瘤性蛛网膜下腔出血37例临床分析

目的 探讨中脑周围池非动脉瘤性蛛网膜下腔出血(PNSH)的病因、临床表现、影像学特点及预后.方法 回顾性分析37例PNSH患者的临床表现、影像学资料、治疗及预后,同时对相关文献进行复习.结果 37例患者均无意识障碍,Hunt - Hess分级Ⅰ～Ⅱ级,所有病例均治愈出院,出院时GOS评分均为优.37例PNSH患者的随访期为1-46个月,平均随访24个月.患者均无再出血、脑血管痉挛和脑积水等.结论 PNSH患者临床表现平稳,影像学特点独特,康复期短,并发症少,预后良好.正确认识、诊断PNSH,可以缩短住院时间,减少重复DSA检查及不必要的开颅探查.     

中脑周围池非动脉瘤性蛛网膜下腔出血的脑血管造影静脉期静脉变异的前瞻性研究

目的 研究中脑周围池非动脉瘤性蛛网膜下腔出血(PNSH)患者的DSA静脉期,比较PNSH患者与动脉瘤性蛛网膜下腔出血(ASAH)患者在深部大脑静脉引流形式有无解剖性变异及其变异类型.方法 在收治的自发性蛛网膜下腔出血(SAH)患者中筛选符合PNSH的患者,均行DSA检查并在静脉期详细阅片,以PNSH患者为病例组,选择同期收治的ASAH患者为对照组,对比两组患者的DSA静脉期,观察PNSH患者深部大脑静脉引流形式有无解剖性变异及其变异类型.结果 两组患者DSA静脉期分别发现三种类型的静脉回流类型.经过x2检验(x2 =21.73 P＜0.05)可初步认为PNSH组和ASAH组深部大脑静脉三种回流形式构成比之间的差异有统计学意义.结论 PNSH患者深部大脑静脉回流变异较大并有一定的规律,其回流多为Ⅱ型及Ⅲ型变异回流形式；ASAH患者中脑周围静脉回流多为Ⅰ型较为普遍的回流形式,因此可以推测其出血原因可能与其静脉变异关系密切.     

蛛网膜下腔出血后迟发性脑血管痉挛与五羟色胺的关系

通过荧光分光方法测定了蛛网膜下腔出血(SAH)后迟发性脑血管痉挛(DCVS)时的病人及实验动物血清与脑脊液(CSF)中5—HT的含量。实验结果显示DCVS时病人及实验动物CSF中5—HT的含量处于很低水平,并且实验动物CSF中5—HT的含量在SAH后的第七天比出血后的第三天还要低。DCVS病人血清中5—HT含量也较正常对照组明显降低。本研究结果提示5—HT与DCVS的发生无明显关系。     

Cognitive and emotional consequences of perimesencephalic subarachnoid hemorrhage

Little is known about the long-term cognitive-functional outcome of patients with perimesencephalic subarachnoid haemorrhage (PM SAH). We investigated the neurological, cognitive and emotional consequences of perimesencephalic subarachnoid haemorrhage in eighteen PM SAH patients admitted between November 1990 and July 1997 to the Neurology/Neurosurgery services of a University Hospital. The follow-up interview, a neurological examination, an headache questionnaire, a neurophysiological evaluation (Mini-Mental State and a complementary battery to assess specific cognitive domains), the Hamilton Depression Rating Scale (HDRS) and the Blessed Dementia Scale. Thirteen patients performed below the 10^th percentile in at least one cognitive domain. Six patients scored more than 12 points on the HDRS. Mini-Mental State and HDRS scores were moderately correlated (r = 0.55). Only three patients left their previous occupation. Minor cognitive deficits and high scores on a depression scale were frequent findings in this cohort of PM SAH patients. Reasurance and treatment of depressive symptoms could be important to improve the long-term outcome of PM SAH patients. Received: 13 September 1999 / Received in revised form: 23 May 2000 / Accepted: 6 June 2000     

蛛网膜下腔出血后脑血管痉挛发病机制的研究新进展

蛛网膜下腔出血(subarachnoid hemorrhage,SAH)后,患者常伴有脑血管痉挛(cerebral vasospasm,CVS),出血后4～14d为高峰期.CVS导致脑组织局部缺血,进而引起神经功能障碍.近年来有大量文献资料和实验数据表明SAH后CVS的发生率约30％～80％,约46％的患者出现临床症状,是导致SAH患者死亡或致残的主要并发症[1].其病因机制复杂,研究表明多种因素与CVS的发生有关.本文就SAH后CVS发病机制的研究进展综述如下.     

中脑周围非动脉瘤性蛛网膜下腔出血的临床特点与治疗

目的总结中脑周围非动脉瘤性蛛网膜下腔出血（PNSH）的临床特点、治疗及预后情况。方法回顾性分析11例PNSH患者的临床表现、影像学资料、诊断及治疗情况,并进行随访,了解预后情况。结果11例PNSH患者发病时均无意识障碍,无神经系统定位体征,临床症状均较轻,Hunt-Hess分级为Ⅰ-Ⅱ级,无脑室内出血,无脑积水,所有病例均治愈出院。随访12~60个月,平均26个月,无患者遗留永久性神经功能障碍,全部患者无再出血,恢复原工作及生活。结论PNSH患者临床症状较轻,并发症少,预后良好。     

细胞凋亡对蛛网膜下腔出血后脑血管痉挛发病机制的研究

脑血管痉挛是蛛网膜下腔出血的重要并发症,也是造成患者死亡和致残最重要的原因.脑血管痉挛已经成为临床研究的热点,尤其是近几年在发病机制、诊断和治疗方面取得了很大进展.凋亡不同于坏死,是细胞的程序性死亡.最近的研究表明蛛网膜下腔出血以后脑血管内皮细胞存在有凋亡的发生,而且此现象在血管痉挛形成机制中起着重要的作用.对脑血管痉挛凋亡机制的深入研究,必将有助于临床上防治脑血管痉挛.     

Systemic interleukin-6 concentrations in patients with perimesencephalic non-aneurysmal subarachnoid hemorrhage

Patients with spontaneous non-aneurysmal subarachnoid hemorrhage (non-aSAH) are considered to have a benign illness in contrast to patients with aSAH. The occurrence of the systemic inflammatory response syndrome has been linked to worse outcomes in patients with aSAH. We analyzed systemic interleukin (IL)-6, a proinflammatory cytokine, to determine whether its concentration differs between patients with non-aSAH and those with aSAH, reflecting the more benign illness. Daily systemic IL-6 levels were measured in the acute phase in 11 patients with non-aneurysmal perimesencephalic SAH (pmSAH), with bleeding strictly located around the midbrain, and in nine patients with non-aneurysmal non-perimesencephalic (non-pmSAH), with hemorrhage extending into adjacent cisterns (group 1). IL-6 levels were compared with those from patients suffering from aSAH with cerebral vasospasm (CVS) (group 2) and without CVS (group 3). The mean IL-6 level (±standard error of the mean) was significantly lower in group 1 compared to group 2 (9.9±1.9 vs. 29.1±6.7 pg/mL, p=0.018). The difference in mean IL-6 level between group 1 and 3 fell short of significance (9.9±1.9 vs. 14.9±1.1 pg/mL, p=0.073). Patients in group 1 had a significantly better outcome (Glasgow Outcome Scale score 4-5) compared to group 2 (p<0.001) and a trend towards better outcome compared to group 3 (p=0.102). A subgroup analysis revealed a higher mean IL-6 concentration in patients with non-pmSAH compared to patients with pm-SAH (p=0.001). We concluded that systemic IL-6 concentration reflects the severity of the inflammatory stress response and course of the illness. The more benign illness and good prognosis of patients with pmSAH or non-pmSAH in contrast to patients with aSAH is reflected by the lower concentrations of IL-6.     

尼莫地平不同给药途径治疗蛛网膜下腔出血后脑血管痉挛

脑血管痉挛(CVS)一直被认为是蛛网膜下腔出血(SAH)后严重的并发症.本文回顾了尼莫地平不同给药途径治疗SAH后CVS的研究进展.尼莫地平作为第二代双氢吡啶类钙离子拮抗剂能有效降低SAH后的全脑梗塞和不良预后.尼莫地平局部应用可增加药物浓度,减少全身应用引起的副作用,有效扩张血管管腔,改善术中CVS,减少手术后症状性CVS的发生,改善动脉瘤SAH患者的预后.尼莫地平口服、静脉应用对于治疗SAH后CVS已取得肯定的效果,更加深入研究其局部应用治疗SAH后CVS的作用及其作用机理,可进一步提高尼莫地平的疗效.     

Multiplexed protein profiling after aneurysmal subarachnoid hemorrhage: Characterization of differential expression patterns in cerebral vasospasm

Cerebral vasospasm is a major contributor to delayed morbidity following aneurysmal subarachnoid hemorrhage. We sought to evaluate differential plasma protein levels across time in patients with aneurysmal subarachnoid hemorrhage to identify potential biomarkers and to better understand the pathogenesis of cerebral vasospasm. Nine female patients with aneurysmal subarachnoid hemorrhage underwent serial analysis of 239 different serum protein levels using quantitative, multiplexed immunoassays (DiscoveryMAP 250+ v2.0, Myriad RBM, Austin, TX, USA) on post-hemorrhage days 0 and 5. A repeated measures analysis of variance determined that mean protein concentration decreased significantly in patients who developed vasospasm versus those who did not for alpha-2-macroglobulin (F [1.00,7.00] = 16.33, p = 0.005), angiogenin (F [1.00,7.00] = 7.65, p = 0.028), apolipoprotein A-IV (F [1.00,7.00] = 6.308, p = 0.040), granulocyte colony-stimulating factor (F [1.00,7.00] = 9.08, p = 0.020), macrophage-stimulating protein (F [1.00,7.00] = 24.21, p = 0.002), tetranectin (F [1.00,7.00] = 5.46, p < 0.039), vascular endothelial growth factor receptor 3 (F [1.00,7.00] = 6.94, p = 0.034), and significantly increased for vitronectin (F [1.00,7.00] = 5.79, p = 0.047). These biomarkers may be of value in detecting cerebral vasospasm, possibly aiding in the identification of patients at high-risk prior to neurological deterioration.     

Trapidil对蛛网膜下腔出血后脑血管痉挛作用的实验研究

目的 探讨蛛网膜下腔出血（SAH）后脑血管痉挛的发生机制及其可能的治疗方法。方法 利用家兔枕大池内注血构建SAH模型，观察血小板衍生生长因子（PDGF）拮抗剂trapidil对脑基底动脉的影响。结果 脑基底动脉于SAH后48h明显变细；静脉或动脉内持续灌注trapidil 15min（1．5mg／min）后，数字减影脑血管造影（DSA）显示痉挛血管已明显扩张变粗，30min时达高峰。结论 PDGF可能参与脑血管痉挛发生的病理过程，PDGF拮抗剂trapidil可有效缓解实验性SAH后脑血管痉挛，有望成为脑血管痉挛的治疗药物。     

蛛网膜下腔出血后脑血管痉挛中钾通道的研究进展

脑血管痉挛（cerebral vasospasm，cvs）是蛛网膜下腔出血（subarachnoid hemorrhage，SAH）后高致死率、致残率的主要原因之一，发生率约为45％。过去数十年来国内外学者们做了大量动物实验和临床试验，从细胞、分子水平对CVS的发病机制进行了论述，然而至今仍未完全阐明。目前，普遍认为SAH后CVS是由多因素所致，可能与内皮的损伤、平滑肌细胞内离子泵功能的紊乱和蛋白激酶（PKC）的激活、血管壁炎症反应以及血管细胞的增殖等有关。二十世纪八十年代以来，随着分子生物学技术的发展，以及电压钳和单细胞通道记录等新技术的应用，医学界对钾通道的认识逐渐深入，在钾离子生理药理的研究领域特别是钾通道开放剂的开发项目上屡有重大突破，而后者也有望成为继钙通道阻滞剂后又一通过作用于离子通道而改善血管痉挛的临床用药。本文结合国内外最新相关文献报道，主要就SAH后钾通道的生理状态与CVS之间关系的研究进展做一综述。     

蛛网膜下腔出血后脑血管痉挛实验研究

目的　在兔蛛网膜下腔出血 (SAH)模型上 ,尝试建立经颅多普勒超声 (TCD)及血管造影 ,监测椎基动脉脑血管痉挛 (CVS)的新方法。方法　兔枕大池一次性注血 ,同时行逆行颈总动脉插管椎基动脉造影及开骨窗TCD监测。结果　逆行性脑血管造影能清晰显示椎基底动脉系统 ,注血前后血管直径差异明显 (P <0 .0 5 ) ,平均血流速度注血后明显增快 ,但中、重度痉挛之间基底动脉血流速度变化无明显差异。结论　一侧颈总动脉逆行插管椎基动脉造影 ,操作简便 ,结果可靠。采取开骨窗以提高TCD超声频率的方法 ,可获得兔基底动脉稳定的频谱图并易于重复。     

甲基强的松龙对兔实验性脑血管痉挛的作用

目的探讨大剂量甲基强的松龙对蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的作用。方法将24只雄性新西兰白兔随机分成2组:SAH对照组和SAH 大剂量甲基强的松龙(MP,18mg/kg)治疗组。通过枕大池二次注血法构建SAH模型,观察MP对脑基底动脉的影响。应用酶联免疫生化技术检测各组兔基底动脉血管平滑肌细胞膜蛋白激酶C(PKC)活性。结果经脑血管造影证实该剂量甲基强的松龙明显减轻实验性脑血管痉挛的严重程度,与对照组相比,PKC活性在大剂量甲基强的松龙治疗组没有明显提高。结论大剂量甲基强的松龙能够明显减轻脑血管痉挛程度,通过抑制血管平滑肌细胞来防治脑血管痉挛的发生发展。     

甲基强的松龙对兔实验性脑血管痉挛的作用

目的探讨大剂量甲基强的松龙对蛛网膜下腔出血（SAH）后脑血管痉挛（CVS）的作用。方法将24只雄性新西兰白兔随机分成2组：SAH对照组和SAH＋大剂量甲基强的松龙（MP，18mg／kg）治疗组。通过枕大池二次注血法构建SAH模型，观察MP对脑基底动脉的影响。应用酶联免疫生化技术检测各组兔基底动脉血管平滑肌细胞膜蛋白激酶C（PKC）活性。结果经脑血管造影证实该剂量甲基强的松龙明显减轻实验性脑血管痉挛的严重程度，与对照组相比，PKC活性在大剂量甲基强的松龙治疗组没有明显提高。结论大剂量甲基强的松龙能够明显减轻脑血管痉挛程度，通过抑制血管平滑肌细胞来防治脑血管痉挛的发生发展。     

Dysfunction of nitric oxide induces protein kinase C activation resulting in vasospasm after subarachnoid hemorrhage

We hypothesize that the interaction between protein kinase C (PKC) and nitric oxide (NO) plays a role in the modulation of cerebral vascular tone, and the disturbance of this interaction following subarachnoid hemorrhage (SAH) results in vasospasm. To prove this hypothesJs with direct evidence, PKC activities of smooth muscle cells of canine basilar arteries in the control and in the SAH groups were measured by an enzyme immunoassay method. Nw-nitro-L arginine (L-NA), an inhibitor of NO production, enhanced PKC activity. This enhancement was inhibited neither by 8-bromo-guanosine 3’5’-cyclic monophosphate (8-bronio-cGMP) nor SIN-7, a NO releasing agent. PKC activity in the SAH was significantly higher than in the control; however, no furtherenhancement was produced with L-NA. In the SAH, PKC activity was not inhibited either by 8-bromo~cGMPor SIN-7. We conclude that NO maintains an appropriate vascular tone through inactivation of PKC, and that this effect is disturbed following SAH, resulting in PKC-dependent vascular contraction, such as vasospasm. On the other hand, once PKC has been activated, NO precursors do not inhibit PKC. These facts indicate NO inactivates PKC through the inhibition of phosphatidylinositol breakdown. [Neural Res 1997; 19: 558-562]     

Vascular risk factors for perimesencephalic nonaneurysmal subarachnoid hemorrhage

No data have been published on the role of vascular risk factors for perimesencephalic nonaneurysmal subarachnoid hemorrhage (PMSAH). In a case-control study we compared the prevalence of vascular risk factors in 40 consecutive patients who suffered a perimesencephalic subarachnoid hemorrhage with that in two controls groups: (a) 120 subjects registered with a general practitioner (GP; matched at a 3 : 1 ratio for age and sex) and (b) 81 proxies of patients of a hospital outpatient clinic. A conditional multivariate logistic regression model was performed taking into account the matched design. Hypertension was more frequent among PMSAH patients than among the two control group subjects for men and women. Among women, smoking was more common in PMSAH than in the GP control group. The conditional multivariate logistic regression model confirmed that hypertension was an independent risk factor for PMSAH (P = 0.036) Hypertension is a preventable risk factor of PMSAH. Received: 11 August 1998 Received in revised form: 26 November 1998 Accepted: 3 December 1998