蛛网膜下腔出血后脑血管痉挛的发病机制

脑血管痉挛是蛛网膜下腔出血最严重和最常见的并发症之一，临床治疗效果不理想。为加深对脑血管痉挛的认识，提高防治意识，文章综述了蛛网膜下腔出血后脑血管痉挛的病理变化和发生机制。     

急性蛛网膜下腔出血与脑血管痉挛的关系

目的：研究蛛网膜下腔出血（ SAH）量、部位与脑血管痉挛程度的相关性。方法：病例为沈阳军区总医院神经内科从2013年6月~2014年1月间以蛛网膜下腔出血入院患者71例,全部患者均在发病48h内经头颅CT证实确诊为蛛网膜下腔出血后进一步经CTA、 DSA证实为颅内动脉瘤破裂所致。我们通过蛛网膜下腔出血的量、部位通过Fisher分级比较。结果：全部蛛网膜下腔出血的患者中,42位患者经CTA或DSA没有发生脑血管痉挛（为无血管痉挛组）,有9人存在脑血管痉挛但未发生神经系统缺损症状（无症状脑血管痉挛组）,有20人确定存在脑血管痉挛且出现神经系统缺损症状（症状性脑血管痉挛组）。症状性脑血管痉挛组与无症状的脑血管痉挛组相比,蛛网膜下腔出血的量与部位相比有统计学意义（P〈0．005）。结论：提示脑血管痉挛的程度与蛛网膜下腔出血的量及位置相关。     

尼莫地平预防蛛网膜下腔出血后脑血管痉挛36例疗效观察

脑血管痉挛是蛛网膜下腔出血患者致残和死亡的主要原因,通常发生在出血后第1-2周,表现为病情稳定后再出现神经系统定位体征和意识障碍,因脑血管痉挛所致缺血性脑梗死所引起。本组对使用尼莫地平防治蛛网膜下腔出血后脑血管痉挛的疗效进行了临床观察。现报告如下。     

颅内动脉瘤并发脑血管痉挛的观察及护理体会

脑血管痉挛是颅内动脉瘤致蛛网膜下腔出血患者的最主要致死原因之一．文献报道．蛛网膜下腔出血后4～14天脑血管痉挛的发生率高达40％，严重者可引起脑梗死。2000～2001年．我院收治颅内动脉瘤致蛛网膜下腔出血患者17例，现将护理体会报告如下。     

原发性蛛网膜下腔出血后的脑血管痉挛

蛛网膜下腔出血后的脑血管痉挛是原发性蛛网膜下腔出血(SAH)的最常见并发症,可导致病情加重,增加死亡及病残率。本文对脑血管痉挛(CVS)发生的相关因素、发病机理、诊断、治疗及预后作如下综述。1 SAH 后脑血管痉挛的相关因素与发病机理1.1 血液对血管壁机械性刺激动脉瘤破裂时对血管壁的撕裂,血液在蛛网膜下腔中的占位效应造成纤维小梁对血管的牵拉以及破裂前动脉瘤囊内血液的突然牵     

自由基清除剂防治蛛网膜下腔出血后脑血管痉挛

脑血管痉挛是蛛网膜下腔出血后的常见并发症,其病理生理学机制未完全明确.越来越多的研究表明,自由基在诱发脑血管痉挛中起着十分重要的作用.近年来,有关自由基清除剂防治蛛网膜下腔出血后脑血管痉挛的研究不断增多.文章对多类自由基清除剂在蛛网膜下腔出血后脑血管痉挛防治中的作用进行了综述.     

自发性蛛网膜下腔出血52例临床及头颅CT分析

目的探讨自发性蛛网膜下腔出血（SAH）的临床特点与头颅CT特点，明确蛛网膜下腔出血的病因，以指导治疗及预后评估。方法回顾性分析内科治疗的52例自发性蛛网膜下腔出血病人的临床资料及头颅CT。结果动脉瘤是自发性蛛网膜下腔出血的主要病因,CT Fisher分级高提示预后不良，再出血及继发脑血管痉挛（CVS）为主要死因。结论头颅CT能对自发性蛛网膜下腔出血的病因及位置进行评估，自发性蛛网膜下腔出血病死率高，但致残率较其他脑血管病低。治疗应针对病因治疗，预防再出血及继发脑血管痉挛与良好的预后有关。     

一氧化氮、一氧化氮合酶与蛛网膜下腔出血后脑血管痉挛

多年以来,脑血管痉挛一直被视为影响蛛网膜下腔出血患者预后的重要因素之一.研究表明,蛛网膜下腔出血后脑血管痉挛与一氧化氮和一氧化氮合酶有关,而调节一氧化氮合成可在脑血管痉挛的治疗中起积极作用.     

蛛网膜下腔出血后继发脑血管痉挛的早期诊断与外科治疗

目的 探讨早期外科治疗蛛网膜下腔出血后继发脑血管痉挛（CVS）的合理有效方法。方法 采用早期显微手术动脉瘤颈夹闭术18例，在清除血肿和成功夹闭动脉瘤后局部使用罂粟碱治疗脑血管痉挛。微弹簧圈血管内栓塞2例，超选择性动脉内灌注罂粟碱。结果 早期外科治疗蛛网膜下腔出血后继发脑血管痉挛总有效率95％。结论 早期外科治疗蛛网膜下腔出血后继发脑血管痉挛可使病人临床症状和神经功能恶化得到明显改善，对提高病人病情预后有一定的实际意义。     

蛛网膜下腔出血后脑血管痉挛的在体动物模型

迟发性脑血管痉挛是蛛网膜下腔出血患者死亡的主要原因.一个成功的蛛网膜下腔出血后脑血管痉挛在体动物模型,有助于探讨脑血管痉挛的发生、发展等复杂多样的病理生理学机制,为临床干预提供重要信息.     

Effects of Ginkgo biloba extract on somatosensory evoked potential, nitric oxide levels in serum and brain tissue in rats with cerebral vasospasm after subarachnoid hemorrhage

This study aimed to investigate the protective effects of Ginkgo biloba extract on cerebral vasospasm and neural damage following subarachnoid hemorrhage (SAH) in rats. It was found that the regional cerebral blood flow decreased immediately and persistently after SAH in SAH rats. The latency of somatosensory evoked potential delayed progressively. The nitric oxide levels in serum and brain tissue decreased and increased, respectively, after SAH. Ginkgo biloba extract effectively antagonized the changes of above parameters. It was concluded that somatosensory evoked potential is useful for the judgement of cerebral ischemic damage during cerebral vasospasm after SAH. Decrease in serum nitric oxide and increase in brain tissue nitric oxide are important factors leading to cerebral vasospasm and neural damage, respectively, after SAH. Ginkgo biloba extract relieves cerebral vasospasm and cerebral ischemic damage by reversing the pathological alteration of nitric oxide.     

蛛网膜下腔出血后脑脊液细胞因子水平与脑血管痉挛的关系

脑血管痉挛是蛛网膜下腔出血(SAH)的一种常见并发症。目前,脑血管痉挛的确切发生机制还不完全清楚,也缺乏有效控制脑血管痉挛发生和发展的方法。近年来,一些学者发现,SAH后脑脊液和血清某些细胞因子水平可能发生改变,细胞因子所引起的炎症反应可能与脑血管痉挛有一定关联。因此,检测脑脊液和血清细胞因子水平对预测SAH的严重程度、转归和及早治疗均有重要意义。     

尼莫地平对兔蛛网膜下腔出血后症状性脑血管痉挛的影响

目的探讨尼莫地平对兔蛛网膜下腔出血（SAH）后症状性脑血管痉挛的影响。方法建立症状性脑血管痉挛动物模型，SAH＋尼莫地平组静脉内应用尼莫地平。观察对比神经功能缺损症状改善、血液流变学及电镜结果。结果SAH＋尼莫地平组随着尼莫地平的应用,神经功能缺损症状逐渐好转、血液流变学得到改善、透射电镜见基底动脉病理改变较SAH组减轻。结论SAH后早期应用尼莫地平对症状性脑血管痉挛具有明显的改善作用。     

蛛网膜下腔出血患者血清与脑脊液中NO和CGRP水平变化及意义

目的观察伴和不伴脑血管痉挛蛛网膜下腔出血（SAH）患者血清与脑脊液中一氧化氮（NO）和降钙素基因相关肽（CGRP）水平的变化。方法根据是否合并脑血管痉挛，将53例SAH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及1、2、3和4周时分别抽血和采取脑脊液，分别测定血清和脑脊液中NO和CGRP水平。结果出血后，三组患者脑脊液和血清NO与CGRP水平逐渐降低，1～2周时降低最明显，随后逐步回升；1、2、3周时痉挛组血清和脑脊液中NO和CGRP水平较非痉挛组明显降低。结论SAH后脑脊液和血清NO与CGRP水平降低可能是引起脑血管痉挛的重要因素。     

Attenuation of canine cerebral vasospasm after subarachnoid hemorrhage by protein kinase C inhibitors despite augmented phosphorylation of myosin light chain

The purpose of the present study is to assess the roles of protein kinase C (PKC) isoforms, especially PKC delta and alpha, and 20-kD myosin light chain (MLC(20)) phosphorylation in the mechanism of cerebral vasospasm following subarachnoid hemorrhage (SAH). We had shown that those PKC isoforms are involved in the development of cerebral vasospasm. Using PKC isoform-specific inhibitors in a 'two- hemorrhage' canine model, we examined changes in the development of cerebral vasospasm, translocation of PKC isoforms and MLC(20) phosphorylation level in canine basilar arteries. A PKC inhibitor (5 microM rottlerin for PKC delta or chelerythrine for PKC alpha) was injected into the cisterna magna on day 4 before the second hemorrhage. The treatment was continued daily until day 7. Rottlerin inhibited the initial phase of vasospasm and PKC delta translocation, but did not significantly inhibit PKC alpha translocation. Chelerythrine inhibited cerebral vasospasm, and the translocation of both PKC delta and alpha throughout the entire course of the study. Although cerebral vasospasm after SAH was inhibited by each PKC inhibitor, the MLC(20) phosphorylation level remained elevated as in the untreated hemorrhage-control study. We conclude that cerebral vasospasm following SAH depends on PKC delta and alpha, while the enhancement of MLC(20) phosphorylation contributes little to this form of vasospasm.     

Interactive role of protein kinase C-delta with rho-kinase in the development of cerebral vasospasm in a canine two-hemorrhage model

BACKGROUND: We previously reported that protein kinase C (PKC)-delta was initially translocated from the cytosol to the membrane fraction (on day 4), followed by PKC-alpha, with the progression of cerebral vasospasm after subarachnoid hemorrhage (SAH) on day 7. Rho/Rho-kinase pathways have also been proposed to be involved in the vasospasm. Thus we investigated the interactive role of Rho-kinase and PKC in the development of cerebral vasospasm after SAH. METHODS: The cerebral vasospasm was produced using a 'two-hemorrhage' canine model. The animals were treated with Y-27632, a Rho-kinase inhibitor, and rottlerin, a PKC-delta inhibitor, both injected into the cisterna magna. RESULTS: Y-27632 inhibited the vasospasm, 20-kDa myosin light chain (MLC20) phosphorylation, and PKC-delta translocation after the second injection of autologous blood on day 4. In contrast, Y-27632 did not affect the vasospasm on day 7. Rottlerin also inhibited the vasospasm on day 4, but had no effect on MLC20 phosphorylation and RhoA translocation. The vasospasm was accompanied with the phosphorylation of caldesmon (CaD), an actin-linked regulatory protein, which was strongly attenuated by Y-27632 and rottlerin. The application of PKC-delta to skinned strips of isolated canine basilar arteries caused a contraction and an increase in CaD phosphorylation. CONCLUSION: The development of cerebral vasospasm after SAH (on day 4) is caused by at least two mechanisms: one involves MLC20 phosphorylation mediated by the inhibition of MLC20 phosphatase by Rho-kinase, and the other CaD phosphorylation mediated by the activation of PKC-delta by Rho-kinase, which results in the alleviation of the inhibition by CaD of myosin Mg2+-ATPase activity.     

细胞外调节蛋白激酶在蛛网膜下腔出血中的研究进展

细胞外调节蛋白激酶(ERK)是丝裂原活化蛋白激酶(MAPK)家族中的一类,磷酸化激活的ERK由胞质转位于胞核,激活下游的信号分子,从而发挥相应的生物学效应。近期的研究表明,该蛋白在蛛网膜下腔出血(SAH)后的炎症、自噬、凋亡及脑血管痉挛中发挥着重要的作用。进一步阐述SAH后ERK参与炎症、自噬、凋亡及脑血管痉挛的相关分子机制,以ERK作为分子靶点,有效地利用该激酶在SAH病理条件下表达的变化,将为研究SAH提供新的方向。     

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.     

Angiographically documented cerebral vasospasm following transsphenoidal surgery for pituitary tumors

Symptomatic cerebral vasospasm (CVS) after transsphenoidal surgery (TSS) is very rare compared with vasospasm resulting from aneurysmal subarachnoid hemorrhage (SAH). Fewer than six cases documented by cerebral angiography have been reported. We evaluated the records of 15 patients in whom SAH developed after TSS. Their clinical symptoms, radiological and laboratory findings were analyzed. Among 15 patients with postoperative SAH, 11 did not show CVS during their postoperative course. However, four patients presented with various clinical symptoms suggestive of CVS on postoperative days 7–9. They showed an abrupt drop of serum sodium level 1 or 2 days before the onset of CVS symptoms. Patients with TSS-related SAH should be managed with proactive and aggressive treatment. Hyponatremia, which usually occurs around the first week after TSS, should not be ignored as a matter of metabolic or hormonal disequilibrium commonly encountered after pituitary surgery.     

Involvement of Rho-kinase-mediated phosphorylation of myosin light chain in enhancement of cerebral vasospasm

Subarachnoid hemorrhage (SAH) often induces a long-term narrowing of the cerebral artery called cerebral vasospasm. Myosin light chain (MLC) in the spastic basilar artery was reported previously to be phosphorylated by Ca(2+)/calmodulin-dependent MLC kinase. Because Rho-kinase, which is activated by the small GTPase Rho, phosphorylates not only MLC but also myosin phosphatase at its myosin-binding subunit (MBS), thus inactivating myosin phosphatase, we examined whether Rho-kinase is involved in the development of vasospasm. Cerebral vasospasm was produced in the canine basilar artery by a 2-hemorrhage method, and vasocontractions were induced by topical application of 80 mmol/L KCl or 0.5 micromol/L serotonin to the canine basilar artery exposed transclivally. The phosphorylation of MLC in the basilar artery was increased concurrently with an enhancement in the intensity of vasospasm with the passage of time after SAH. In addition, Rho-kinase in the basilar artery was activated concurrently with an increase in the phosphorylation of MBS at Ser854 in vasospasm. The Rho-kinase activation levels in vasospasm on days 0 and 2 were comparable to those in KCl- and serotonin-induced sustained vasocontraction, respectively, and those in vasospasm on day 7 were markedly high. The topical application of Y-27632, a specific inhibitor of Rho-kinase, to the exposed spastic basilar artery on day 7 induced a dose-dependent dilation, and the intensities of vasospasm and the phosphorylation of MBS and MLC were simultaneously decreased by 10 micromol/L Y-27632, although the decrease in MBS phosphorylation was more marked than the decrease in MLC phosphorylation. These results indicate that the activation of Rho-kinase and the phosphorylation of MLC and MBS occur concomitantly during vasospasm induced by SAH and suggest that Rho-kinase is involved in the enhancement of cerebral vasospasm in addition to Ca(2+)/calmodulin-dependent MLC kinase by increasing the phosphorylation of MLC directly or indirectly as a result of the inhibition of myosin phosphatase by its phosphorylation.