腰穿脑脊液生理盐水置换术防治蛛网膜下腔出血并发脑血管痉挛及脑积水(附461例报告)

目的 评价腰穿脑脊液生理盐水置换术防治蛛网膜下腔出血(SAH)并发脑血管痉挛(CVS)及正常压力脑积水(NPH)的疗效及安全性。方法 将符合入选标准的患者分为实验组(461例)和对照组(388例)，实验组给予反复腰穿、椎管内分次注入生理盐水30～60ml进行脑脊液置换，对照组常规治疗。观察两组患者临床症状及头颅CT变化。评价其疗效。结果CVS和NPH发生率分别为实验组6．9％(32例)、4．3％(20例)。对照组17．2％(67例)、9．5％(36例)．总有效率实验组94．8％，对照组82．5％。结论该方法在防治SAH并发CVS及NPH方面疗效肯定。     

不同剂量尼莫地平对SAH患者ET-1、NO及大脑中动脉平均血流速度的影响

目的 探讨应用尼莫地平预防蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)的最佳剂量.方法 将60例原发性SAH患者随机分为SAH1、SAH2、SAH3、SAH4组各20例,分别予2、1、0.5、0.2 mg/h尼莫地平静滴,在第1、3、7、10、14 d观察血浆和脑脊液(CFS)中内皮素-1(ET-1)和NO动态变化,并用经颅多普勒(TCD)监测各组大脑中动脉(MCA)的平均血流速度(Vm).结果 与SAH3组及SAH4组比较,SAH1组及SAH2组血浆和CSF中ET-1水平明显升高、NO明显降低(P<0.05),MCA的Vm明显降低;SAH1组及SAH2组分别有7例(35%)和1例(5%)因血压下降退出试验(P<0.05).结论 1 mg/h尼莫地平(静滴)为防治SAH后CVS的适宜剂量.     

老年蛛网膜下腔出血患者脑脊液中溶血磷脂酸含量的动态变化

目的观察老年蛛网膜下腔出血(SAH)患者脑脊液中溶血磷脂酸(LPA)含量动态变化的特点与脑血管痉挛(CVS)的关系。方法选择经临床和辅助检查确诊的SAH患者67例为SAH组,另选同期住院的非SAH患者55例为对照组,分别于发病后1、7、14及28天测定脑脊液中LPA的含量,又将SAH组患者经脑血管造影和经颅多普勒超声确诊后分为CVS组(21例)和无CVS组(46例)。结果SAH组患者发病1天时脑脊液中LPA含量与对照组比较差异无显著性意义;SAH组患者发病7天时明显升高(P<0.01);14天时仍高(P<0.01),28天降至基线水平。CVS组患者发病1天时脑脊液中LPA含量与无CVS组比较差异无显著性意义;CVS组患者发病7天时明显升高(P<0.01);14天时仍高(P<0.01),28天降至基线水平。结论SAH后7和14天脑脊液中LPA含量与CVS的发生明显关联。检测脑脊液中LPA含量对预测CVS的发生可能具有重要意义。     

蛛网膜下腔出血继发脑血管痉挛

脑血管痉挛 (CVS)是 SAH的常见并发症 ,继发于 CVS的脑缺血性损伤也称为迟发性缺血性损伤 ,其具有很大危害性 ,是患者致残及致死的主要原因之一。据报道 ,SAH继发CVS的发生率为 70 % ,迟发性缺血性损伤的发生率为 36 %。临床上 ,将血管造影发现的 CVS称为“造影性”CVS;可引起脑缺血或脑梗死症状的 CVS称为“症状性”CVS。一般“造影性”CVS不出现临床症状 ,其原因可能与脑侧支循环供血的有效性、CVS的严重程度及持续时间 ,以及颅内高压或静脉病变等有关。单电子发射断层扫措 (PET)示 CVS引起脑血流量 (CBF)小于 2 0 ml/ (…     

蛛网膜下腔出血后脑血管痉挛与脑利钠肽及低钠血症的关系

目的探讨蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)与血浆脑利钠肽(BNP)及低钠血症的关系。方法对30例SAH病人发病后0~3d,4~6d,7~9d及10~12d 4个时段测定血浆BNP浓度和血钠,并进行相关性分析;无CVS组与无症状CVS组及有症状CVS组病人BNP浓度比较,低钠血症组与非低钠血症组BNP浓度比较,与16名健康对照组BNP浓度比较。结果SAH病人BNP浓度明显高于对照组(P<0.01),无CVS组和无症状CVS组BNP浓度逐渐下降,有症状CVS组第三时段BNP浓度明显高于第一时段(P<0.01),也明显高于前两组(P<0.01)。低钠血症组中第三时段BNP浓度明显高于第一时段(P<0.01)及非低钠血症组,而非低钠血症组BNP浓度呈下降趋势。结论BNP浓度升高可诱导低钠血症,引起有症状CVS及迟发性脑梗死,BNP可作为预测SAH后出现症状性CVS及预后的一个重要指标。     

脑脊液溶血磷脂酸含量与蛛网膜下腔出血后脑血管痉挛的关系

目的:观察蛛网膜下腔出血(SAH)患者脑脊液溶血磷脂酸(LPA)含量动态变化的特点及其与脑血管痉挛(CVS)的关系,探索CVS的发病机制.方法:选取经临床和辅助检查确诊的SAH患者67例,分别于发病后24 h、7 d、14 d和28 d测定脑脊液LPA含量,并与对照组进行比较,同时观察LPA含量与CVS在时程上的相关性.结果:67例SAH患者中共有29例(43.3%)发生CVS,平均发生时间为6.6 d.发病24 h时,SAH患者脑脊液LPA含量与对照组无显著差异;发病7 d时显著高于对照组(P＜0.001);发病14 d时显著高于对照组(P＜0.01),但显著低于发病7 d时(P＜0.01);发病28 d时降至基线水平,与对照组无显著差异.发病24 h时,CVS组脑脊液LPA含量与无CVS组无显著差异,发病7 d时显著高于无CVs组(P＜0.001),发病14 d时仍显著高于无CVS组(P＜0.01);发病28 d时两组之间无显著差异.结论:SAH患者脑脊液LPA水平在发病后7～14 d显著升高,并且在时程上与CVS发生显著关联.检测脑脊液12A含量对预测CVS的发生可能具有重要意义.     

蛛网膜下腔出血患者症状性脑血管痉挛的预测

蛛网膜下腔出血（SAH）后的脑血管痉挛（CVS）是SAH的重要并发症之一,尤其是症状性CVS能够导致迟发性神经功能缺损。因此,准确预测SAH后症状性CVS的发生具有重要临床意义。2001年7月～2004年10月,我们对76例SAH患者分别进行了脑血管造影（DSA）、经颅多谱勒超声（TCD）检查及Fisher量表分析,探讨其对SAH后症状性CVS的预测价值。现报告如下。     

蛛网膜下腔出血后脑血管痉挛的预测

脑血管痉挛(CVS)是蛛网膜下腔出血(SAH)重要的并发症,是引起SAH后脑缺血和脑梗死的病理基础,其发生率30％左右,出现时间多在SAH后3～21天。CVS分为两个阶段:急性痉挛和迟发性痉挛(DCV)。急性痉挛发生在SAH后24小时,常在24小时内缓解。迟发性痉挛不同于急性痉挛,病理解剖学可观察到血管平滑肌细胞发生形态学上的改变,一旦发生很难逆转,对血管扩张剂的反应性差。因此,迟发性痉挛的关键在于预防,有早期发现、早期用药,才能取得一定的疗     

脑脊液置换术治疗蛛网膜下腔出血160例疗效观察

目的观察脑脊液置换术治疗蛛网膜下腔出血（以下简称SAH）的疗效。方法将蛛网膜下腔出血患者,采用随机数字分配法分为置换组（160例）和对照组（150例）,置换组行脑脊液置换术,隔日1次,共置换3~5次,每次腰穿放出血性脑脊液5~10 m l,以等量生理盐水进行缓慢置换,重复2次,间隔5 m in,最后1次加地塞米松5 mg鞘内注射。对照组按SAH传统方法治疗。结果 160例经置换脑脊液后头痛能迅速缓解,平均为4.6 d,而对照组150例头痛缓解时间平均为13.2 d,置换组神志不清恢复正常的时间及头痛缓解时间均较对照组缩短（P〈0.05）。脑血管痉挛致脑梗死的发生,置换组0例,而对照组20例,置换组无脑积水的病例发生,而对照组发生脑积水25例。结论应用脑脊液置换术治疗SAH是一种缓解头痛,减少脑血管痉挛、梗阻性脑积水的有效方法。     

c-jun氨基末端激酶在兔蛛网膜下腔出血后脑血管痉挛中的作用

目的观察兔蛛网膜下腔出血(SAH)后基底动脉中原癌基因c-jun氨基末端激酶(JNK)的表达规律,以探讨其与脑血管痉挛(CVS)的关系。方法将72只新西兰大白兔随机分为2组:①对照组:12只;②SAH组:60只。SAH组又随机分为注血后1、3、5、7、10 d,共5组,每组12只。采用枕大池二次注血法建立稳定的兔CVS模型,应用苏木素-伊红染色和Western印迹分别观察兔基底动脉的形态学改变和JNK的表达情况,并通过测量管径的变化来判断CVS的严重程度。结果 SAH组的基底动脉出现相应的病理学改变,管腔狭窄呈急性期收缩和迟发性痉挛双相改变;SAH组的JNK表达升高,在第7天时达到高峰(P<0.01),第10天后表达稍下降,但仍高于对照组(P<0.01)。结论在兔CVS模型的基底动脉中JNK的表达明显上调,呈现一定的时序性变化规律,与迟发性CVS的严重程度一致,在CVS的发生和发展过程中起了重要的作用。     

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。     

蛛网膜下腔出血后海马区微血管痉挛及血管内转染一氧化氮合酶基因的影响

目的研究蛛网膜下腔出血(SAH)后海马CA1区神经元及微血管的变化,观察血管内转染内皮型一氧化氮合酶(eNOS)基因后,海马CA1神经元及微血管改变,探讨eNOS基因转染预防脑血管痉挛的作用。方法 24只兔随机分为对照组、SAH组、转染携带eNOS基因重组腺病毒组(AdeNOS组)。每组8只。采用枕大池二次注血法制备兔SAH后脑血管痉挛模型。兔于首次注血后7d进行灌注固定,留取海马区脑组织标本,在电镜和光镜下观察海马神经元及微血管的变化。结果光镜下SAH组海马CA1区神经元较对照组明显减少,微血管周围间隙增宽,管腔狭窄,管壁增厚;电镜下SAH组海马神经元细胞肿胀,结构不完整,细胞核固缩,线粒体空泡化;AdeNOS组损伤较SAH组明显减轻。结论 SAH后脑血管痉挛可引起海马CA1区神经元变性,可能与海马区微血管痉挛改变有关,eNOS基因转染可明显减轻海马神经元损伤,预防SAH后脑血管痉挛的发生。     

Expression of the receptors of VEGF and the influence of extract of Ginkgo biloba after cisternal injection of autologus arterial hemolysate in rats

The study was aimed to investigate the alterations of vascular endothelial growth factor (VEGF) receptors and the influence of extract of Ginkgo biloba (EGb) after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, vehicle, EGb1 (lower dose), and EGb2 (higher dose) groups. Autologus arterial hemolysate was injected into cisterna magna to induce SAH. The non-SAH rats received cisternal injection of saline instead. Rats underwent RT-PCR determination of one of the VEGF receptors flt-1mRNA, and immunohistochemistry for VEGF receptors Flt-1 and Flk-1. The results revealed that there was only slight expression of flt-1mRNA in the brain tissue in non-SAH rats. The expression in SAH group was enhanced 24 hours and 72 hours after cisternal injection. No Flt-1 and Flk-1 positive cell was observed in the brain in non-SAH group. A good few Flt-1 and Flk-1 positive cells were found in cortex and other regions of the brain in SAH group. The expression of flt-1mRNA, Flt-1 and Flk-1 proteins were increased by the use of two doses of EGb. It was concluded that the up-regulated expression of the two kinds of VEGF receptors may be an intrinsic protective mechanism in the process of SAH, which can be enhanced by EGb.     

Effects of blockade of cerebral lymphatic drainage on regional cerebral blood flow and brain edema after subarachnoid hemorrhage

The study was designed to observe the influence of blockade of cerebral lymphatic drainage on the regional cerebral blood flow (rCBF) and brain edema after experimental subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, and SAH plus cervical lymphatic blockade (SAH + CLB) groups. Autologous arterial hemolysate was injected into rat's cisterna magna to induce SAH. The rCBF was recorded continuously by a laser Doppler flowmeter. Intracranial pressure (ICP) was also monitored. After 24 hours and 72 hours of SAH, the rats were sacrificed and the brain was harvested for water content detection. It was found that there was no obvious change of rCBF and brain water content during the experiment in non-SAH group. An immediate and persistent drop in rCBF was found in SAH group. The drop in rCBF was more obvious in SAH + CLB group. CLB also worsened the SAH-induced increase in ICP. The brain water content 24 hours and 72 hours after induction of SAH in SAH group increased significantly. CLB led to a further increase of brain water content. In conclusion, blockade of cerebral lymphatic drainage pathway deteriorates the secondary cerebral ischemia and brain edema after SAH.     

Beneficial effects of systemic administration of recombinant human erythropoietin in rabbits subjected to subarachnoid hemorrhage

Cerebral vasospasm and ischemic damage are important causes of mortality and morbidity in patients affected by aneurysmal subarachnoid hemorrhage (SAH). Recently, i.p. administration of recombinant human erythropoietin (r-Hu-EPO) has been shown to exert a neuroprotective effect during experimental SAH. The present study was conducted to evaluate further the effect of r-Hu-EPO administration after SAH in rabbits on neurological outcome, degree of basilar artery spasm, and magnitude of neuronal ischemic damage. Experimental animals were divided into six groups: group 1 (n = 8), control; group 2 (n = 8), control plus placebo; group 3 (n = 8), control plus r-Hu-EPO; group 4 (n = 8), SAH; group 5 (n = 8), SAH plus placebo; group 6 (n = 8), SAH plus r-Hu-EPO. r-Hu-EPO, at a dose of 1,000 units/kg, and placebo were injected i.p. starting 5 min after inducing SAH and followed by clinical and pathological assessment 72 h later. Systemic administration of r-Hu-EPO produced significant increases in cerebrospinal fluid EPO concentrations (P < 0.001), and reduced vasoconstriction of the basilar artery (P < 0.05), ischemic neuronal damage (P < 0.001), and subsequent neurological deterioration (P < 0.05). These observations suggest that r-Hu-EPO may provide an effective treatment to reduce the post-SAH morbidity.     

阿托伐他汀对大脑中动脉栓塞大鼠尿激酶溶栓治疗的影响

目的研究阿托伐他汀联合尿激酶溶栓对大鼠大脑中动脉急性脑梗死的疗效。方法选择SD大鼠48只,采用血栓栓塞法制备大鼠大脑中动脉急性脑梗死模型,随机分为阿托伐他汀组、尿激酶组、联合治疗组和对照组,每组12只。缺血3h给予阿托伐他汀或生理盐水,缺血4h给予尿激酶或生理盐水治疗。治疗前和缺血24h行神经功能缺损评分,缺血24h取脑行2,3,5-氯化三苯基四氮唑染色检测脑梗死体积。结果与对照组比较,阿托伐他汀组缺血24h神经功能显著改善[(6.5±4.3)分vs(12.5±4.3)分],脑梗死体积明显降低[(13.8±7.5)%vs(30.5±23.4)%,P<0.05]。与阿托伐他汀组比较,尿激酶组和联合治疗组神经功能改善程度及脑梗死体积降低程度更显著(P<0.05)。与尿激酶组比较,联合治疗组神经功能改善、脑梗死体积减小,但差异无统计学意义(P>0.05)。结论阿托伐他汀对脑梗死组织有保护作用,阿托伐他汀与尿激酶联合治疗有进一步提高疗效的趋势。     

M4型瞬时受体电位通道在蛛网膜下腔出血大鼠脑血流自主调节障碍中的作用

目的 探讨M4型瞬时受体电位通道(TRPM4)在蛛网膜下腔出血(SAH)大鼠模型中对脑血流量自主调节障碍的作用。方法 选择清洁级健康雄性SD大鼠120只,按随机数字表法分为假手术、SAH、阴性对照及治疗组,剔除死亡大鼠。采用立体定向仪鞍上池注射法建立SAH模型,分别向假手术组和阴性对照组注射等渗盐水0.2 ml,分别向SAH组和治疗组注射自体尾动脉血0.2 ml。通过置入式微量泵分别向假手术组和SAH组大鼠的侧脑室持续泵入等渗盐水,向阴性对照组和治疗组持续泵入浓度为0.03 mol/L的TRPM4阻滞剂(9-Phenanthrol),4组大鼠分别于第3、5和7天接受大脑皮质局部血流量和全脑血流量的检测。结果 120只SD大鼠中共有106只(88.3%)存活至研究时间点,4组分别以21只大鼠(各时点分别为7只)进行数据分析。第3、5、7天,假手术、SAH、阴性对照和治疗组大脑皮质局部和全脑血流量的差异均有统计学意义(均P0.05);SAH组皮质局部血流量[第3、5、7天分别为(141±18)、(148±24)、(168±19)PU]和全脑血流量[第3、5、7天分别为(93±5)、(85±5)、(85±6)ml/(100 g·min)]均较假手术组[皮质局部:(235±17)、(220±24)、(224±20)PU,全脑:(141±10)、(147±8)、(143±8)ml/100 g·min]明显降低(均P0.05),治疗组大脑皮质局部和全脑血流量[皮质局部:(183±26)、(173±26)和(187±15)PU,全脑:(114±10)、(104±9)和(119±5)ml/(100 g·min)]均较SAH组明显增加(均P0.05)。结论 TRPM4对改善SAH后脑血流自主调节障碍有明显作用。     

Experimental and clinical study on effect of endovascular dilation on symptomatic cerebral vasospasm

Objective To undertake animal experimentation and clinical study on the safety and efficacy of percutaneous transluminal angioplasty (PTA) and intraarterial papaverine (IAP) infusion for treatment of refractory symptomatic cerebral vasospasm (CVS). Methods In the experimental study, vasospasm was induced in rabbits by double injections of blood into the cisterna magMa, IAP infusion was given on either the 4th day or the 7th day after occurrence of subarachnoid hemorrhage (SAH), and then neurological observation, angiography, light and electron microscopy were done, In the clinical study, since September 1996, 22 patients with refractory symptomatic CVS involving 50 vascular territories received dilation therapy by PTA and IAP within 24 hours of clinical neurological deterioration. Results In the experimental study, all the rabbits except two in the ‘the 4th day‘ group showed angiographic dilation in all of the spastic basilar arteries, and neurological improvement; in the ‘the 7th day‘ group angiographic dilation appeared in 4 (57. 1% ) out of 7 rabbits. After 24 hours, 1 rabbit in each group had recurrence of neurological deficits and angiographic constriction. In the clinical study after aneurysm clipping or endovascular coil embolization was done, within 72 hours of SAH all patients underwent endovascular treatment: PTA alone in 3 cases, IAP alone in 14 cases, PTA and lAP in the remaining 5 cases. All vessel segments were dilated satisfactorily after endovascular treatment. Clinical improvement was significant in 13 eases,moderate in 7, minimal or none in 2; 2 cases died on the 7th day after endovascular dilation treatment. Conclusion Endovascular dilating techniques, namely, PTA, IAP and a combination of PTA and IAP, are safe and effective for treatment of symptomatic CVS refractory to medical therapy.