尼莫地平防治创伤性蛛网膜下腔出血早期脑血管痉挛

目的探讨观察尼莫地平防治创伤性蛛网膜下腔出血早期脑血管痉挛的疗效。方法对我院2007-10—2010-10收治的60例创伤性蛛网膜下腔出血患者随机分为2组,对照组30例采用常规综合治疗,治疗组30例在此基础上给予尼莫地平注射液持续静脉泵入。结果 2组治疗后MCA血流速度均有所降低,且治疗组下降程度较对照组更为明显（P〈0.05）;治疗组的CVS发生率、病死率明显低于对照组（P〈0.05）;2组再出血率相比较,差异无统计学意义（P〉0.05）。结论尼莫地平治疗创伤性蛛网膜下腔出血早期脑血管痉挛的疗效确切,可明显改善患者预后,值得临床借鉴。     

尼莫地平预防创伤性蛛网膜下腔出血所致的脑血管痉挛

本文观察尼莫地平预防创伤性蛛网膜下腔出血(SAH)所致的脑血管痉挛(CVS)。将创伤性SAH病人136例分为两组,尼莫地平组(65例)于伤后24小时内给予尼莫地平治疗,对照组(71例)采用一般综合治疗各三周。结果提示尼莫地平组死亡率(24.6％)、CVS发生率(26.1％)分别低于对照组(33.8％和36.6％),说明尼莫地平预防创伤性SAH所致的CVS有效。     

尼莫地平治疗蛛网膜下腔出血脑血管痉挛疗效观察

目的观察尼莫地平治疗蛛网膜下腔出血脑血管痉挛的应用效果,以期进一步明确其机制,提高治疗效果。方法选取98例蛛网膜下腔出血脑血管痉挛患者给予尼莫地平治疗作为观察组,与以往未予以尼莫地平治疗的95例蛛网膜下腔出血脑血管痉挛者进行对比观察(对照组),同时对2组患者临床症状、体征改善情况及平均住院时间和大脑中动脉血流平均速值等内容予以观察、对比且对相关数据进行统计学分析。结果观察组临床症状及体征改善率优于对照组,且平均住院时间较对照组明显缩短(P<0.05);观察组患者大脑中动脉血流平均速值低于对照组(P<0.05),且未出现严重不良事件。结论尼莫地平在蛛网膜下腔出血所致的脑血管痉挛中应用效果良好且安全可靠,值得临床推广。     

内皮素与脑血管痉挛

蛛网膜下腔出血引起的脑血管痉挛是一个复杂的病理生理过程,其确切的病因和发病机理至今仍不十分明确。近年来,有关内皮素——一种由内皮细胞产生的、具有强烈缩血管作用的肽类物质与脑血管痉挛发生的关系被引起广泛的注意。研究表明,内皮素在脑血管痉挛发生的病理生理过程中起到重要的作用。本文在简要介绍内皮素的基础上,着重阐述内皮素与脑血管痉挛的关系。     

尼莫地平防治蛛网膜下腔出血后脑血管痉挛临床观察

目的观察尼莫地平防治蛛网膜下腔出血后脑血管痉挛的疗效。方法选择蛛网膜下腔出血患者56例,随机分为尼莫地平治疗组30例和对照组26例,2组均于48 h内接受治疗,对照组用脱水、止血等常规治疗,尼莫地平治疗组在常规治疗基础上加用尼莫地平持续静脉泵给药(1 mg/h)14 d,之后改为口服20 mg,3次/d,14 d,同时进行血压监测以调整用药剂量。结果 1个月后治疗组脑血管痉挛的发生率、病死率低于对照组(P<0.05),再出血发生率2组比较差异有统计学意义(P>0.05)。结论尼莫地平防治蛛网膜下腔出血后脑血管痉挛疗效确切,且会增加再出血的危险性。     

尼莫地平治疗蛛网膜下腔出血后脑血管痉挛的疗效观察

目的探讨尼莫地平治疗蛛网膜下腔出血后脑血管痉挛的临床疗效。方法 86例蛛网膜下腔出血并发脑血管痉挛患者按1∶1比例随机分为2组,每组各43例,对照组给予常规治疗,观察组在对照组基础上给予尼莫地平治疗。结果治疗1个月后,2组总有效率差异有统计学意义(P0.05);观察组GOS评分优于对照组,差异具有统计学意义(P0.05);2组大脑中动脉流速比较差异有统计学意义(P0.05)。结论尼莫地平可迅速改善蛛网膜下腔出血后脑血管痉挛患者的临床症状,提高疗效,且安全性高,值得临床推广应用。     

尼莫地平防治蛛网膜下腔出血后脑血管痉挛疗效观察

脑血管痉挛(CVS)是蛛网膜下腔出血(SAH)最常见、最严重的并发症之一,发生率高达70%,是SAH患者病残和死亡的主要原因,SAH后积极防治CVS的发生有重要临床意义。1资料与方法1.1病例选择2008-06-2011-06我院神经内科收治SAH     

尼莫地平治疗动脉瘤性蛛网膜下腔出血所致的血管痉挛

现在普遍的观点认为动脉瘤性蛛网膜下腔出血所致的脑动脉痉挛和梗塞是致死致残的主要原因,治疗脑血管痉挛才是治疗动脉瘤性蛛网膜下腔出血的关键所在。钙拮抗剂可防止血管平滑肌持续收缩导致的血管痉挛。10年来大量的研究表明尼莫地平是目前应用较广的一种钙拮抗剂,对治疗脑血管痉挛效果较好.     

Effect of vardenafil on cerebral vasospasm following experimental subarachnoid hemorrhage in rats

We examined the effects of the phosphodiesterase 5 (PDE-5) inhibitor vardenafil on cerebral vasospasm in an experimental rat subarachnoid hemorrhage (SAH) model. Thirty-two albino Wistar rats were divided into five groups: G1, no experimental intervention; G2, administered subarachnoid physiological saline after sham surgery; G3, subjected to SAH; G4, subjected to SAH and administered low-dose (0.5 mg/kg) vardenafil treatment; and G5, subjected to SAH and administered high-dose (5 mg/kg) vardenafil treatment. For animals in G3, G4 and G5, SAH was induced by an injection of autologous non-heparinized blood into the cisterna magna. Immediately after SAH, for animals in G4 and G5, vardenafil was administered by gavage at intervals of 8 hours for 2 days. The rats were then decapitated, and basilar arteries and blood samples were taken for biochemical and histopathological examination. Malonyldialdehyde values in G2 (p = 0.004) and G3 (p = 0.002) were significantly higher than those in G1. G4 and G5 had significantly lower values than G2 and G3 (p = 0.014, G4 v. G2; p = 0.005, G4 v. G3; p = 0.005, G5 v. G2; p = 0.002, G5 v. G3). Total antioxidant capacity (TAC) values in G3 were significantly lower than those in G1 (p = 0.041). TAC values in G4 and G5 were significantly higher than those in G3 (p = 0.043). Mean luminal diameter in G3 was significantly smaller compared with G1 and G2 (p = 0.002), but larger in G4 (p = 0.002) and G5 (p = 0.001) compared with G3. Mean luminal diameter was also significantly larger in G5 than in G2 (p = 0.008) and G4 (p = 0.038). Mean wall thickness in G2 (p = 0.015) and G3 (p = 0.002) was significantly thicker compared with G1. Wall thickness was significantly thinner in G4 and G5 compared with G2 and G3 (p = 0.008, G4 v. G2; p = 0.001, G4 v. G3; p = 0.005, G5 v. G2; p = 0.001, G5 v. G3). Our results confirm that vardenafil may induce vasodilatation and provide potential benefits in SAH therapy by preventing vasospasm.     

17β-雌二醇对大鼠蛛网膜下腔出血后迟发型脑血管痉挛的作用

目的研究17β-雌二醇(E2)对蛛网膜下腔出血(SAH)后迟发型脑血管痉挛(DCV)的抑制作用。方法雄性Wistar大鼠50只随机分为5组:①空白组,②假穿刺组,③SAH组,④SAH+E2组,⑤SAH+安慰剂组。采用酶联免疫吸附法(ELISA)检测血浆中内皮素-1(ET-1)含量,末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记法(TUNEL)检测颞叶神经元凋亡情况,通过测定基底动脉血管横截面积判断脑血管痉挛情况。结果实验结果显示SAH后7 d SAH+E2组基底动脉横截面积与SAH组和SAH+安慰剂组相比明显变大(P<0.01);与SAH组和SAH+安慰剂组相比,SAH+E2组血浆ET-1浓度明显减少(P<0.01);TUNEL染色显示SAH+E2组颞叶皮质神经元凋亡程度较SAH组和SAH+安慰剂组显著性减轻。结论持续给予E2维持其生理浓度可以有效预防SAH后迟发型脑血管痉挛,部分可能与E2可以抑制ET-1的产生有关。     

Effect of melatonin on cerebral vasospasm following experimental subarachnoid hemorrhage

OBJECT: The current study was undertaken to determine whether melatonin therapy reverses vasospasm and prevents apoptosis by inhibiting lipid peroxidation in an experimental subarachnoid hemorrhage (SAH) model. MATERIALS AND METHODS: The rabbits were divided into four groups as follows: Group 1, SAH + melatonin (5 mg/kg/i.p. BID) simultaneously with SAH (n = 6); Group 2, SAH + melatonin (5 mg/kg/i.p. BID) treated 2 hours after SAH (n = 6); Group 3, control group (n = 4); Group 4, SAH only (n = 6). Light microscopic examinations of the basilar arteries were performed to demonstrate the pathophysiological changes of the arterial wall with hematoxylin- eosin. Apoptosis: Immunohistology using the ApopTag Peroxidase In Situ Apoptosis Detection Kit was used to demonstrate apoptosis in a cross section of basilary arteries. Apoptotic index was calculated as the number of the immunoreactive nuclei per total number of endothelial cells, and expressed as a percentage. RESULTS: The results of measurements of diameters of the vessels between groups were significantly different (p = 0.028). While basilar arteries of the SAH only group showed 57% constriction, Groups 1 and 2 were calculated as 33 and 26% constriction, respectively, compared with the control group (p < 0.05). And also Groups 1 and 2 showed significant protection of apoptosis compared with Group 4. The difference between the four groups was tested by Kruskal-Wallis test and the significance between the two groups was tested by Mann- Whitney U-test. CONCLUSION: Melatonin with its strong antioxidant effect can prevent SAH-induced vasospasm and apoptosis of endothelial cells of vessels.     

Effects of ebselen versus nimodipine on cerebral vasospasm subsequent to experimental subarachnoid hemorrhage in rats

We investigated the effect of ebselen relative to nimodipine in an animal model of subarachnoid hemorrhage. Thirty Wistar albino rats were divided into 5 groups: G1, no intervention; G2, sham surgery without subarachnoid hemorrhage (SAH); G3, SAH only; G4, SAH plus nimodipine treatment; G5, SAH plus ebselen treatment. For G2 animals, physiological saline (0.9% NaCl) was injected into the cisterna magna. For G3, G4 and G5 animals, SAH was induced by injecting autologous non-heparinized blood into the cisterna magna. One hour after injection, G4 animals received nimodipine at 6-hour intervals and G5 animals received ebselen twice a day for 48 hours. After treatment, brain tissue and blood samples were taken for biochemical and histopathological examination. Mean malonyldialdehyde concentration was significantly higher in G3 than in G1 (p < 0.0001), G2 (p = 0.01), G4 (p = 0.002) and G5 (p = 0.014), and significantly higher in G5 than in G1 (p = 0.013). Mean superoxide dismutase activity was significantly lower in G4 than in both G1 (p = 0.025) and G2 (p = 0.02). Mean wall thickness was significantly greater in G3 than in G1 (p < 0.0001), G2 (p = 0.01), G4 (p < 0.0001) and G5 (p < 0.0001). Mean wall thickness was also significantly greater in both G1 and G2 than in G4 (p < 0.0014 and p < 0.0001) and G5 (p < 0.0001 and p < 0.0001). Mean luminal diameter of the basilar artery was significantly smaller in G3 than in G2 (p = 0.02), G4 (p < 0.018) and G5 (p < 0.001). Our results confirm that ebselen may have neuroprotective effects by acting to prevent vasospasm.     

尼莫地平防治蛛网膜下腔出血后脑血管痉挛疗效观察

目的 探讨尼莫地平防治蛛网膜下隙出血后脑血管痉挛的疗效.方法 将70例蛛网膜下腔出血后脑血管痉挛的患者随机分为尼莫地平组(观察组)和对照组,对照组用脱水、止血等常规疗法,观察组在常规疗法基础上加用尼莫地平.结果 尼莫地平组防治蛛网膜下腔出血后脑血管痉挛疗效优于对照组,2组疗效比较差异有统计学意义(P＜0.01) .结论 尼莫地平防治蛛网膜下隙出血后脑血管痉挛安全有效.     

盐酸法舒地尔对蛛网膜下腔出血后血管痉挛的实验研究

目的通过建立大鼠蛛网膜下腔出血（SAH）模型,探讨盐酸法舒地尔对蛛网膜下腔出血后血管痉挛的缓解作用和神经保护作用,并与尼莫地平对比,观察疗效。方法通过枕大池二次注血法建立大鼠SAH模型,观察基底动脉和海马神经元形态变化,测量基底动脉管径和管壁厚度,计算海马CA1区神经元密度,检测基底动脉内皮型一氧化氮合成酶（eNOS）的表达。结果各组模型大鼠的基底动脉均出现血管痉挛,海马CA1区正常神经元数目明显减少,多数神经元发生变性,基底动脉的eNOS表达明显减弱。但注射法舒地尔组与其他模型组相比能较大程度的缓解以上变化,具有统计学差异（P〈0.05）,且优于尼莫地平。结论法舒地尔可以有效缓解SAH后的迟发性脑血管痉挛,具有神经保护作用,其缓解迟发性脑血管痉挛作用和神经保护作用与动脉壁产生的一氧化氮（NO）有关。     

运动诱发电位对脑动脉瘤蛛网膜下腔出血后迟发性脑血管痉挛的诊断性意义分析

目的研究运动诱发电位(motor evoked potential,MEP)对脑动脉瘤蛛网膜下腔出血(aneurysmal subarachnoid hemorrhage,a SAH)后迟发性脑血管痉挛(vasospasm,VS)的诊断意义。方法选取2015年5月~2017年5月在陕西省第四人民医院和第四军医大学西京医院神经外科重症监护病房(Intensive Care Unite,ICU)住院治疗的高分级(Hunt-Hess分级Ⅲ-Ⅴ级)的伴有或不伴有迟发性VS的a SAH患者35例,运用经颅磁刺激运动诱发电位仪来检测MEP刺激阈值的变化,运用数字减影血管造影(digital subtraction angiography,DSA)检查结果作为判定是否存在确定性a SAH后迟发型性VS的金标准。并对MEP诊断VS的敏感性、特异性、阳性和阴性预测值进行计算。结果出现大脑皮质运动区供血动脉迟发性VS的患者,MEP的刺激阈值最小增加值为45 m A,平均增加值为61.55 m A;在未出现迟发性VS的患者,MEP的刺激阈值最大增加值为25m A,平均增加值为12.59m A;二者比较有明显差异(P0.05)。MEP的刺激阈值增加45m A或以上对诊断迟发性VS有临床意义,其敏感性为0.85,特异性为0.86,阳性预测值为0.85,阴性预测值为0.86。结论 MEP检查能够比较准确地诊断a SAH后迟发性VS,其可以作为一种床旁实时诊断VS的较为可靠方法。     

黄芪甲苷对大鼠蛛网膜下腔出血后迟发性脑血管痉挛的影响

目的 探讨黄芪甲苷对大鼠蛛网膜下腔出血（SAH）后迟发性脑血管痉挛的影响及机制。方法 将40只成年雄性SD大鼠随机分为假手术组、黄芪甲苷组（腹腔注射用0.1%二甲基亚砜助溶的黄芪甲苷溶悬液）、模型组和溶媒组（腹腔注射等体积0.1%二甲基亚砜），每组10只。采用颈内动脉刺破法制作SAH模型。SAH后24 h根据改良Garcia神经功能评分评定大鼠神经功能。SAH后6 d，HE染色测量基底动脉横截面积评估血管痉挛，免疫组化染色检测基底动脉p-Akt表达，免疫荧光染色检测基底动脉C-myc和α-SMA表达。结果 与假手术组相比，模型组和溶媒组改良Garcia神经功能评分明显降低（P<0.05），基底动脉横截面积明显减小（P<0.05），基底动脉α-SMA表达水平明显降低（P<0.05），基底动脉p-Akt和C-myc表达水平明显增加（P<0.05）；而模型组和溶媒组均无统计学差异（P>0.05）。与溶媒组相比，黄芪甲苷组改良Garcia神经功能评分明显提高（P<0.05），基底动脉横截面积明显增加（P<0.05），基底动脉α-SMA表达水平明显增加（P<0.05），基底动脉p-Akt和C-myc表达水平明显降低（P<0.05）。结论 黄芪甲苷可能通过抑制Akt信号通路下调C-myc的表达、促进α-SMA表达，影响SAH大鼠基底动脉血管平滑肌表型转换和增殖，增加基底动脉横截面积，从而缓解基底动脉痉挛。     

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。