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1.
目的 研究血管紧张素Ⅱ-1型受体拈抗剂奥美沙坦(OLM)在自发性高血压大鼠脑出血中的神经保护作用. 方法 自发性高血压大鼠采用完全随机数字表法分成正常组、脑出血组、治疗对照组、OLM治疗组,每组11只.正常组不做任何处理,后3组经右侧基底节注射胶原蛋白酶Ⅶ制作实验性脑出血模型.脑出血后1 h,OLM组经胃管给予单剂量鼻饲OLM(10 mg/kg或3mg/kg,溶入1 mL羧甲基纤维素钠中),治疗对照组给予等量羧甲基纤维素钠,脑出血组不予处理.脑出血后6h,在动物清醒状态下,用无创鼠尾血压计测平均动脉血压;脑出血后24 h,按改良型肢体平衡试验法进行行为学检测,干湿法测脑组织含水量,RT-PCR分析受体和靶基因mRNA表达水平. 结果 脑出血组平均动脉血压[(121.4+3.5)mm Hg]与正常组基础血压[(120.2+3.8)mm Hg]比较差异无统计学意义(P>0.05);10 mg/kg OLM组平均动脉血压[(105.6+3.5)mm Hg]较脑出血组明显下降,差异有统计学意义(P<0.05);但3 mg/kg OLM组和治疗对照组没有引起血压的明显下降[分别为(120.8±3.1)mm Hg,(118.6±3.9)mm Hg],与脑出血组比较差异无统计学意义(P>0.05).3 mg/kgOLM组大鼠出血侧脑组织含水量[(80.02±0.32)%]较脑出血组[(80.90±0.36)%]减少,差异有统计学意义(P<0.05);治疗对照组大鼠出血侧脑组织含水量[(80.81±0.32)%]较脑出血组稍低,但差异无统计学意义(P>0.05).3 mg/kg OLM组表现出更少的神经功能缺失(神经功能评分为5.03±0.71),与脑出血组(6.62±0.55)比较差异有统计学意义(P<0.05);治疗对照组神经功能评分(6.41±0.55)与脑出血组比较差异无统计学意义(P>0.05).3 mg/kg OLM组脑出血侧ATIR及靶基因(HO-1、COX-2、IL-6和VCAM-1)的mRNA表达均比脑出血组低,差异有统计学意义(P<0.05),而治疗对照组和脑出血组比较差异无统计学意义(P>0.05). 结论 在白发性高血压大鼠脑出血中,小剂量OLM能促进神经功能的恢复并产生许多神经保护作用,包括减轻脑水肿、抑制炎症反应和氧化应激反应等.  相似文献   

2.
目的在比较自发性高血压大鼠(SHR)与同龄无高血压Wistar大鼠永久性大脑中动脉阻塞(pMCAO)后脑缺血损伤情况并初步分析其可能机制。方法雄性SHR和Wistar大鼠各30只分别随机分为:pMCAO模型6 h组、假手术6 h组、pMCAO模型24 h组、假手术24 h组和正常组(均n=6)。采用线栓法制作pMCAO模型,术后6、24 h对大鼠进行神经功能学评分后处死,制作脑冠状切片。术后6 h处死大鼠脑部切片行尼氏染色后在组织学层面上观察神经元损伤情况;术后24 h处死大鼠脑部切片行尼氏染色后计算脑梗死体积和水肿程度百分比。正常组脑部切片经苏木精-伊红染色后计算脑部小血管壁/腔比。结果术后6和24 h,不同品系大鼠神经功能学评分差异无统计学意义(P0.05);术后6 h尼氏染色示SHR神经元损伤重于Wistar大鼠。术后24 h SHR脑梗死体积百分比[(28.05±2.38)%]大于Wistar大鼠[(25.23±1.33)%],差异有统计学意义(P0.05)。两品系大鼠之间脑水肿程度差异无显著性。脑部小血管壁/腔比SHR[(11.46±3.74)%]较Wistar大鼠[(8.73±1.73)%]增大(P0.05)。结论 pMCAO术后SHR的脑缺血损伤程度重于Wistar大鼠,可能与高血压引起的脑侧支循环血管壁增厚、僵硬,自我调节能力降低有关。  相似文献   

3.
目的:模拟人类高血压致大脑动脉瘤的病理过程,利用肾性高血压及脑血流动力学变化制备大鼠脑动脉瘤模型,通过观测脑动脉瘤形成过程中大鼠血浆内皮素一1(ET-1)的变化,探讨ET-1在脑动脉瘤发生发展中的作用。方法:将雄性SD大鼠随机分为肾性高血压组(RH)、假手术组,体重为200~250g,自发性高血压(SHR)大鼠购自中国医学科学院动物所,于术后1周、2周、4周、8周、12周、16周分别测定大鼠尾动脉收缩压、血浆ET-1含量。手术16周后处死动物,在光镜下观察脑动脉瘤的发生及部位。结果:①RH及SHR大鼠在术后第2周血压开始升高,血浆ET-1水平随血压升高而增加,在术后第4周时达到高峰,两组大鼠血压及血浆ET-1含量均明显高于同期假手术组。②在手术16周后处死动物,其中10只SHR大鼠、6只RH大鼠形成脑动脉瘤,有脑动脉瘤形成的大鼠血浆ET-1水平明显高于同组未形成动脉瘤的大鼠。③结论:肾性高血压时,随着血压增高缩血管物质ET-1血浆水平增高,ET-1可能通过导致脑血管内皮细胞功能紊乱、血管内皮结构破坏参与了脑动脉瘤的形成。  相似文献   

4.
目的 探讨局灶性脑缺血再灌注损伤(CIR)大鼠外周血内皮祖细胞(EPCs)数量的变化及其意义.方法 50只健康雄性SD大鼠随机分为正常对照组(5只)、假手术组(5只)、CIR模型组(15只)、糖尿病模型组(5只)、糖尿病假手术组(5只)和糖尿病合并CIR组(15只).由链脲佐菌素(STZ)诱导制作糖尿病大鼠模型;采用线栓法制作CIR大鼠模型.各模型大鼠采用Longa评分标准进行神经功能评分.CIR模型组与糖尿病合并CIR组各取5只大鼠采用2,3,5-三苯基氯化四氮唑(TTC)染色,计算其脑梗死体积.用流式细胞仪计数各组大鼠外周血EPCs的数量.结果 糖尿病合并CIR组大鼠神经功能评分[(2.8±1.0)分]明显高于CIR模型组[(1.5±0.3)分],且脑梗死体积[(464.1±169.3)mm3]明显大于CIR模型组[(101.3±57.4)mm3](均P<0.05).各组中,CIR模型组大鼠外周血EPCs数量最多,糖尿病合并CIR组最少,正常对照组与假手术组多于糖尿病模型组与糖尿病假手术组(均P<0.01).结论 CIR大鼠外周血EPCs数量增加,有助于修复血管及保护受损脑组织;糖尿病大鼠外周血EPCs数量明显减少,且合并CIR后减少更甚.外周血EPCs数量的检测有助于CIR病情及预后的评估.  相似文献   

5.
目的 探讨脑膜炎患者脑脊液(CSF)中肿瘤坏死因子α(TNF-α)、乳酸脱氢酶(LDH)及其同工酶检测的临床意义.方法 收集53例化脓性脑膜炎患者(化脑组)、58例病毒性脑膜炎患者(病脑组)、49例结核性脑膜炎患者(结脑组)、60例非神经系统感染性疾病患者(对照组)的CSF样本,采用酶联免疫吸附法(ELISA)测定TNF-α水平,采用酶测速率法测定LDH的活性,采用琼脂糖凝胶电泳法测定LDH同工酶含量,并进行比较.结果 3组脑膜炎患者CSF TNF-α含量明显高于对照组[(25.64±20.08)pg/L],其中化脑组[(462.24±368.13)pg/L]明显高于病脑组[(73.47±68.74)pg/L]及结脑组[(62.97+40.58)pg/L](均P<0.01),病脑组与结脑组间差异无统计学意义.化脑组CSF LDH水平[(201.37±148.06)U/L]显著高于其他各组(均P<0.01),结脑组[(170.32±86.45)U/L]明显高于病脑组[(79.54±43.71)U/L](P<0.01);但病脑组[(79.54±43.71)U/L]与对照组[(64.56±49.68)U/L]间差异无统计学意义.化脑组LDH4[(22.83±2.08)U/L]、LDH5[(35.26±2.18)U/L]明显高于其他各组,LDH1[(7.84±1.15)U/L]、LDH2[(13.01±1.46)U/L]明显低于其他各组(均P<0.01);结脑组LDH3[(29.48±3.24)U/L]较对照组[(16.13±3.95)U/L]明显升高(P<0.01);而病脑组同工酶谱与对照组比较差异无统计学意义.结论 CSF中TNF-α、LDH及LDH同工酶水平检测有助于不同类型脑膜炎的鉴别诊断.  相似文献   

6.
目的探讨全麻对颈动脉重度狭窄支架置入术后过度灌注综合征发生的预防作用。方法选择单侧颈动脉起始段重度狭窄患者92例行颈动脉支架置入术,根据麻醉方式分为局麻组39例和全麻组53例。记录平均手术时间、平均住院时间、术中并发症发生率、术中收缩压标准差及血压变异系数、术后5 d内并发症发生率、术后3个月卒中发生率以及术后脑过度灌注综合征发生率。结果两组间平均住院时间、术中并发症发生率、术后5 d内并发症发生率、术后3个月卒中发生率差异无统计学意义(均P0.05)。全麻组平均手术时间延长(P0.05)。全麻组收缩压标准差[(11.77±1.74)mm Hg]小于局麻组[(17.35±3.39)mm Hg](P0.001),全麻组收缩压变异系数[(10.71±1.05)%]小于局麻组[(12.68±2.35)%](P0.001)。局麻组术后发生脑过度灌注综合征5例,全麻组发生脑过度灌注综合征1例,两组发生率差异具有统计学意义(P=0.047)。结论全麻可降低重度单侧颈动脉狭窄患者支架置入术后过度灌注综合征的发生率,其机制可能在于全麻可以更好的控制术中血压。  相似文献   

7.
经弹力酶和胶原酶联合处理的动脉瘤模型   总被引:4,自引:0,他引:4  
目的 试图建立形态、病理和行为表现都更加逼真的顶端动脉瘤动物模型。方法 采用大白兔8只,将双侧颈总动脉显微吻合重建成为类似于基底动脉顶端的形态,将经过弹力酶和胶原酶处理的动脉段移植到动脉弓的顶端,形成顶端动脉瘤模型。分别于动脉瘤建立后即刻和2周后测量动脉瘤的直径,并于2周后取出动脉瘤及其载瘤动脉进行病理研究。结果 共制作顶端动脉瘤模型8个,1枚动脉瘤模型建立术后24h破裂,1个动脉瘤术后2周破裂。动脉瘤由早期的平均直径(2.0±10.21)mm(n=8)生长到2周后(3.12±0.50)mm(n=6),两者之间有显著性差异。2周后的动脉瘤壁明显薄弱,病理检查发现动脉瘤壁厚度不足正常动脉的1/5,可见炎症细胞浸润。弹力纤维染色和胶原纤维染色显示瘤壁的弹力层和胶原纤维明显减少或消失,仅由薄层的结缔组织构成。结论 移植弹力酶和胶原酶联合处理后的动脉段所建立的顶端动脉瘤动物模型,具有自发生长、破裂的行为表现,形态和病理上与临床动脉瘤更加相似。  相似文献   

8.
目的探讨实验性大鼠动脉瘤形成过程中基质金属蛋白酶2(MMP-2)、基质金属蛋白酶9(MMP-9)的表达规律。方法制作肾性高血压大鼠脑动脉瘤模型,通过免疫组化在蛋白水平系统动态观察肾性高血压大鼠脑动脉瘤形成过程中MMP-2、MMP-9表达的变化。结果实验组在术后1 w脑动脉壁即可见MMP-2、MMP-9表达增加,随着术后时间的推移和大鼠血压的增高,其表达也迅速增加,术后1个月基本达最高峰并一直持续至4个月,其中MMP-9较正常状态的增加比MMP-2的表达增加更为显著。对照组脑动脉壁MMP-2、MMP-9也有微弱表达,且MMP-2表达较MMP-9略强。结论脑动脉壁MMP-9、MMP-2特别是MMP-9的过度表达导致的脑动脉壁胶原纤维及内弹力层破坏是脑动脉瘤形成的主要原因之一。  相似文献   

9.
目的建立一个新型的具有高血压及脑小血管病理改变的脑白质病变(white matter lesions,WMLs)动物模型。方法 13只雄性Sprague-Dawley大鼠,随机分为假手术组(n=6)与易卒中型肾血管性高血压-改良的2VO组(stroke-prone renovascular hypertensive rat-modified 2 vessel occlusion RHRSP/Modified 2VO)(n=7),RHRSP/Modified 2VO组先行双肾双夹术制作RHRSP模型,12周后间隔1周先后夹闭双侧颈总动脉。双肾双夹术后20周对大鼠进行水迷宫试验观察大鼠是否存在空间记忆功能的受损,组织病理学检测观察是否存在脑白质病变及相应的脑小血管病理学改变。结果双肾双夹术后12周,RHRSP/Modified 2VO组7只大鼠收缩压均大于180 mm Hg;水迷宫实验:RHRSP/Modified 2VO组的逃避潜伏期较假手术组明显升高(P0.05),穿越平台次数及原平台象限停留时间比较假手术组明显降低[(2.5±1.05 vs.5±1.67);(28.04%±14.13%vs.49.69%±13.12%)],差异具有统计学意义(P0.05);RHRSP/Modified 2VO组脑白质病变的分级明显高于假手术组(2.17±0.75 vs.0.33±0.52),差异具有统计学意义(P0.05),且RHRSP/Modified 2VO大鼠存在脑小血管的病理改变(小动脉管壁增厚、血脑屏障破坏及静脉胶原沉积)。结论 RHRSP/Modified 2VO是适用的WMLs动物模型,可用于探究WMLs的发病机制及治疗靶点。  相似文献   

10.
目的 探讨吗啡依赖戒断焦虑行为与海马CA1、CA3区突触界面结构和突触素表达变化之间的相关性.方法 剂量递增法建立大鼠吗啡依赖模型,高架十字迷宫检测焦虑行为,透射电镜技术结合图像分析系统、免疫组织化学比较对照组、模型组和治疗组(各6只)大鼠海马CA1、CA3区突触界面结构和突触素(P38)的表达.结果 (1)行为学:模型组开放臂的次数和时间均少于对照组和治疗组[最小有意义差异t检验(下同),P<0.01或P<0.05).(2)突触界面结构:模型组CA1区突触后致密物厚度[(10.7±0.9)nm]、突触活性区长度[(45±4)am]、突触间隙宽度[(3.80±0.30)nm]和突触界面曲率(1.37±0.12)均高于对照组和治疗组(P<0.01或P<0.05);模型组CA3区突触后致密物厚度[(12.7±1.1)nm]、突触活性区长度[(53±8)nm]、突触间隙宽度[(3.81 ±0.59)nm]、突触界面曲率(1.39±0.30)亦均高于对照组和治疗组(P<0.01或P<0.05).(3)突触素表达:模型组CA1、CA3区突触素吸光度(A)值分别为(0.42±0.06)和(0.43±0.05),显著高于对照组(0.2±0.02,0.25±0.03)和治疗组(0.27±0.04,0.26±0.03).结论吗啡戒断焦虑行为与海马CA1、CA3区突触形态结构可塑性及突触素表达水平有一定的相关性.  相似文献   

11.
目的 比较弹性蛋白酶诱导的兔囊状动脉瘤与人颈内动脉眼动脉段动脉瘤的形态学差异.方法 采用弹性蛋白酶诱导的方法制作兔右颈总动脉起始部囊状动脉瘤模型18例,3周后行DSA并三维重建.测量动脉瘤瘤高、瘤宽、瘤颈宽、高径比(AR值)、颈宽角、载瘤动脉直径和载瘤动脉夹角,并与人眼动脉段动脉瘤对应指标进行比较.结果 瘤高:兔动脉瘤组(5.32±1.65 )mm,人眼动脉段动脉瘤组(3.69±1.95) mm.两组差异有统计学意义(P <0.05);AR值:兔动脉瘤组1.34±0.57,人眼动脉段动脉瘤组0.94±0.56,两组差异有统计学意义(P<0.05);兔动脉瘤组与人眼动脉段动脉瘤组的瘤宽、瘤颈宽、颈宽角、载瘤动脉直径和载瘤动脉夹角等差异均无统计学意义(P>0.05).结论 弹性蛋白酶诱导的兔囊状动脉瘤在形态学上与人颈内动脉眼动脉段动脉瘤相似.  相似文献   

12.
目的 探讨核转录因子(NF-κB)的激活及单核细胞趋化蛋白-1(MCP-1)和基质金属蛋白酶-9(MMP-9)的表达及在脑动脉瘤(CA)形成中的作用.方法 新西兰兔24只,雌雄各半,随机分成4组:A组(对照组)、B组(1周组)、C组(2周组)、D组(3周组),每组6只.用弹性蛋白酶(EA)滴注法建立兔右颈总动脉瘤模型,并用CTA和HE染色观察模型动脉瘤的形态及病理变化,同时用免疫组化分析NF-κB、MCP-1和MMP-9蛋白表达,RT-PCR检测其mRNA的表达.结果 (1)1周后实验兔行CTA检查,18只实验兔均发现作用血管段形成明显的梭形或囊性动脉瘤,其中可见血栓形成,并且血管有闭塞现象,正常对照组6只兔未发现动脉瘤样病变.HE染色检查,实验组动脉瘤瘤壁变薄,弹性纤维断裂,最终消失,平滑肌细胞减少萎缩,降解明显,对照组也有少量炎性细胞浸润,但未观察到弹力纤维降解和平滑肌退行性变.(2)对照组免疫组化显示未见NF-κB及MCP-1表达,MMP-9极少量表达,RT-PCR结果显示均见少量表达;实验组NF-κB及MCP-1均于1周时表达达高峰,3周时表达明显降低,MMP-9表达呈逐渐增强趋势.结论 NF-κB的活化可能是脑动脉瘤发生与发展的始动因素之一,MCP-1及MMP-9表达增高在脑动脉瘤发生发展过程中起着重要作用.
Abstract:
Objective To study the effects of nuclear factor Kappa B( NF - κB) , MCP - 1 and MMP -9 at the early phase of cerebral aneurysm(CA). Methods 24 healthy New Zealand rabbits, half female and half male, were randomly divided into 4 groups: group A (control group), group B( 1 week), group C(2 weeks), group D (3 weeks), 6 rabbits per - group. The morphologic change of the right common carotid artery and formation of the aneurysm were detected by CT angiography and HE dyeing. Aneurysm samples were collected, and immunohistochemistry and real - time rolymerase chain reaction ( Real - time PCR)used to detect the expression of the proteinum and mRNA of NF - κB, MCP - 1 and MMP - 9. Results (1) After a week, using CT angiography to detect all the 18 experimental rabbits, all of them have found visible fusiform or cystiform aneurysms where the elastase was dropped, and also found that some vessels were obstructed. Aneurysms have not found in all the control group rabbits. The pathological examination of the experimental aneurysms showed that the wall of aneurysm becoming thinner, the internal elastic layers were disrupted or disappeared and the reduced medial vascular smooth muscle cell becoming atrophy or degradation obviously. Inflammatory cell infiltrate were also observed in the control group, but the internal elastic layers degradation and vascular smooth muscle degeneration were not found. (2) The result of immunohistochemistry and Real - time PCR indicate that NF - kB and MCP - 1 reached the peak at 1 week, and decreased at 3 weeks. MMP -9 was increased gradually. The expression of NF - kB and MCP -1 were not found in control group. Conclusion NF - κB activation may be one of the initiating agents in the development of the cerebral aneurysm. MCP - 1 and MMP - 9 significantly increased in CA that play an important role in the pathogenesis of cerebral aneurysm (CA).  相似文献   

13.
目的 通过简单手术方法建立形态学和组织学上类似人颅内囊状动脉瘤的动脉瘤模型.方法 第一组采用弧形动脉瘤夹临时夹在兔右颈总动脉起始部及部分右锁骨下动脉上,向动脉残腔内注入猪胰弹性蛋白酶溶液消化20 min;第二组使用生理盐水代替胰弹性蛋白酶;第三组弧形动脉瘤夹夹在右颈总动脉起始部上3 mm,胰弹性蛋白酶诱导.结果 第一组成功建立动脉瘤模型,病理显示瘤壁完全缺失弹力层,术后6个月内各观察时期动脉瘤大小差异无统计学意义(P>0.05).第二组和第三组造影检查均形成残端.结论 胰弹性蛋白酶和动脉瘤夹的位置是决定该模型成功的关键.  相似文献   

14.
We experienced 94 unruptured cerebral aneurysms in 80 patients in our clinic between April 1979 and March 1985, and analyzed them in the light of the symptomatological factor, diagnostical factor, significance of aneurysm itself and its treatment. Based on these clinical analysis, unruptured cerebral aneurysms were classified into the following 4 groups; Group 1: intact aneurysm in multiple aneurysms in patients with subarachnoid hemorrhage, Group 2: asymptomatic aneurysm discovered incidentally during the investigation of various diseases other than cerebral aneurysm, Group 3: symptomatic aneurysm with compression or ischemic clinical signs, or subjective symptoms due to aneurysm, Group 4: asymptomatic aneurysm screened by a noninvasive method in healthy humans, or in patients with a risk factor for cerebrovascular diseases, with diseases predisposed to aneurysm, and with minor subjective symptoms unrelated to aneurysm. Group 1 included 36 aneurysms in 31 patients, with internal carotid aneurysms being predominant; the size of 3 mm was most frequently found and those smaller than 10 mm formed in 92%. An operation for aneurysm was performed in 17 patients without operative morbidity and mortality. Among 14 unoperated patients one died of hemorrhage from an unruptured cerebral aneurysm. Indication for operation in Group 1 is determined depending on the patient's severity due to initial SAH. Group 2 was composed of 13 aneurysms in 12 patients; internal carotid aneurysm and anterior cerebral aneurysm, 5 each, being dominant. The size of 3 mm was most frequently seen and all were smaller than 7 mm. An operation was performed in 5 patients all showing a favorable course.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

15.
目的 建立雌激素缺乏的颅内动脉瘤模型,并在此基础上初步研究雌激素缺乏对颅内动脉瘤形成、生长的影响及其可能机制. 方法 雌性Wistar大鼠30只按随机数字表法分为实验组(切除双侧卵巢+颅内动脉瘤模型)、实验对照组(切除双侧卵巢旁与其大小相当的一块脂肪+颅内动脉瘤模型)、空白对照组(每组各10只).大鼠去势模型或腹部假手术模型制作后2周用猪胰弹性蛋白酶滴加到颈外动脉及分叉处动脉壁周围,在颈外动脉距分叉处约1.5 mm位点用两根手术线结扎颈外动脉,在两根线之间剪断颈外动脉,使颈外动脉的盲段形成颈内动脉的一个动脉瘤.动脉瘤模型制作6周后取右心房全血2mL,离心取上清液后于-20℃冰箱保存,用于检测大鼠血清中雌激素的含量,同时游标卡尺测量颅内动脉瘤长度和直径,并取实验组及实验对照组的颅内动脉瘤组织和空白对照组相应的一段颈外动脉组织用于常规组织切片染色. 结果 实验组血清中雌激素水平为(105.00±12.96)pmol/L,实验对照组为(178.50±25.96)pmol/L,空白对照组为(180.40±18.70)pmol/L,实验组与实验对照组及空白对照组组间比较差异有统计学意义(P<0.05).实验组颅内动脉瘤长度扩张率为(131.31±6.63)%,直径扩张率为(125.10±5.49)%,实验对照组为(109.90±3.44)%和(106.82±2.49)%,比较差异有统计学意义(P<0.05).结论 雌激素缺乏对颅内动脉瘤的形成、生长有一定的促进作用.本研究使用肓段法结合酶消化法制作颅内动脉瘤模型简便可行.  相似文献   

16.
In order to elucidate hemodynamic characteristics of the circle of Willis in patients with saccular aneurysms and the causative relationship linking saccular aneurysms and hypertension, branches of the circle of Willis from 21 patients with ruptured aneurysms and of seven normotensive and eight hypertensive controls were histometrically investigated. The 21 aneurysm cases consisted of 12 single, four multiple and five single giant aneurysms. Among these 21 patients, 11 had no clinical history of systemic hypertension. Histometric analysis revealed that the average thickness of the media of the resistance vessels in the circle of Willis in all 21 patients was significantly greater than that of the normotensive control group (P < 0.001), and that the mean thickness of the whole aneurysm group was almost equal to that of the hypertensive control group (t= 0.102). Moreover, the difference between 11 aneurysm patients without clinical history of hypertension and 10 aneurysm patients with clinical history of hypertension was insignificant (t= 1.293). Based on these data, we conclude that an increased local hemodynamic stress with hypertensive alterations of the arterial wall is prerequisite for the development of cerebral saccular aneurysm even in patients without a history of systemic arterial hypertension.  相似文献   

17.
目的 探讨选择性血管结扎法对大鼠脑动脉瘤形成的影响.方法 SD大鼠50只,随机分为3组:(1)A组20只:结扎左侧颈总动脉+两侧肾动脉后支(各侧1支);(2)B组20只:"8"字形结扎左侧颈内、外动脉+电凝并切断两侧肾动脉(各侧只留1个分支);(3)C组为假手术组10只.术后喂养含0.9%的盐及0.12%β-氨基丙腈的饲料.4周后处死,取大鼠脑动脉Willis环,在光镜下观察其病理的变化.结果 A组大鼠ACA/OA分叉处均未见有进展期动脉瘤,仅3个早期动脉瘤样改变.B组大鼠中发现12个进展期动脉瘤和2个早期动脉瘤样改变.C组中未见动脉瘤形成.结论 血管壁结构的破坏或变弱和高血液动力学压力是动脉瘤形成的主要因素.  相似文献   

18.
微血管多普勒在脑动脉瘤夹闭术中的应用   总被引:3,自引:0,他引:3  
目的探讨微血管多普勒(MVD)在脑动脉瘤夹闭术中的应用价值。方法在23例26个脑动脉瘤夹闭前、后,使用MVD对动脉瘤、载瘤动脉和相关穿支动脉检测血流动力学的改变。动脉瘤夹闭后,瘤体内涡流存在时,加强瘤颈的夹闭力,载瘤动脉或穿支动脉血流降低或消失时,改变动脉瘤夹夹闭位置,使载瘤动脉和或穿支动脉的血流恢复至正常。结果所有动脉瘤均检测到涡流或毛刺样血流信号。21个动脉瘤夹闭术后,瘤体内涡流消失,载瘤动脉及其分支血流频谱良好;3个动脉瘤行孤立术后,瘤体内频谱消失,2个巨大动脉瘤行动脉瘤夹闭加清除术。动脉瘤夹闭术中,不完全夹闭2个动脉瘤,4个动脉瘤载瘤动脉血流速度增快,调整动脉瘤夹夹闭位置后,血流速度恢复正常。术后头颅CT示,所有病例无脑梗死。3例眼动脉瘤、2例小脑后下动脉瘤和1例小脑上动脉瘤出院前作DSA检查,动脉瘤消失,载瘤动脉和相关血管无闭塞或狭窄现象。其他病例均作CTA复查,载瘤动脉及周围血管保留良好,动脉瘤消失。结论MVD在动脉瘤夹闭术中是一种安全直接,快速简便和经济有效的监测方法。  相似文献   

19.
目的 探讨微血管多普勒超声(MVD)在颈内动脉瘤手术中的应用.方法 采用探头频率20MHz、直径1.5 mm,对32例颈内动脉瘤患者(共计36个动脉瘤)进行动脉瘤夹闭前后血流动力学监测.术后血管造影进行评估.结果 所有患者均能在动脉瘤顶或瘤体部监测到涡流样或毛刺样血流信号、闻及杂音.动脉瘤夹闭术后即刻监测,发现载瘤动脉狭窄8例,闭塞1例;动脉瘤夹闭不全2例,均经调整瘤夹位置,显示载瘤动脉远段的血流频谱形态和音频信号正常,术后经DSA/CTA证实.以上情况的发生与动脉瘤大小及载瘤动脉有粥样硬化斑块有关.结论 MVD可作为颅内动脉瘤手术的常规检测方法,尤其对瘤颈粗、甚至无明显瘤颈的巨大型动脉瘤手术具有指导意义.  相似文献   

20.
Two pairs of sisters with identical cerebral aneurysms are reported. In the first family, a sibship of three, the two female members presented with subarachnoid haemorrhages from identical, left internal carotid artery bifurcation aneurysms. The subarachnoid haemorrhage occurred in one of the sisters at the age of 20 and at the age of 50 in the other. The remaining healthy sibling, a 40-year-old male, underwent elective cerebral angiography, which was normal. The other sibship, two 48-year-old female identical twins, had identical right middle cerebral artery aneurysms. The first twin became symptomatic after subarachnoid haemorrhage. The aneurysm in her identical twin was identified by screening angiography. There were no verified subarachnoid haemorrhages among the parents and grandparents in either family. No systemic anomalies were identified and collagen type 3 deficiencies were excluded. The identical location of these familial aneurysms, particularly in view of the relatively rare location in the first family, suggests that local factors in the developing vascular tree may play a role in the pathogenesis of saccular aneurysms in addition to systemic anomalies affecting the general structure of cerebral vascular walls.  相似文献   

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