动脉结扎法诱导大鼠颅内动脉瘤模型的实验研究

目的 运用动脉结扎法诱导大鼠产生颅内动脉瘤，建立一种真实可信的疾病模型。方法 选用S—D大鼠(体重200—300g)40只，实验组30只大鼠同时结扎左侧颈总动脉和双侧肾动脉后支；对照组10只大鼠未给予手术处理。实验组手术一周后，两组动物均以1％盐水替代饮水喂养3个月。取双侧大脑前动脉—眼动脉(ACA-OA)分叉处组织在光镜下进行病理学检查。结果 实验组23只大鼠共发现5个早期动脉瘤改变，其中4个在动脉结扎对侧(右侧)，1个在动脉结扎同侧(左侧)；对照组双侧均未见动脉瘤样改变。结论 该方法诱导的动脉瘤位于颅内，且发病部位、形态与病理改变均与临床颅内动脉瘤十分相似。因此，该方法建立的颅内动脉瘤模型是研究该病发病机理、影响因素及探索药物或基因治疗的理想选择。     

肾血管性高血压大鼠脑动脉瘤模型的建立及发生机制初步探讨

目的 :探讨采用易卒中型肾血管性高血压大鼠建立脑动脉瘤模型。方法 :建立大鼠肾血管性高血压模型 ,再电凝切断左侧颈总动脉 ,然后用光镜和电镜观察右侧大脑前动脉和嗅动脉分叉处及附近的组织学改变。结果 :实验组在 2 0 /2 3只大鼠中可见瘤前、早期及进展期的动脉瘤改变 ,与人类囊状动脉瘤的病理改变相似。结论 :结扎一侧颈总动脉造成血流动力学改变的易卒中型肾血管性高血压大鼠可以作为较理想的脑动脉瘤模型。     

枸杞多糖对颅内动脉瘤大鼠NF-κB信号通路及血管内皮组织炎性损伤的影响

目的 探讨枸杞多糖(LBP)对颅内动脉瘤(IA)大鼠核蛋白因子-κB(NF-κB)蛋白通路及血管内皮组织炎性损伤的影响。方法 取SD雌性大鼠50只,采用切除双侧卵巢并结扎左侧颈总动脉及双侧肾动脉后支以构建IA模型,随机分为IA模型组、LBP低(5 mg/kg)、中(10 mg/kg)、高(20 mg/kg)剂量组,另取10只大鼠,只暴露卵巢、颈总动脉、双侧肾动脉后支,不进行摘除和结扎,作为对照组(Control组); 各组均于手术1周后,开始给药,Control组、IA模型组经灌胃给予生理盐水,LBP各剂量组灌胃给予相应剂量药物,1次/d,共给药30 d; 末次给药12 h后处死,取大鼠血液用酶联免疫吸附法(ELISA)检测血清炎性因子白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)及血管内皮损伤标志物血管内皮生长因子(VEGF)、血管内皮素(ET)水平; 分离取出大鼠脑动脉(Wills)环,在40倍显微镜下检查大脑动脉(Wills)环病理改变,并检测动脉瘤血管壁厚度及动脉瘤体积; 取脑动脉瘤血管组织,用苏木精-伊红染色(HE)检测动脉瘤血管组织病理变化; 蛋白免疫印迹法(Western blot)检测动脉瘤血管组织NF-κB,Toll样受体-4(TLR4)蛋白表达水平。结果 与Control组比较,IA模型组大鼠Willis环上凸起、管壁厚度和肿动脉瘤体积、动脉瘤内皮细胞空泡变性及炎性细胞浸润等病理损伤程度、血清IL-6,TNF-α,VEGF,ET水平、动脉瘤血管组织NF-κB和TLR4蛋白表达水平明显升高(P<0.05); 与IA模型组比较,LBP低、中、高剂量组大鼠Willis环上凸起、管壁厚度和动脉瘤体积、动脉瘤内皮细胞空泡变性及炎性细胞浸润等病理损伤程度、血清IL-6,TNF-α,VEGF,ET水平、动脉瘤血管组织NF-κB和TLR4蛋白表达水平明显降低(P<0.05),且LBP各剂量组上述指标水平呈剂量依赖性降低。结论 LBP可能通过抑制TLR4/NF-κB通路激活、降低炎症反应来减轻IA血管内皮组织损伤。     

诱发鼠大脑动脉瘤的实验模型

1980年京都大学在鼠身上通过(1)β-ancino-propionitrile(一种生山黧豆毒素)(2)结扎双侧肾动脉后支以产生高血压(3)以1%氯化钠溶液作为饮用水4)结扎单侧颈动脉。制作了一个产生脑血管囊性动脉瘤的实验模型。Suzuki证明了他们的发现。有些学者指出,生山黧豆素可能诱发血管壁炎症,不用这种物质而产生的颅内动脉瘤将与人的颅内动脉瘤更相似。作者的研究是为确定一种不用这种物质而诱发颅内动脉瘤的方法,本文将报告鼠的颈动脉端侧吻合结果。材料和方法:5个月雌性Wistar鼠,分成2组,第一组9只结扎两侧肾动脉后支,切断一侧颈总动     

外周血内皮祖细胞数量变化与颅内动脉瘤的生成

背景：动脉内膜损伤是动脉瘤发生的始动因素,内皮祖细胞能修复受损的动脉内膜。 目的：建立大鼠颅内动脉瘤模型,探讨动脉瘤大鼠内皮祖细胞数量变化及意义。 方法：40只SD大鼠随机分为两组,正常组作为正常对照,不给予任何干预。模型组大鼠手术结扎双侧肾动脉后支以及左侧颈总动脉,术后喂食含8%氯化钠鼠粮。于2周,1,2,3个月末测量大鼠内皮祖细胞变化,并与3个月末测量各组大鼠血压及动脉瘤大小,RT-PCR检测willis环相关基因表达。 结果与结论：模型组大鼠内皮祖细胞数目于2周后就开始下降,与正常组比较差异有显著性意义(P < 0.05),一直持续到3个月末(P < 0.01)。模型组大鼠动脉瘤壁基质金属蛋白酶9表达明显高于正常组正常大鼠(P < 0.01),而内皮型一氧化氮合酶明显低于正常(P < 0.05)。结果提示循环内皮祖细胞数量降低可能是动脉瘤生成的一个重要因素。     

骨髓间充质干细胞移植对血管性痴呆大鼠海马胆碱能系统的影响

目的 观察同种异体骨髓间充质干细胞(BMSCs)对血管性痴呆(VaD)模型大鼠海马胆碱能系统的影响.方法 体外分离、扩增大鼠BMSCs,并用BrdU标记.采用双侧颈总动脉结扎法(2-VO)制备VaD模型.将大鼠随机分为3组:A组(BMSCs移植组):于双侧颈总动脉结扎后4周经尾静脉注射BMSCs;B组(对照组):注射同等剂量PBS;C组(假手术组):暴露双侧颈总动脉但不结扎,不进行尾静脉注射.BMSCs注射后4周,采用免疫荧光染色观察大鼠海马BrdU标记细胞;测定海马结构内乙酰胆碱酯酶(ACHE)及胆碱乙酰转移酶(ChAT)的活性.结果 BMSCs移植后4周A组大鼠海马结构可见荧光标记的BMSCs;A、B组AChE和ChAT活性均较C组降低(P＜0.05),且A组较B组显著增强(P＜0.05).结论 静脉移植BMSCs可增强VaD大鼠海马胆碱能系统活性.     

慢性静脉压增高状态下脑微循环的动态研究

目的 研究慢性静脉压增高状态下脑微循环的动态变化。方法 选择Wistar雄性大鼠16只(对照组A n=6;实验组B n=10),全身麻醉下行右侧颈总动脉与右侧颈外静脉端端吻合。利用激光多普勒扫描技术测定吻合前-后以及2周后吻合部结扎前-后脑表25处局部脑血流(ICBF)和局部脑血流量(ICBV)的变化,区域脑血流(rCBF)和区域脑血流量(rCBV)分别用各自的25个数据的中位数表示。A组:单纯右颈总动脉结扎;B组:右颈总动脉与右颈外静脉端端吻合。结果 A组的两侧大脑半球以及B组的左侧大脑半球吻合前后rCBF、rCBV的变化无统计学意义,B组的右侧大脑半球吻合前后rCBF rCBV也无统计学意义,但2周后rCBF显著降低(p<0.05),rCBV显著增高(P<0.05),吻合部结扎后rCBF即刻增高(P<0.05),rCBV即刻降低(P<0.05):结论 一侧颈总动脉-颈外静脉吻合模型对研究慢性静脉压增高状态下脑缺血的研究具有实用价值;在慢性静脉压增高状态下结扎动静脉短路后,脑灌注压迅速上升,CBF得到改善。     

兔皮质引流静脉急性闭塞模型的建立

目的通过双极电凝闭塞皮质引流静脉,建立兔脑皮质引流静脉急性闭塞模型。方法青紫蓝兔35只,随机分为3组,其中A组15只,电凝顶叶皮质引流静脉1支;B组15只,电凝顶叶、枕叶皮质引流静脉各1支;C组(假手术组)5只,仅行开颅加切开硬脑膜处理,3组在造模后8h、24h、48h分别进行DSA检查,脑含水量、脑梗死率和静脉血栓形成率统计,大体标本、光镜对照研究。结果电凝法闭塞兔皮质引流静脉的成功率为100%,造模后经DSA证实所有电凝闭塞的皮质引流静脉已完全闭塞。A、B两组脑组织含水量与C组比较,均有升高(均P0.01),B组造模后8h、24h、48h较A组对应时段脑组织含水量均明显增高(均P0.01)。B组相邻2支皮质引流静脉电凝闭塞后的脑梗死率和静脉血栓形成率较A组均明显增加(均P0.05),假手术组均未见上述异常表现。结论电凝法制作的皮质引流静脉闭塞模型成功率高,稳定性和重复性好,是研究皮质静脉闭塞的理想模型。     

针刺抑制幼鼠HIBD脑组织神经细胞凋亡的实验研究

目的探讨针刺对新生大鼠缺血缺氧性脑损伤(HIBD)脑神经元调亡的保护作用及其机制。方法 (1)选用85只7 d龄清洁级SD大鼠,将大鼠结扎左侧颈总动脉后恢复2 h,置于透明密闭容器中,并入37℃恒温水中以1 L/min的速度通入低氧气体,2.5 h后将动物取出,存活者继续作行为测定,获成功模型72只,随机分为3组,A组为HIBD+针刺Ⅰ组,B组为HIBD+针刺Ⅱ组,C组为HIBD对照组;另设假手术组D组,每组24只。(2)选用幼鼠百会、患侧颞Ⅰ针、内关、曲池、足三里、涌泉,A组于造模后24 h开始针刺,前7 d仅针四肢部穴位,第8天开始加针头部穴位;B组造模后第8 d开始针刺,头、体针同步。针刺均为1次/d,A组连续针刺20 d,B组连续针刺13 d,假手术组干预措施与A组相同,至HIBD后第21天处死取材。采用TUNEL法测定针刺对HIBD大鼠额叶与海马区组织神经元凋亡,用图像分析仪在光镜下计算神经细胞凋亡数目。结果 4组左侧海马CA1区神经元及左侧大脑额叶皮质神经元凋亡数差异有统计学意义(P<0.05),其中D相似文献   

老化血管性痴呆大鼠的制备

目的 探讨老化血管性痴呆大鼠模型的制备方法,使其更接近人类血管性痴呆的病理生理学特点.方法 SD大鼠随机分为两组(正常组6只及模型组17只),其中模型组大鼠D-半乳糖(D-gal)注射4周后行双侧间隔72 h结扎颈总动脉,6周后观察大鼠脑内有无梗死灶形成.正常组大鼠常规饲养,未做结扎.术后6周检测两组大鼠水迷宫试验、事件相关诱发电位潜伏期、海马区锥体细胞和突触素密度.结果 模型组大鼠死亡率较低,脑内未见明显梗死灶,但认知功能较正常组大鼠有显著的损害(P＜0.05),海马区锥体细胞排列紊乱,数目显著减少(P＜0.05),突触素密度也显著下降(P＜0.05).结论 D-gal加双侧间隔颈总动脉结扎法成功复制的大鼠痴呆模型更接近人类血管性痴呆病理生理学特点,且模型死亡率低.     

Involvement of internal elastic lamina in development of induced cerebral aneurysms in rats

To elucidate the role of the internal elastic lamina in the development of cerebral aneurysm, the bifurcation of the anterior cerebral artery and olfactory artery was histologically studied in control and experimental rats treated with unilateral carotid ligation and renal hypertension. Various stages of aneurysm formation were compared, and it was found that early aneurysmal changes were always present just distal to the apical intimal pad on the anterior cerebral artery side. The internal elastic lamina was thinned and fragmented just distal to the pad even in the very early stage of aneurysm formation when the medial layer was still present. In control rats, the internal elastic lamina had a tendency to thin and fragment at the site where aneurysms would develop in experimental rats. Our study shows that changes of the internal elastic lamina were present just distal to the pad even in control rats, which never develop cerebral aneurysms. Under hemodynamic stress augmented by experimental treatments, further degenerative changes of the internal elastic lamina and involvement of the medial layer are considered to occur and result in aneurysm formation there.     

Expressions of PDGF-B and collagen type III in the remodeling of experimental saccular aneurysm in rats

The essential etiologic factors of intracranial berry aneurysm may be the hemodynamic stress on the arterial wall. Vascular remodeling triggered by abnormal hemodynamic stress on the blood vessels may play an important role in the formation, development and rupture of intracranial aneurysms. However, the specific causative mechanisms associated with this remain elusive. In this study, we look for the possible mechanism of platelet-derived growth factor B (PDGF-B) on the pathogenesis of saccular aneurysms in rats. Direct microsurgical destruction of the arterial intima and internal elastic lamina at the bifurcation of the carotid artery was performed in 30 rats to induce saccular aneurysms and the contralateral carotid arteries were ligated in half of them. After 4-5 months, the size of the aneurysms was determined. The expressions of PDGF-B and collagen type III on the walls of the normal carotid arteries and the saccular aneurysms were determined by in situ hybridization and immunohistochemistry. Saccular aneurysms could be induced immediately by destroying the intima and internal elastic lamina at the bifurcation of the carotid artery in rats. Saccular aneurysms grew significantly due to the hemodynamic stress in 4-5 months, and much bigger after the ligation of the contralateral carotid artery which enhanced the hemodynamic stress. There was no PDGF-B expression on the walls of the normal carotid arteries in rats, but it was expressed on the aneurysmal walls and more distinctly with the growth of the saccular aneurysms. However, there was collagen type III expression on the media of the normal carotid artery, but its expression decreased on the aneurysmal walls and further reduced with the growth of the saccular aneurysms. So, PDGF-B may induce the expression of MMP for the degradation of collagen type III on the wall of the saccular aneurysms. This may be one of the important mechanisms on the pathogenesis of the saccular aneurysm.     

A case of symmetrical aneurysms at the bilateral middle cerebral arteries associated with the deep seated arteriovenous malformation in the midline]

A case of symmetrical aneurysms at the bilateral middle cerebral arteries (MCA) associated with the deep seated arteriovenous malformation (AVM) in the midline was presented. Because symmetrical aneurysms at the MCA are 1.17% of all aneurysms, and those associated with the deep seated AVM in the midline are very rare. A 75-year-old female suffered from a sudden onset of a severe headache and a loss of consciousness, and was admitted to our department on June 14, 1996. Computed tomography(CT) showed a subarachnoid hemorrhage (SAH) in the right sylvian fissure (Fisher's Group 4). Bilateral symmetrical MCA's aneurysms and the deep seated AVM were clarified by angiography. The symmetrical aneurysms stood out anterior lateral side and the right aneurysm had bleb. On the other hand, the afferent vessels of the AVM were the branches of bilateral posterior cerebral arteries, and the efferent vessel was the vein of Galen. So we determined SAH due to right MCA aneurysm, and performed the neck clipping of the ruptured aneurysm. The symmetrical aneurysms at the MCA associated with AVM in midline have not been reported. Each parent's artery was not connected each other. These origins, therefore, are suggested to be related not only to acquired factors like hypertension, hemodynamic stress etc, but also to a congenital factor. The origin of the saccular aneurysm is suggested congenital either but it isn't definite.     

椎基底动脉瘤的手术治疗

目的 探讨手术治疗椎基底动脉瘤的方法.方法 26例28个椎基底动脉瘤患者.动脉瘤破裂出血9例;16例基底动脉瘤,10例椎动脉瘤.5例基底动脉顶部动脉瘤经翼点入路,5例基底动脉顶部和2例基底动脉上段动脉瘤用额颞颧(切断颧弓、扩大中颅窝底)入路,4例基底动脉中段动脉瘤采用乙状窦前(岩骨)和远外侧联合入路.10例椎动脉瘤中,4例椎动脉瘤采用乙状窦前(岩骨)和岩骨联合入路,6例取用远外侧-枕骨髁联合入路.11例术中临时阻断血管时间延长或可能影响开通血管患者行血管搭桥术,其中颈内动脉大脑后动脉P2段移植搭桥2例,颈外动脉与大脑后动脉P2段移植搭桥4例,椎动脉移植搭桥2例,枕动脉与小脑后下动脉搭桥3例.结果 术后恢复正常工作,无神经功能障碍者:基底动脉顶端动脉瘤9例,基底动脉干动脉瘤5例,椎动脉瘤10例,良好率为92%.1例基底动脉顶端动脉瘤患者术后有严重神经功能缺失,生活不能自理;1例基底动脉主干动脉瘤术后穿通动脉闭塞引起中脑缺血,术后20 d死亡.结论 选择适合的颅底手术入路有利于术中获得充分的手术操作空间.对于单纯手术夹闭困难的动脉瘤,用血管移植搭桥的方法,可以避免因夹闭动脉瘤和临时阻断载瘤动脉出现术后脑缺血.     

ANNOTATION: AN ANIMAL MODEL OF CEREBRAL ANEURYSMS

Cerebral aneurysms were induced experimentally in rats by ligating the common carotid artery on one side, making the animals hypertensive, and feeding them the lathyrogen beta-aminopropionitrile. On analysis of this experimental model, haemodynamic stress, hypertension and metabolic disorder of the connective tissue proved to be of primary importance as aetiological factors in the development of cerebral aneurysms. The experimentally induced cerebral aneurysms resemble those in man both in location and in microscopic structure; they can thus be regarded as a good model for the study of the pathogenesis of cerebral aneurysms. The initial changes leading to the formation of aneurysms occurred on the distal side of major artery branches adjacent to the apex, but distal to the intimal pad. It is proposed that degenerative changes in the internal elastic lamina and muscle cells of the media, caused by haemodynamic stress at vessel branches and intimal pads, are the basis for aneurysm formation.     

Multiple aneurysms associated with bilateral carotid occlusion and venous angioma: surgical management risk-case report.

A unique case of multiple aneurysms associated with bilateral carotid artery occlusion and venous angioma is described. A 42 year old female presented with subarachnoid haemorrhage. Cerebral angiograms demonstrated(1) a ruptured saccular aneurysm in the right posterior cerebral artery,(2) bilateral occlusion of internal carotid arteries,(3) a rete mirabile in the subtemporal fossa fed by left external carotid artery which connected with the internal carotid artery at the cavernous portion where a saccular aneurysm had formed, and(4) a venous angioma in the posterior fossa. The ruptured aneurysm of the posterior cerebral artery was obliterated preserving the anterior choroidal arteries. However, a left hemiparesis developed and CT scan revealed a small low density area in the right posterior limb of the internal capsule postoperatively. A ruptured aneurysm associated with bilateral extracranial carotid occlusion poses a clinical dilemma and treatment of such cases is challenging and difficult. The non-surgical and surgical outcomes of ruptured cerebral aneurysms associated with internal carotid occlusion are reviewed.     

脑动脉瘤模型制作及高血压对其影响的实验研究

目的 建立脑动脉瘤动物模型并初步探讨高血压对脑动脉瘤的影响.方法 45只雄性SD大鼠按随机数字表法分为高血压组、正常血压组和正常对照组.高血压组行脑动脉瘤模型制作+双侧肾动脉狭窄术:正常血压组只建立脑动脉瘤模型:正常对照组不予任何处理.各组在术前,术后6周、12周三个时间点分别测量各组大鼠动脉收缩压.术后12周测量脑动脉瘤大小,并灌注固定,取脑动脉瘤部位血管组织,应用HE染色、Van Geson染色和Verhoeff染色进行病理检查.结果 高血压组在处死前血压明显升高[(197.48±15.44)mm Hg],与手术前的血压[(104.40±14.70)mm Hg]相比差异有统计学意义(P<0.05);处死前脑动脉瘤的长度[(2.38±0.31)mm]和宽度[(1.89±0.35)mm]与脑动脉瘤制作完成时的长度[(1.62±0.18)mm]和宽度[(1.36±0.09)mm]相比差异有统计学意义(P<0.05);正常血压组和正常对照组无明显变化.病理检查显示高血压组血管内膜消失,弹力层完全断裂;正常血压组尚存部分弹性纤维;正常对照组血管组织无改变.结论本实验采用的脑动脉瘤模型稳定性好,制作方便,具有与人类脑动脉瘤相似的形态和病理结构.高血压对脑动脉瘤的弹力蛋白和胶原蛋白有明显影响,是影响脑动脉瘤增大的重要因素之一.     

Kissing aneurysms of the distal anterior cerebral artery

Kissing aneurysms, a particular type of multiple aneurysm are rare. A kissing aneurysms was identified at the distal anterior cerebral artery (ACA) in a 59-year-old male patient diagnosed with subarachnoid hemorrhage (SAH). The use of three-dimensional intracranial CT angiograms revealed that kissing aneurysms (that is, an aneurysm with a bilateral symmetrical mirror image) were located at the distal ACA and diffuse SAH in basal, sylvian, and interhemispheric cisterns. Both conventional carotid angiograms showed that both distal ACA aneurysms were seen separately on both internal carotid angiograms. Two aneurysms were observed simultaneously on carotid compression of either side. Some particular cautions required in diagnosing and treating kissing aneurysms are discussed, together with a literature review.     

An acute experimental model of saccular aneurysms in the rat

A new and reproducible saccular aneurysm model has been developed at the bifurcation of the common carotid artery in rats. The details of the experimental methods and results are described. It is strongly suggested that the internal elastic lamina is a critical layer in saccular aneurysm formation, because an experimental saccular aneurysm can be produced immediately by transluminally damaging the inside of the arterial wall at the bifurcation of the common carotid artery. This saccular aneurysm model has several advantages: (i) it can be induced quickly and the success rate approaches 100% in rats; (ii) this technique can produce satisfactory experimental saccular aneurysms for other aneurysm studies, and in the future it will also be possible to use this technique to produce experimental saccular aneurysms in cerebral arteries of large animals.