大鼠大脑中动脉的解剖及其在脑缺血模型中的应用

用４５只大鼠脑标本观测大脑中动脉的起始，行程，分支及分布情况，确定制仡中灶性脑缺血模型血管阻断部位。大鼠的大脑中动脉可分三段，中段相对较长，位置恒定，分支较少，表面骨质较薄，易于凿骨开窗，是制作脑缺血模型阻断血管的最佳部位。     

人参皂甙Rd对大鼠脑缺血后丘脑远隔损害的保护作用研究

目的:探讨人参皂甙Rd(GS-Rd)对大鼠脑缺血后对丘脑远隔损害的保护作用。方法:成年SD雄性大鼠,线栓法制备大脑中动脉堵塞脑缺血模型(MCAO),随机分为假手术组,MCAO脑缺血组(1、3、5 d),GS-Rd治疗组(5 mg/kg、10 mg/kg),每组五只。GS-Rd治疗组的大鼠在MCAO手术前30 min,腹腔注射5 mg/kg或10mg/kg GS-Rd,之后每天腹腔注射相应剂量。观察并记录每组大鼠的体重变化;收集大鼠丘脑组织,采用Miliplex试剂盒法检测炎症因子TNF-α、IL-1β、IL-16的含量变化。结果:MCAO脑缺血组大鼠的体重较假手术组减轻(P0.05),而炎症因子TNF-α、IL-1β、IL-16的含量增多(P0.05);与MCAO脑缺血组相比,给予10 mg/kg剂量GS-Rd治疗组的大鼠体重增加(P0.05),而且炎症因子TNF-α、IL-1β、IL-16的含量减少(P0.05);但5mg/kg剂量组较MCAO组体重无显著变化(P0.05)。结论:GS-Rd(10 mg/kg)可能通过减少炎症因子TNF-α、IL-1β、IL-16的含量,减轻大鼠脑缺血后对丘脑等远隔脑区的损害。     

Wistar大鼠永久性局灶性大脑中动脉阻断脑缺血新模型的建立

在Ｗｉｓｔａｒ大鼠用改良的开颅方法两点阻断大脑中动脉,建立一个新的永久性局灶性脑缺血模型（ＰＭＣＡＯ）。通过大鼠脑梗塞后神经功能状况的观察,明胶－墨汁灌注、ＴＴＣ染色计算机图像分析及病理形态学的方法对模型进行研究评价。Ｗｉｓｔａｒ大鼠大脑中动脉阻断后２４　ｈ,神经功能为２级;模型组梗塞面积稳定,占对侧面积５７±５％,其梗塞灶位于脑皮质和纹状体外侧;病理形态学表现为典型的缺血性改变。结果表明,用本方法阻断大脑中动脉,阻断确切,梗塞灶的大小、位置恒定。这一模型为局灶性脑缺血机制的研究以及治疗药物的疗效观察提供了一个可重复、稳定可靠的动物模型。     

大脑中动脉及分支的研究

随着显微血管外科的普及和提高,为颅内、外动脉吻合术闭塞性脑血管的外科治疗提供形态学资料。作者于1993年11月～1995年10月用成人脑标本,对大脑中动脉的位置、走行、分支类型、口径及吻合进行了观察和测量,并对临床应用意义进行探讨。 材料与方法 用成人50例(男32例,女18例)防腐固定的完整头部和脑标本,去颅后细心地剥离蛛网膜,掰开大脑外侧裂,然后用弯脚规,直脚规,游标卡尺等观察和测量大脑中动脉主干及分支的口径、类     

构建大脑中动脉阻塞脑缺血模型大鼠的类型分析

背景：线栓法造成短暂性大脑中动脉阻塞是研究大鼠局灶性脑缺血普遍使用的模型制作方法。但制作大鼠脑缺血模型的类型存在一定差异,可能导致实验结果的偏差。 目的：分析大脑中动脉阻塞线栓法制作大鼠脑缺血模型的类型及其影响因素。 方法：雄性SD大鼠166只,参照Longa线栓法造模,术后24 h行MRI扫描,根据扫描结果将大鼠分成皮质梗死组、皮质下梗死组及无梗死组,分析造模时线栓插入的深度。 结果与结论：皮质梗死组、皮质下梗死组和无梗死组大鼠的线栓插入深度分别为(19.9±0.9),(19.0±1.1)和(17.7±1.3) mm,皮质梗死组大鼠的线栓插入最深,而无梗死组的线栓插入最浅(P < 0.01)。提示插入深度不同导致的大鼠脑梗死的类型也不同,线栓插入越深,皮质梗死的概率可能越大。     

大脑中动脉分叉处动脉瘤夹闭术中显露大脑中动脉M1段的手术策略

目的 探讨大脑中动脉分叉处(MCBIF)动脉瘤开颅夹闭术中安全显露大脑中动脉M1段的手术策略。方法 回顾性分析2012年3月—2018年3月山西大医院神经外科手术治疗的60例(65个)MCBIF动脉瘤患者的临床资料,其中男29例、女31例,发病年龄35～65(40±0.5)岁。动脉瘤出血Hunt-Hess分级0级3例,Ⅰ级13例,Ⅱ级13例,Ⅲ级16例,Ⅳ级7例,Ⅴ级8例。在冠状位最大密度投影(MIP)图像上观察到,动脉瘤指向上方27个、指向外侧22个、指向下方16个。测量动脉瘤同侧大脑中动脉M1段的长度,观察M1段的曲度,模拟翼点开颅手术入路;采取近端或远端入路手术,指向下方和外侧的动脉瘤从上方显露大脑中动脉M1段,指向上方的动脉瘤从下方显露大脑中动脉M1段,并选择合适的动脉瘤夹夹闭动脉瘤。随访并观察动脉瘤复发情况,预后评价采用格拉斯哥预后评分(GOS),并比较不同指向动脉瘤的预后差异。结果 大脑中动脉M1段长度为8.2～16.5( 13.5±0.3)mm。M1段曲度向下,动脉瘤指向上;M1段曲度向上,动脉瘤指向下;M1段平直向外,动脉瘤指向外。 CTA三维影像模拟手术入路中动脉瘤以及与周围血管的解剖关系与手术中所见解剖结构完全相符。所有动脉瘤夹闭可靠,术后6个月复查头颅CTA未见动脉瘤复发。随访6～36(18.0±2.5)个月,末次随访结果GOS评分:5分37例,4分10例,3分4例,2分3例,1分6例,不同指向动脉瘤的预后良好率比较差异无统计学意义(P＞0.05)。结论 充分利用CTA三维重建技术,明确动脉瘤的指向、大脑中动脉M1段的长度和曲度,精确评估大脑中动脉分叉处动脉瘤和M1段在侧裂内的投影方位,避开动脉瘤顶,采取合适的策略显露M1段,有效做到近端控制,是手术安全进行的可靠保障。     

大鼠大脑中动脉的衰老性变化

目的：观测大鼠大脑中动脉的衰老性变化。方法：在常规光镜、透射电镜下观察,并应用图像分析系统作测量。结果：衰老后,大鼠大脑中动脉管壁厚度几乎无改变,管腔增大;平滑肌细长,内弹性膜变薄、断裂、分层及脂质沉积。结论：高龄大鼠大脑中动脉管壁的形态和超微结构都具有显著的衰老性改变。     

肝细胞生长因子对大鼠大脑中动脉梗塞后凋亡变化的实验分析

目的 探讨大鼠大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型中肝细胞生长因子(hepatocyte growth fac-tor,HGF)对凋亡影响的作用.方法 62只SD大鼠随机分为Sham组、MCAO组及HGF组,MCAO组及HGF组均采取线栓法建立MCAO模型.各...     

MR T1加权像大脑中动脉高信号血管征在急性及亚急性脑梗死中的意义

目的 探讨急性及亚急性脑梗死患者MR T₁WI大脑中动脉高信号血管征(HVS)的临床意义。方法 回顾性分析2013年1月—2015年3月安徽医科大学第一附属医院收治的92例急性及亚急性大脑中动脉供血区脑梗死患者(脑梗死组)的临床及影像学资料,其中男54例、女38例,年龄41～94岁、平均(66.0±13.9)岁;收集同期非脑梗死脑部疾病患者及健康成人34例影像资料为对照组。所有研究对象行MRI平扫,其中脑梗死患者有68例行头颅3D时间飞跃法MRA(3D-TOF MRA)和/或CTA检查。观察所有研究对象MRI T₁WI大脑中动脉HVS,对比HVS阳性组与HVS阴性组患者脑梗死范围、血管病变程度、DWI-Alberta中风早期CT评分(DWI-ASPETS)以及临床表现。结果 对照组34例研究对象T₁WI均未出现HVS。92例脑梗死患者中有43例存在HVS(HVS阳性组),49例无HVS(HVS阴性组);两组间年龄、性别构成及合并基础疾病等一般临床情况比较,差异均无统计学意义(P值均>0.05);但入院时,HVS阳性组患者肌力低于HVS阴性组,差异有统计学意义(Z=1.978,P=0.048)。HVS阳性组平均梗死范围为(4.0±1.1)个脑叶、DWI-ASPETS中评分≤6分者占83.7% (36/43),HVS阴性组平均梗死范围为(2.5±0.9)个脑叶、DWI-ASPETS中评分≤6分占26.5% (13/49),两组比较差异均有统计学意义(P值均<0.01)。68例行MRA和/或CTA检查中,HMCA阳性组35例,其中动脉闭塞占71.4%(25/35),动脉狭窄占28.6%(10/35);HMCA阴性组33例,其中动脉闭塞占45.5%(15/33),动脉狭窄占39.4%(13/33),未见异常占15.1%(5/33);两组间差异有统计学意义(χ²=5.724,P＜0.05)。结论 急性及亚急性脑梗死患者MR T₁WI大脑中动脉HVS征提示动脉闭塞或严重狭窄,该征象可作为患者预后差的指标之一;认识HVS的意义,有助于理解梗死的发病原因,指导临床治疗以及判断预后。     

MR imaging of postischemic neuronal death in the substantia nigra and thalamus following middle cerebral artery occlusion in rats

The goal of this study was to investigate apparent diffusion coefficient (ADC) and T(2) relaxation time (T(2)) in the substantia nigra and thalamus after middle cerebral artery occlusion in rats. In the substantia nigra ipsilateral to infarct, ADC was significantly lower and T(2) was significantly higher on the third and fourth days, but they did not change significantly on the first, second, eighth and 15th days. In the ipsilateral thalamus, ADC and T(2) did not change significantly between the first and fourth days, but were significantly lower on the eighth and 15th days. This combination of MR findings suggested that secondary degeneration in the thalamus was different from that in the substantia nigra.     

Thalidomide protects against ischemic neuronal damage induced by focal cerebral ischemia in mice

We aimed to examine whether thalidomide might inhibit the neuronal damage resulting from focal cerebral ischemia, and if so to explore the neuroprotective mechanism. Focal cerebral ischemia was induced by permanent middle cerebral artery occlusion (MCAO) in mice, and thalidomide was intraperitoneally administered a total of three times (at 10 min before, just before, and 1 h after MCAO). Thalidomide significantly reduced (a) the infarct area and volume at 24 and 72 h after MCAO and (b) the neurological score at 72 h after MCAO. Brains were also histochemically assessed for apoptosis and lipid peroxidation using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining and an antibody recognizing 8-hydroxy-2′-deoxyguanosine (8-OHdG), respectively. Thalidomide reduced both the number of TUNEL-positive cells and the oxidative damage. However, post-treatment of thalidomide [20 mg/kg, three times (at just after, 1 h after, 3 h after MCAO)] did not reduce the infarct volume. In an in vitro study, we examined the effects of thalidomide on lipid peroxidation in mouse brain homogenates and on the production of various radical species. Thalidomide inhibited both the lipid peroxidation and the production of H₂O₂ and O₂ · ⁻ (but not HO⁻) radicals. We also measured the brain concentration of TNF-α by ELISA. The TNF-α level in the brain was significantly increased at 9–24 h after MCAO. However, thalidomide did not reduce the elevated TNF-α level at either 12 or 24 h after MCAO. These findings indicate that thalidomide has neuroprotective effects against ischemic neuronal damage in mice, and that an inhibitory action of thalidomide against oxidative stress may be partly responsible for these neuroprotective effects.     

虫草素对大脑中动脉局灶性脑缺血模型大鼠氧化应激和脑损伤的影响

目的　研究虫草素对大脑中动脉局灶性脑缺血模型大鼠氧化应激指标和脑组织Caspase-3和p53表达的影响。 方法　首先，给药组大鼠每天分别腹腔注射虫草素5、10、20 mg/kg，连续10 d；然后，采用改良Zea Longa线栓法制备大脑中动脉闭塞（middle cerebral artery occlusion，MCAO）模型；造模24 h后，盲法进行神经功能评分，称重法检测脑含水量，HE染色观察脑组织病理损伤，Tunnel染色检测脑细胞凋亡，RT-PCR检测Bcl-2、Bax、Caspase-3和p53 mRNA表达，Western blotting检测Bcl-2、Bax、Caspase-3和p53蛋白表达，试剂盒检测SOD，MDA，GSH水平。 结果　给药组与MCAO组相比，神经功能评分显著降低，脑含水量显著减少，细胞损伤减轻，细胞凋亡率显著减少，Bax mRNA及蛋白表达显著下调，Bcl-2 mRNA及蛋白表达显著上调，MDA含量显著下降，SOD和GSH含量显著上升，Caspase-3和p53 mRNA及蛋白表达显著下调，且这些效果随着虫草素给药量的增加更加显著。 结论　虫草素能够缓解大脑中动脉局灶性脑缺血引起的神经功能障碍和降低脑缺血引起的脑含水量升高，并能抑制大脑中动脉局灶性脑缺血模型大鼠氧化应激和细胞凋亡，从而减缓大脑中动脉局灶性脑缺血造成的损伤。     

用大鼠制作脑缺血模型血管阻断部位的选择

利用 4 5只经墨汁、乳胶混和液灌注的大鼠脑标本 ,观测大脑中动脉的起始、行径及表面投影。大鼠的大脑中动脉可分三段 ,中段较长 ,分支较少 ,表面为蝶骨大翼覆盖。制作局灶性脑缺血模型血管的最佳阻断部位是大脑中动脉中段 ,经蝶骨大翼行颅骨开窗可达此部位     

线栓法大鼠局灶性脑缺血模型制作方法的改进及评价

目的:改进线栓法大鼠大脑中动脉梗死局灶性脑缺血模型的制作方法,并运用多个指标评价该模型的使用价值。方法:采用体质量300～350 g的雄性Wistar大鼠,分成模型组、模型对照组和假手术组。所有动物均采用水合氯醛麻醉,模型组在手术过程中用丝线结扎翼腭动脉,从颈内动脉将直径0.25 mm的渔线插入大脑中动脉起始处,并恢复颈总-颈外动脉血流。结果:模型组成功率为80%,神经缺损症状出现率为100%,24 h存活率为75%。模型对照组成功率为73.9%,神经缺损症状出现率为88.2%,24 h存活率为80%。与假手术组比,模型组及模型对照组大鼠神经缺损评分、脑梗死体积、脑指数、脑含水量及体质量下降率均明显升高。结论:选用体质量均衡的大鼠,采用丝线结扎翼腭动脉,同时不结扎颈总动脉,从而保持颈总-颈内动脉血流畅通,能提高模型成功率和稳定性。     

开颅法制作大鼠局灶性脑缺血再灌注模型的改良研究

目的:改良传统的开颅造模法,建立一种稳定、可靠的大鼠脑缺血再灌注模型。方法:20只SD大鼠随机分为假手术与缺血再灌注组,每组10只,分别行假手术操作及改良模型制作。改良模型为,大鼠开颅后暴露左侧大脑中动脉(middle cerebral artery,MCA),将直径0.12 mm的不锈钢丝放置于MCA下,近其主干,钢丝两端架于颞骨表面120 min,撤去钢丝即再灌注。假手术仅暴露MCA,不进行缺血及再灌注。大鼠再灌注24 h,通过神经功能缺失评分,TTC染色,神经元计数及病理形态学的方法对模型进行评价。结果:改良后的造模成功率为100%,梗死灶位于额、顶叶皮层,病理形态学表现为典型的缺血性改变,正常神经元数减少(P0.01)。神经功能缺失评分1.3±0.5,脑梗死体积比率为5.32%±1.28%,与假手术组相比均有统计学意义(P0.01)。结论:这一改良模型阻断及恢复MCA血流明确,梗死灶的大小、位置稳定,死亡率低,为脑缺血再灌注机制的研究及治疗方法的探讨提供了有益帮助。     

Comparison between coated vs. uncoated suture middle cerebral artery occlusion in the rat as assessed by perfusion/diffusion weighted imaging

Differences among models in the temporal evolution of ischemia after middle cerebral artery occlusion (MCAO) in rats may considerably influence the results of experimental treatment studies. Using diffusion and perfusion imaging, we compared the spatiotemporal evolution of ischemia in Sprague-Dawley rats after permanent MCAO (pMCAO) with different types of sutures. Male Sprague-Dawley rats were randomly assigned to pMCAO produced with either 4-0 silicone coated (n=8), or 3-0 uncoated monofilaments (n=8). Serial determination of quantitative cerebral blood flow (CBF) and apparent diffusion coefficient (ADC) maps were performed up to 3 h after pMCAO. Lesion volumes were calculated by using previously validated thresholds and correlated with infarct volume corrected for edema defined by 2,3,5-triphenyltetrazolium chloride (TTC) staining at 24 h after MCAO. The ADC/CBF-defined mismatch volume in the 4-0 coated suture model was present significantly longer (up to 120 min) compared to the uncoated 3-0 suture model (30 min). The TTC-derived infarct volume was significantly larger in the coated model (290.3+/-32.8 mm(3)) relative to the uncoated model (252.3+/-34.6 mm(3)). This study demonstrates that the type of suture may significantly influence the spatiotemporal evolution of the ADC/CBF-mismatch as well as the final infarct volume. These inter-model variations must be taken into account when assessing new therapeutic approaches on ischemic lesion evolution in the rat MCAO model.     

Neuroprotective properties of prostaglandin I2 IP receptor in focal cerebral ischemia

We and others have identified that inhibition of cyclooxygenase might not be the optimal approach to limiting brain damage after stroke. Now we are investigating the unique properties of the various prostaglandin receptors to determine whether blocking those that mediate toxicity or stimulating those that reduce toxicity will improve neurological outcomes. Here, we determined the respective contribution of the prostaglandin I₂ (PGI₂) receptor in transient middle cerebral artery (MCA) occlusion (tMCAO) and permanent MCAO (pMCAO) preclinical stroke models by using male wildtype (WT) and IP receptor knockout (IP^−/−) C57Bl/6 mice. In addition, we investigated the putative preventive and therapeutic effects of the IP receptor agonist beraprost. The infarct volumes and neurological deficit scores (NDS) were significantly greater in IP^−/− than in WT mice after both tMCAO and pMCAO. Interestingly, beraprost pretreatment (50 or 100 μg/kg p.o.) 30 min before tMCAO and post-treatment (100 μg/kg p.o.) at 2 or 4.5 h of reperfusion significantly reduced the neurological deficit score and infarct volume in WT mice. Post-treatment with beraprost (100 μg/kg p.o.) 4.5 h after pMCAO also significantly decreased neurological deficits and infarct volume in WT mice. Together, these novel findings suggest for the first time that PGI₂ IP receptor activation can attenuate anatomical and functional damage following ischemic stroke.