改良光化学法的大鼠大脑中动脉血栓形成模型溶栓评价

目的 评价改良光化学法大鼠大脑中动脉(MCA)血栓形成模型用于溶栓治疗研究的价值。材料与方法 用氦-氖激光和血卟啉衍生物形成大鼠MCA血栓，夹闭双侧颈总动脉60min。电镜动态观察血栓变化，光镜、电镜和MRI动态观察梗死灶的变化。行静脉尿激酶(UK)溶栓试验，手术显微镜下直接观察血栓溶解情况。结果 手术显微镜下见MCA形成闭塞性白色血栓，电镜下为血小板血栓，随时间延长纤维蛋白逐渐增多，至24h有大量纤维蛋白呈网状，与人脑血栓形成的血小板纤维素血栓类似。形成的梗死灶具有可重复性，光镜和电镜特点也与人的相似。血栓可经静脉用UK溶解。结论 改良的光化学大鼠MCA血栓形成模型是较理想的研究溶栓治疗的模型。     

大鼠大脑中动脉血栓形成模型的建立

应用外径约 0 .3mm的导管从大鼠颈外动脉逆行插管至颈内动脉 ,一直到距大脑中动脉 (MCA)起始处 2～ 3mm处 ,注射凝血酶诱导血栓形成。于手术后 3、6、12h观察行为障碍并评分 ,手术后 12h取脑观察Willis环、脑梗死体积及病理改变。结果表明 ,该模型行为障碍和脑梗死体积较为恒定 ,观察Willis环可见MCA起始部血栓形成 ,所形成的血栓是混合血栓 ,脑梗死体积与本研究室应用线栓法建立的大鼠MCA缺血模型的梗死体积无明显差异。该模型操作简便 ,缺血效果可靠 ,梗死部位恒定 ,而且较接近人类脑血栓形成的临床特点 ,适用于评价溶栓治疗效果的实验研究     

大鼠大脑中动脉血栓成模型的建立

应用外径约0．3mm的导管从大鼠外动脉逆行插管至颈内动脉，一直到距大脑中动脉（MCA）起始处2－3mm处，注射凝血酶诱导血栓形成，于手术后3、6、12h观察行为障碍并评分，手术后12h取脑观察Willis环、脑梗死体积及病理改变。结果表明，该模型行为障碍和脑梗死体积较为恒定，观察Willis环可见MCA起始部血栓形成，所形成的血栓是混合血栓，脑梗死体积与本研究室应用线栓法建立的大型MCA缺血模型的梗死体积无明显差异，该模型操作简便、缺血效果可靠，梗死部位恒定，而且较接近人类脑血栓民的临床特点，适用于评价溶栓治疗效果的实验研究。     

一种新型的适用于延迟溶栓治疗的大鼠脑血栓模型的制作

目的 通过对血栓大小的改良,建立适用于延迟溶栓治疗的大鼠脑血栓模型.方法 将10个长度0.8～1.0 mm、宽度0.35 mm的白色血栓经颈内动脉分别注入栓塞脑动脉,形成局灶性脑血栓模型.接受脑血管栓塞的138只SD雄性大鼠被随机分为两大组,分别为单纯缺血组(n=68)和延迟溶栓治疗组(n=70).单纯缺血组不接受任何治疗;延迟溶栓治疗组分别在血栓注入3、6和9 h后,将10 mg/kg的rt-PA自股静脉缓慢注入.使用MRI评价梗死灶的位置、大小、栓塞后不同时间的相对脑血流量.末次MRI检查结束后,大鼠脑组织用4%甲醛固定,作病理检查.结果 共有131只大鼠在血栓注入后脑内形成明确梗死灶,模型成功率为95%,脑梗死仅位于同侧大脑半球占84.7%(111/131),局限于左侧顶叶皮质或(和)左侧基底节的占79.4%(104/131),局灶性脑梗死体积占同侧大脑半球(23.12±6.04)%;对侧大脑半球也同时出现梗死灶占14.5%(19/131).发生局灶性出血11只,大面积出血1只,出血率为9.2%(12/131),均发生在延迟溶栓组.单纯缺血组大鼠,在血栓注入后3、6和9 h的rCBV分别为(34.13±17.55)%、(40.67±25.91)%和(40.72±26.51)%,各组之间rCBV均无显著差异(分别为3 h和6 h,Z=-0.958,P=0.338,3 h比9 h,Z=-1.147,P=0.251).延迟溶栓后成活率高(24 h死亡13只;48 h死亡1只,溶栓后8 d和12 d各死亡1只).结论 改良后的大鼠脑血栓模型是可靠的可重复性的类似于人类大脑中动脉分支栓塞的脑血栓模型,适用于研究延迟溶栓治疗的大鼠脑血栓模型.     

参芪脑保颗粒对光化学诱导的大鼠局灶性脑梗死治疗作用的实验研究

目的 研究中药参芪脑保颗粒对大鼠局灶脑梗死的疗效。方法 采用光化学法制成大鼠局灶脑缺血模型，随机分为对照组、参芪脑保颗粒大、中、小剂量组、溶栓胶囊治疗组、金纳多片治疗组，分别于光照后3h、1、2、3、4d给予灌胃治疗，并观察各组大鼠的体重及神经功能评分变化。第5d处死，用TTC及HE染色观察梗死灶体积及病理改变。结果 参芪脑保颗粒治疗组的体重恢复较对照组及金纳多组快，大、中剂量组的梗死灶体积明显小于对照组(P＜0．001)及金纳多治疗组(P＜0．05)，大剂量组的梗死灶体积小于小剂量组(P＜0．05)，与溶栓胶囊治疗组相比差别不显(P＞0．05)。参芪脑保颗粒治疗组神经元缺血性损伤较对照组及金纳多组轻。结论 参芪脑保颗粒对大鼠局灶脑梗死有治疗作用。     

经皮血栓旋切抽吸术加内支架植入术在下肢动脉闭塞性病变中的应用

目的探讨经皮血栓旋切抽吸术加内支架植入术治疗下肢动脉闭塞性病变的疗效。方法1例右股浅动脉中下段闭塞17d,溶栓3d无效,行经皮血栓旋切抽吸术,开通后残留狭窄70％。术后26h血栓形成,立即溶栓后,再植入内支架。结果通过上述方法,患者右股浅动脉、胭动脉及其以远动脉开放。随访6个月后仍正常。结论经皮血栓旋切抽吸术加内支架植入术对下肢动脉闭塞性病变治疗效果确切。     

脑血栓的微导管溶栓治疗

目的 探讨脑血栓用微导管溶栓治疗的时间、方法及后处理,以提高脑血栓治疗的疗效。资料与方法 本组16例,其中颈内动脉血栓形成5例,大脑中动脉血栓形成8例,椎基底动脉血栓形成3例。从出现症状到溶栓治疗时间：10min 1例,4h1例,6h7例,8h5例,22h2例。15例经CT证实无脑出血。行股动脉穿刺插管选择性动脉造影,明确血栓部位,将微导管超选择插入靶动脉内,采用接触＋贯穿法溶栓。尿激酶用量最大者60万U,最小35万U。结果 颈内动脉和大脑中动脉血栓形成13例,其中11例血栓完全溶解,肌力从0级升至Ⅳ级,肢体运动功能恢复,预后良好;2例血栓不全溶解,动脉造影复查显示靶动脉通畅70％,3d后肌力从0级升至Ⅱ级。3例椎基底动脉溶栓后造影显示2例血栓完全溶解,1例血管复通40％;3例中,1例预后良好,2例死于呼吸衰竭。结论 （1）溶栓时间越早越好,如果能在超梗死期开始溶栓其预后是良好的。（2）接触＋贯穿法溶栓,可加速血栓溶解,缩短脑细胞的缺血时间,提高溶栓效果,同时可明显减少尿激酶的用量。     

颈动脉内膜剥离术后新发脑梗死MRI分布特点

目的分析颈动脉内膜剥离术并发脑梗死的MRI特点及其与交通动脉开放的关系。方法前瞻性分析2016年12月～2017年7月期间的30例CEA术后并发脑梗死MRI特点,包括新发脑梗死的形态、大小、数量及分布等特点。新发梗死灶根据发生部位及血供特点分为手术侧颈动脉供血区梗死与非手术侧颈动脉供血区梗死,后者分为手术对侧前循环及后循环新发梗死。依据DSA和脑超声多普勒观察记录非手术侧颈动脉供血区梗死相应前、后交通动脉开放状态,分析梗死灶来源。采用独立样本t检验分析术前有无临床症状、有无新发梗死灶以及斑块表面形态,对术后新发梗死灶个数的相关性。结果 30例中新发梗死灶共计125个,除1例为片状梗死灶外,其余均为小圆点状或小斑片状梗死灶。30例中,手术侧与非手术侧颈动脉供血区梗死均为21例(70. 0%,30);非手术侧前循环新发梗死16例(76. 2%,21),后循环新发梗死13例(61. 9%,21),并且有9例(42. 9%,21)无手术侧颈动脉区梗死而直接引起非手术侧颈动脉供血区梗死。非手术侧前循环新发梗死16例中,13例发现前交通动脉开放,3例无前交通动脉开放;后循环新发梗死13例中,5例发现相应后交通动脉开放,余8例未发现相应后交通动脉开放。独立样本t检验显示术前有无临床症状、有无新发梗死灶以及斑块的形态与术后新发脑梗死数量没有显著的相关性(均P 0. 05)。结论 CEA术后新发脑梗死病灶小、数量少、分布广、无神经系统症状和体征。CEA术后梗死灶既分布在手术侧颈动脉供血区、也分布于wilis环开放或不开放的非手术侧颈动脉供血区,提示其形成机制的多样性。     

碱性成纤维细胞生长因子对大鼠局灶性脑缺血的保护作用与bax表达

目的 观察动脉内溶栓与碱性成纤维细胞生长因子（bFGF)联合治疗对大鼠缺血性脑梗死面积的影响,并探讨bFGF的保护机制。方法 将50只雄性Wistar大鼠,用血栓栓塞法制备大脑中动脉缺血模型,于缺血4h后随机分为：1、单纯溶栓组;2．溶栓与bFGF联合治疗组。分别在治疗后不同时间点观察大鼠神经功能缺陷的和MRI T2WI显示病变面积的变化,采用免疫组化法检测各时间点bax的表达,结果 在单纯溶栓组,脑缺血再灌注3h时,bax表达开始增加,再灌注12h时达到高峰;与单纯溶栓组比较,溶栓与bFGF联合治疗6h后,MRI T2WI显示病变面积显著缩小（P＜0．05）,bax表达明显减弱（P＜0．05）。结论 bFGF对大鼠局灶性缺血具有保护作用,可降低bax表达,抑制细胞凋亡可能是其作用机制之一。     

脑梗死潜在溶栓治疗时间窗实验研究

目的 观察缺血脑组织动态病理改变,探索大鼠脑梗死潜在溶栓治疗时间窗。方法 采用光镜、电镜、免疫组化、辅以图像分析系统,对大鼠大脑中动脉闭塞（MCAO）后缺血脑组织内神经元、胶质细胞、微血管内皮细胞病理改变及白细胞浸润情况进行动态（MCAO后10min-7d)观察和量化分析。结果 MCAO6h内,缺血脑组织表现为局灶性可逆性病理改变。MCAO12h出现不可逆性病理改变,病变累及整个大脑中动脉供血区。MCAO＜12h组与MCAO≥12h组大鼠脑梗死体积存在显著性差异（t=3.329,P=0.0025)。结论 大鼠大脑中动脉闭塞后,潜在的最长溶栓治疗时间窗为6－12h。     

Post-traumatic cerebral infarction caused by thrombus in the middle cerebral artery

A woman in her 80s was found unconscious after being hit by a car while crossing a road. After admission to hospitals, computed tomography (CT) scans revealed traumatic brain injury (TBI), and the patient was treated symptomatically. However, despite improvement of TBI in CT images, she died unexpectedly. Postmortem CT demonstrated cerebral infarction in the territory of the right middle cerebral artery (MCA). Histopathological examination revealed lumen-obstructing thrombosis and intimal injury upstream of the thrombosis in the right MCA. These findings suggested that the intimal injury in the MCA had led to thrombus formation, and thromboembolism in the region distal to the injury leading to post-traumatic cerebral infarction (PTCI). Both postmortem CT and autopsy were able to reveal the final condition of the deceased, which had not been fully anticipated by the clinicians who had treated her after the accident. The longitudinal antemortem to postmortem course revealed by multiple CT images and the histopathological examination provided crucial clues to the pathogenesis of PTCI in this case.     

超急性动脉闭塞性脑梗塞CT和DSA对比检查研究

目的：了解CT和DSA各自对超急性脑动脉闭塞性脑梗塞的诊断价值及相互之间在影像学方面的关联,方法：10例患者,上均因突发性语一肢体偏瘫,无明显神志障碍,且在发病6h内就诊,所有患者均经神经内科医生检查,疑诊为脑梗塞后先行头部CT扫描,再行DSA检查,并在诊断明确的基础上进行动脉介入栓治疗。结果：2例4级脑动脉分支闭塞患者的CT和DSA检查结果基本相符,5例脑动脉主干闭塞的患者尽管CT发现脑梗塞灶,但其范围明显小于动脉的供血范围;1例DSA见动脉闭塞, 但CT未见低密度改变,1例DSA见动脉闭塞,CT仅见局部脑肿胀改变;1例患者CT和DSA发病6h内检查均为阴性,24h后CT复查见脑梗塞灶。结论：DSA在显示脑动脉闭塞或狭窄方面具有较高的敏感性,CT只是在缺血脑组织的病理变化发展到一定阶段时才能检测出来,尽管如此,我们仍然认为CT是诊断急性缺血性脑梗塞的首选检查方法,DSA只是在进行动脉内介入溶栓治疗时予以使用。     

大鼠超急性脑梗死弥散-灌注磁共振成像的实验研究

目的：应用弥散－灌注磁共振成像技术对改良线栓法制作的鼠大脑中动脉阻塞超急性脑梗死进行实验研究。材料与方法：34只SD大鼠，随机分成5组，其中2只为假手术A组，其余按栓塞时间30分钟，13，6小时分成B，C，D，E4组，A组于2，24小时后，B，C，D＜E组分别于栓塞后30分钟，1，3，6小时以及线栓拔出后2，24小时行弥散和灌注成像扫描。结果：假手术A组弥散，灌注成像无异常信号，实验B，C，D，E组的均见灌注异常信号且范围无变化，弥散高信号区随时间延长而范围增大，6小时后与灌注异常信号区一致。栓塞2小时后T2WI显示高信号。结论：弥散磁共振成像可信号超急性脑梗死灶大小及其演变规律，灌注成像显示脑梗死缺血范围。     

Endovascular Mechanical Thrombectomy of an Occluded Superior Division Branch of the Left MCA for Acute Cardioembolic Stroke

Cardiac embolism accounts for a large proportion of ischemic stroke. Revascularization using systemic or intra-arterial thrombolysis is associated with increasing risks of cerebral hemorrhage as time passes from stroke onset. We report successful mechanical thrombectomy from a distal branch of the middle cerebral artery (MCA) using a novel technique. A 72-year old man suffered an acute ischemic stroke from an echocardiographically proven ventricular thrombus due to a recent myocardial infarction. Intra-arterial administration of 4 mg rt-PA initiated at 5.7 hours post-ictus failed to recanalize an occluded superior division branch of the left MCA. At 6 hours, symptomatic embolic occlusion persisted. Mechanical extraction of the clot using an Attracter-18 device (Target Therapeutics, Freemont, CA) resulted in immediate recanalization of the MCA branch. Attracter-18 for acute occlusion of MCA branches may be considered in selected patients who fail conventional thrombolysis or are nearing closure of the therapeutic window for use of thrombolytic agents.     

LEO stent monotherapy for the endovascular reconstruction of fusiform aneurysms of the middle cerebral artery

We present the case of a patient with a fusiform aneurysm of the M1 segment of the middle cerebral artery (MCA) in which endovascular stent placement without coiling was performed. A 3.5-mm x 25-mm LEO self-expanding stent was deployed along the fusiform aneurysm of the horizontal MCA M1 segment. Digital subtraction angiography showed progressive thrombosis at 6 months and complete thrombosis of the fusiform MCA aneurysm at 12 months.     

一种不开颅的微创家犬局灶性脑梗塞疾病模型

目的 :建立一种适合影像学研究的家犬局灶性脑梗塞疾病模型。材料和方法 :10只健康成年家犬 ,手术组 7只 ,假手术对照组 3只。股动脉插管 ,DSA透视下将导管选择到一侧颈内动脉 ,注入聚氯乙烯酒精颗粒 (polyvinylalcohol,PVA)栓子。假手术对照组除不注入栓子外 ,其他操作步骤同手术组。分别从DSA、MRI、神经功能评分、形态学检查等方面评价模型效果。结果 :手术组动物术后出现不同程度的神经功能缺陷 ,MRI示同侧大脑中动脉区信号改变 ,DSA造影示血管中断。形态学检查出现相应缺血改变。假手术组动物未见异常改变。结论 :该种家犬脑梗塞疾病模型适于影像学及其他亚急性、慢性脑缺血实验研究。     

SWI 在超急性大面积脑梗死中的应用价值

目的：探讨磁敏感加权成像(SWI)在超急性大面积脑梗死中的应用价值。方法连续纳入40例大脑中动脉供血区超急性大面积脑梗死患者,扫描序列包括常规 MRI、DWI、MRA 及 SWI,由2位高年资神经影像医师分析 MRI 图像并记录结果,比较SWI 和常规序列大脑中动脉血栓检出数及 MRA 显示动脉狭窄或闭塞数,比较 SWI 和常规序列显示血栓长度及梗死区静脉增多情况。结果SWI 血栓检出数与常规 MRI 比较有显著差异(23 vs 12,χ2=6.146,P =0.013),与 MRA 比较无显著差异(23 vs 24,χ2=0.052,P =0.820)。2例患者 SWI 同时观察到大脑中动脉主干及分支血栓。SWI 显示血栓长度与常规序列比较有显著差异(25.7 mm±9.4 mm vs 14.6 mm±8.5 mm,t=14.395,P =0.000),SWI 显示脑梗死区静脉增多病例数与常规序列比较有显著差异(21 vs 12,χ2=4.178,P =0.041)。结论SWI 在超急性大面积脑梗死中有较大应用价值。     

Metabolism of 99mTc-ethylcysteinate dimer in infarcted brain tissue of rats.

Brain SPECT with 99mTc-ethylcysteinate dimer (99mTc-ECD) reveals a subacute cerebral infarct as a hypoactive area, even in the presence of postischemic hyperperfusion. The brain retention of 99mTc-ECD depends on hydrophilic conversion mediated by enzymes, and impaired enzymatic trapping is hypothesized to depress the retention efficiency in the infarcted region. The aim of this study was to determine whether the metabolic rate of 99mTc-ECD is actually reduced in infarcted brain tissue. METHODS: In 50 mmol/L phosphate buffer (pH 7.4), 99mTc-ECD was incubated for 30 min with homogenates of rat brain tissue with and without triphenyltetrazolium chloride (TTC) staining. The ratio of polar products was determined by thin-layer chromatography as a function of incubation time, and metabolic rates were obtained. Permanent focal ischemia was induced by occlusion of the right middle cerebral artery (MCA) in rats. The brain was removed 24 h after MCA occlusion, and the infarcted area was defined by TTC staining. The metabolic rate of 99mTc-ECD was determined in homogenates of infarcted tissue, contralateral noninfarcted tissue, and tissue sampled from sham-operated rats. The infarct volume was measured by direct and indirect methods to assess volume expansion caused by edema, and the metabolic rate in infarcted tissue was corrected for the effect of edema. RESULTS: TTC staining had no effect on the metabolic rate of 99mTc-ECD. The metabolic rates in the infarcted tissue were 0.222%/min +/- 0.054%/min and 0.285%/min +/- 0.064%/min before and after correction for edema, respectively. These rates were significantly lower than those in the contralateral noninfarcted tissue (0.426%/min +/- 0.028%/min) and the tissue sampled from the sham-operated rats (0.439%/min +/- 0.031%/min). No substantial difference in rates was observed between the contralateral tissue and the tissue from the sham-operated rats. CONCLUSION: The results of this study showed that infarction decreases the activity of enzymes that mediate the hydrophilic conversion of 99mTc-ECD in the brain and suggest that reduced metabolic activity is related to decreased accumulation of 99mTc-ECD in hyperperfused infarcts.