一种氯化铁诱导血栓生成的小鼠大脑中动脉远端缺血模型

目的 建立稳定的小鼠大脑中动脉远端氯化铁血栓模型，评价其造成的脑损伤及神经功能损伤程
度。
方法 C57BL6/J雄性小鼠随机分为脑缺血组和假手术组。脑缺血组用10%氯化铁（ferric chloride，
FeCl3）溶液诱导右侧大脑中动脉远端形成血栓。在术前、术后10 mi n、术后1 d和7 d观测术侧脑血流
和手术动脉血流量的变化。术后1 d观察脑组织梗死率。术后1 d、3 d、5 d、7 d用3种神经学评分[改良
加西亚评分（modified Garcia score，mGS）、改良神经损伤严重程度评分（modified neurological severity
scores，mNSS）和15分神经学评估表（15-point neurological evaluation scale，NES）]和胶黏纸测试评价小
鼠神经功能。术后7 d免疫荧光染色标记神经细胞核观察脑组织损伤，标记CD16/32、CD206和Iba1观
察胶质细胞表达。
结果 与假手术组相比，脑缺血组术后10 mi n、1 d、7 d脑表面血流和手术动脉血流下降，术后1 d脑
皮层梗死明显，术后7 d仍有明显脑组织损伤；脑缺血组术后1 d、3 d、5 d和7 d时3种神经学评分及胶
黏纸测试均提示小鼠神经功能不同程度损伤。术后7 d脑缺血组梗死周围皮层M1和M2型胶质细胞表
达增加。
结论 FeCl3溶液可诱导形成稳定的小鼠脑缺血模型，该模型可造成手术侧大脑中动脉远端及脑表
面血流量降低，皮层脑梗死，小鼠神经功能受损，梗死周围胶质细胞表达上调。本研究建立了稳定
氯化铁诱导血栓形成的小鼠脑缺血模型，为脑血栓形成和抗栓药物治疗提供了一种可靠的研究工
具。     

一种改进的更为稳定可靠的远端大脑中动脉闭塞模型

目的 建立一种稳定可靠的脑缺血研究模型.方法 (1)远端大脑中动脉闭塞(dMCAO)模型的制作:SD大鼠(270～350 g),异氟烷麻醉,永久阻断左侧大脑中动脉远端并夹闭双侧颈总动脉30 min即制作成功dMCAO模型.(2)模型的评定:分别于术后10 h行PET扫描、术后24 h行MRI扫描;术后48 h行TTC染色进行梗死面积的评定;分别于术前,术后1、2、7、10、14、21、30、37、44、51、60 d进行行为学评定;CV染色评定细胞受损情况;并计算死亡率.结果 MRI测定梗死面积为45.30%±2.35%(95%可信限:42.94～47.86),TTC测得梗死面积为43.39%±2.33%(95%可信限:40.94～45.84),PET测得缺血面积为54.50%±3.15%(95%可信限:49.49～59.51).术后60 d CV染色测得梗死面积为30.10%±2.22%(95%可信限:28.05～32.15),行为学评定:基线评分两组无差异,60 d总评分差异有统计学意义,在术后各时间点梗死组与对照组相比差异也有统计学意义.模型制作过程中无个体排除,无死亡.结论 30 min一过性阻断双侧颈总动脉加永久性阻断左侧大脑中动脉远端所产生的dMCAO模型稳定、可靠,适用于脑缺血研究.     

大鼠自体血栓大脑中动脉闭塞模型的改良

目的 进一步改良大鼠自体血栓大脑中动脉闭塞（MCAO）模型。方法 通过神经功能缺损评分，MRI，TTC染色，墨汁染色和病理观察。对改良血栓和普通血栓的栓塞效果进行比较。同时对不同体重大鼠对血栓直径的要求进行了观察。结果 6个改良血栓可形成与12个普通血栓相同的MCAO，两组之间神经功能缺损评分，梗死面积无显著性差异。结论 改良后保证了Willis环后半部的完整；动物不需两次手术，使操作时间明显缩短，使模型推广成为可能。     

大脑中动脉高密度征与磁敏感血栓征对大脑中动脉闭塞比较研究

目的比较研究大脑中动脉高密度征(HMCAS)和磁敏感血栓征(SVS)显示大脑中动脉(MCA)闭塞血栓的差异。方法回顾性分析41例临床及影像证实MCA近段闭塞急性脑梗死患者CT及MRI(包含SWI及MRA序列)影像资料。分析HMCAS、SVS显示责任血管血栓灵敏度、特异性、阳性预测值、阴性预测值及其相关性。结果 41例MCA区域急性脑梗死患者中,MRA显示27例同侧MCA近段闭塞,SWI显示21例SVS,CT显示22例HMCAS。HMCAS、SVS显示责任血管血栓灵敏度(78%,78%)、特异性(93%,100%)、阳性预测值(95%,100%)、阴性预测值(68%,70%)。在所有患者中,HMCAS与SVS对预测MCA近段是否闭塞具有高度的一致性(κ值分=0.853);在MRA证实MCA近段闭塞患者中,HMCAS与SVS有无对预测MCA近段是否闭塞具有良好的一致性(κ值分=0.786)。结论 HMCAS、SVS在显示MCA近段血栓具有较好的灵敏度及高度的特异性,并且两者之间具有良好的一致性。     

建立大鼠可逆性大脑中动脉闭塞的局灶脑缺血模型

通过应用４－０单股尼龙外科线沿颈内动脉进入颅内阻断大鼠大脑中动脉血流，制成大鼠短暂性局灶脑缺血模型。大鼠大脑中动脉阻塞后，均出现各种神经病学征象。氯化三苯四氮唑染色能清楚地显示梗塞范围。光镜和电镜观察大鼠短暂性局灶脑缺血后的病理变化，结果显示细胞超微结构的病理损害在电镜下可被观察。该实验表明此模型是比较理想的短暂性局灶脑缺血模型。     

完全血栓化的大脑中动脉动脉瘤2例报告并文献复习

目的探讨完全血栓化的大脑中动脉动脉瘤的临床特征及治疗方式。方法回顾性分析2例完全血栓化的大脑中动脉动脉瘤患者的临床资料,并对相关文献进行复习。结果本组2例患者均为中年女性,表现为头痛(不剧烈)和发作性头晕。经头颅CT、MRI和DSA检查诊断为完全血栓化的大脑中动脉动脉瘤;予以观察随访。结合文献复习,完全血栓化的颅内动脉瘤以女性多见,首发症状多为头痛,均为未破裂动脉瘤,多发于大脑中动脉。其术前易误诊为颅内海绵状血管瘤或肿瘤等,多采用动脉瘤孤立切除或血管重建术治疗。结论完全血栓化的大脑中动脉瘤易与颅内海绵状血管瘤等相混淆。当病灶位于动脉主干或分支远端时,应高度考虑完全血栓化的动脉瘤存在;若其无占位效应,则以观察为主,定期随访复查。     

犬大脑中动脉栓塞时动脉静脉溶栓治疗的对比研究

目的 对比性探讨尿激酶在犬大脑中动脉急性栓塞时动脉与表解雇溶栓治疗的疗效。方法 建立犬自体血栓大脑中动脉栓塞（ＭＣＡＯ）模型,血管造证实大脑中动脉（ＭＣＡ）完全阻塞后３小时,经ＭＣＡ注射尿激酶或静脉滴注尿激酶,监测各时相点的静脉凝血象变化,治疗后９６小时进行病理学评定。结果 动脉溶栓组的平均ＭＣＡ系统残留血栓重量极显著低于对照组和静脉溶栓组,动脉溶栓组的脑梗死容积亦小于其他两组。结论 犬急性缺血性     

超声评价法优化三氯化铁诱导大鼠颈总动脉血栓模型的研究

目的探讨采用连续超声评价法优化不同三氯化铁浓度梯度和作用时间诱导大鼠颈总动脉血栓模型,为溶栓及取栓研究提供合适的在体血栓模型。方法选取20只(Sprague–Dawley)SD大鼠,每组5只,分别采用20%、30%、40%、50%四种三氯化铁浓度外敷大鼠单侧颈总动脉,使用14 L高频超声探头,分别在外敷10min、15 min、20 min三个时间点观察血管二维超声图像及彩色多普勒血流情况。选取血管闭塞最佳组大鼠,于干预120 min后观察血管自发再通率及静脉注射尿激酶后的血管再通率。实验结束后,取出干预血管甲醛固定,石蜡包埋,切片,进行HE染色病理分析。结果三氯化铁外敷大鼠颈总动脉20 min、50%浓度组血管闭塞率100%,40%、30%、20%浓度组外敷20 min血管闭塞率分别20%、0%、0%(P0.001)。外敷120 min后,50%浓度组组血管自发再通率0%、40%、30%、20%组血管自发再通率100%(P0.001),50%三氯化铁浓度造模组尾静脉注射尿激酶后血管部分再通率为40%。50%浓度组镜下病理显示血栓结构致密,尿激酶干预后管腔部分再通,血栓结构松散。结论采用50%三氯化铁浓度外敷大鼠颈总动脉20 min,可能是在体血栓模型形成的有效条件,该动物模型可能适合溶栓研究。     

猫大脑中动脉闭塞后缺血脑组织早期葡萄糖代谢的研究

目的 通过正电子发射体层摄影术（PET）检查,了解猫大脑中动脉闭塞（MCAO）后缺血区脑组织葡萄糖代谢的变化。方法 经眶电凝猫左侧MCA,制成永久性局灶性脑缺血模型,在电凝MCA前15min,静脉注射18氟化脱氧葡萄糖（fluorine-18-fluorodeoxyglucise,^18FDG),MCAO后15min,1h,3h及6h分别行^18FDG-PET数据采集,并与对照组及对侧相应区域比较,以了解MCAO早期缺血脑组织葡萄糖代谢的变化;同时行神经功能评分及病理学检查,以证实梗死范围,结果 脑缺血后,左侧MCA皮层分布区的葡萄糖代谢明显增高,且随着时间的延长该代谢增高区逐渐集中;病理检查证实,该代谢增高区与缺血区相一致,其最后的浓聚区即为坏死中心区。结论 脑缺血后,脑组织缺血区早期出现葡萄糖代谢增高现象,与以往报道的脑缺血PET的实验结果相反。     

Distal Middle Cerebral Artery M4 Aneurysm Surgery Using Navigation-CT Angiography

Unruptured non-traumatic dissecting aneurysm in the M4 segment of the middle cerebral artery (MCA) accompanied by complete occlusion of the ipsilateral internal cerebral artery (ICA) has never been reported. A 41-year-old man presented with an infarction manifesting as left-sided weakness and dysarthria. Magnetic resonance angiography revealed a subacute stage infarction in the right MCA territory and complete occlusion of the right ICA. Angiography demonstrated aneurysmal dilatation of the M4 segment of the right MCA. Surgery was performed to prevent hemorrhage from the aneurysm. The aneurysm was proximally clipped guided by Navigation-CT angiography and flow to the distal MCA was restored by superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis. We report this rare case with literature review.     

大脑后动脉偏侧优势对同侧大脑中动脉病变卒中严重程度及预后的影响

目的探讨同侧大脑后动脉偏侧优势(posterior cerebral artery laterality,PCAL)对同侧大脑中动脉(middle cerebral artery,MCA)M1段严重狭窄或闭塞后急性卒中患者梗死范围、卒中严重程度和短期预后的影响。方法于2010年1月-2015年11月,前瞻性连续性纳入郑州大学第一附属医院MCA M1段严重狭窄(狭窄率70%~90%)或闭塞的161例急性缺血性卒中患者,根据患者有无PCAL分组,比较两组临床基线资料及3个月随访改良Rankin量表(modified Rankin scale,mRS)评分的差异。结果 161例患者中共76例PCAL阳性,85例PCAL阴性。PCAL阳性组既往卒中者少(P=0.021),基于弥散加权成像的Alberta卒中项目早期CT评分(diffusion weighted imaging-Alberta Stroke Programme Early CT Score,DWI-ASPECTS)更高(P=0.045),出院时美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分更低(P=0.009),3个月mRS评分更低(P=0.002),临床短期预后更好,差异有显著性。多因素Logistic回归分析可见,入院NIHSS评分[OR(odds ratio)1.266,95%CI(confidence interval)1.139~1.407,P0.01]是预后不良的预测因子,PCAL阳性(OR 0.355,95%CI 0.146~0.864,P=0.022)是预后良好的预测因子。结论 MCA M1段严重狭窄或闭塞的急性缺血性卒中患者,PCAL阳性者梗死范围更小,短期临床预后更好。     

动脉硬化性大脑中动脉狭窄或闭塞所致脑梗死类型

目的探讨动脉硬化性大脑中动脉狭窄或闭塞性疾病(MCAOD)所致脑梗死的类型。方法对50例经颅脑MRA或DSA确诊的症状性MCAOD患者进行研究,依据其头部弥散加权成像(DWI)和T2W的改变对脑梗死分型。结果50例患者共发现57条动脉硬化性大脑中动脉狭窄或闭塞,未发现病灶的有6(占12．0%)个大脑半球,多发性脑梗死和单发脑梗死分别见于13(占22．8%)个和38(占66．7%)个大脑半球。脑分水岭梗死、流域性脑梗死、半卵圆区脑梗死、多发性散在点状脑梗死(MSSI)、腔隙性脑梗死分别见于18(占31．6%)个、12(占21．1%)个、6(占10．5%)个、2(占3．5%)个和1(占1．8%)个大脑半球。结论MCAOD可引起各种类型的脑梗死,脑分水岭梗死约占1/3,动脉粥样硬化性血栓形成约占1/5,纹状体内囊梗死约占1/5,主要发病机制与动脉-动脉栓塞和低灌注有关。     

长期大脑中动脉闭塞后远隔部位MAP—2和GFAP变化

目的 :探讨长期MCAO后丘脑、黑质网状部 (SNr)微管相关蛋白 2和胶质纤维酸性蛋白的变化。方法 :3 5只SD大鼠分为 7组 ,每组 5只。Tamura法制作动物模型。脑切片分别用鼠脑MAP 2、GFAP抗体 ,ABC法染色。观察丘脑的面积改变 ,SNr面积和长度的改变 ;SNr神经细胞和胶质细胞数的变化。结果 :丘脑面积逐渐缩小 ;SNr面积长度及神经细胞减少 ,胶质细胞增加。脑缺血后 1个月MAP 2减少 ,GFAP增加 ,6个月GFAP丝极消失。结论 :神经细胞减少和胶质细胞增加可能是长期MCAO后丘脑和SNr萎缩的基础     

Accumulated Mannitol and Aggravated Cerebral Edema in a Rat Model of Middle Cerebral Artery Infarction

Objective

Repeated administration of mannitol in the setting of large hemispheric infarction is a controversial and poorly defined therapeutic intervention. This study was performed to examine the effects of multiple-dose mannitol on a brain edema after large hemispheric infarction.

Methods

A middle cerebral artery was occluded with the rat suture model for 6 hours and reperfused in 22 rats. The rats were randomly assigned to either control (n=10) or the mannitol-treated group (n=12) in which intravenous mannitol infusions (0.8 g/kg) were performed six times every four hours. After staining a brain slice with 2,3,5-triphenyltetrazolium chloride, the weight of hemispheres, infarcted (IH) and contralateral (CH), and the IH/CH weight ratio were examined, and then hemispheric accumulation of mannitol was photometrically evaluated based on formation of NADH catalyzed by mannitol dehydrogenase.

Results

Mannitol administration produced changes in body weight of -7.6±1.1%, increased plasma osmolality to 312±8 mOsm/L. It remarkably increased weight of IH (0.77±0.06 gm versus 0.68±0.03 gm : p<0.01) and the IH/CH weight ratio (1.23±0.07 versus 1.12±0.05 : p<0.01). The photometric absorption at 340 nm of the cerebral tissue in the mannitol-treated group was increased to 0.375±0.071 and 0.239±0.051 in the IH and CH, respectively from 0.167±0.082 and 0.162±0.091 in the IH and CH of the control group (p<0.01).

Conclusion

Multiple-dose mannitol is likely to aggravate cerebral edema due to parenchymal accumulation of mannitol in the infarcted brain tissue.     

无症状大脑中动脉闭塞的临床研究

目的 探讨无症状大脑中动脉闭塞患者的临床和影像学特点.方法 回顾性分析2016年1月-2019年1月连续住院并行头颅MRA检查患者的临床及影像学资料,选择无症状性大脑中动脉主干闭塞患者作为研究对象,分析其临床和影像学特点.结果 研究共筛查3967例行头颅MRA检查的患者,其中无症状大脑中动脉闭塞者23例(0.58％),...     

External Carotid Artery Angioplasty and Stenting Followed by Superficial Temporal Artery to Middle Cerebral Artery Anastomosis

A 31-year-old man presented with right hemiparesis, and magnetic resonance imaging revealed a small infarct at left basal ganglia. Digital subtraction angiography showed left cervical internal carotid artery (ICA) occlusion and severe stenosis of the ipsilateral external carotid artery (ECA) with collateral cerebral circulation fed by ECAs. Based on the results of a functional evaluation of cerebral blood flow, we performed preventive ECA angioplasty and stenting for advanced ECA stenosis to ensure sufficient blood flow to the superficial temporal artery. Eight weeks later, superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis was performed. His postoperative course was uneventful and no additional transient ischemic attacks have occurred. To our knowledge, this is the first report of preventive angioplasty and stenting for advanced narrowing of an ECA before STA-MCA anastomosis for ipsilateral ICA occlusion.     

Occlusion of the Middle Cerebral Artery Branch Mimicking Aneurysm

A 26-year-old man was admitted to our department due to intermittent left hemiparesis for 3 months. Magnetic resonance image showed subacute infarction in the right precentral gyrus. Digital subtraction angiography and magnetic resonance angiography revealed an aneurysmal protrusion at the right middle cerebral artery (MCA) bifurcation. It was difficult to differentiate the aneurysm from the occlusion of the middle trunk of the MCA trifurcation. Brain single photon emission computerized tomography showed a decrease in perfusion in the right posterior frontal lobe without vascular reserve. Therefore, we planned a superficial temporal artery-MCA anastomosis with an exploration of the right MCA bifurcation. Intraoperatively, the aneurysmal opacification on preoperative angiography proved to be the proximal stump of the occluded middle trunk of the MCA trifurcation. An aneurysmal protrusion at the MCA bifurcation does not always indicate an aneurysm. In diagnosing protruding vascular lesions at the MCA bifurcation, the possibility of a vascular stump should be considered according to their angioanatomical appearance and the history of the patient.