大鼠脑干缺血模型制备及早期超微结构观察

目的:制备脑干缺血动物模型并观察大鼠脑干缺血后早期组织学病理的超微结构。方法:应用两点电凝基底动脉的方法制作鼠脑干缺血动物模型。结果:病理学观察发现脑干缺血2小时即可出现超早期病理变化,并随时间的延长缺血性损害逐渐加重。结论:两点电凝基底动脉后可以造成稳定的脑干缺血,对急性脑干缺血的病理学研究有一定的价值。     

短暂局部预缺血对脑梗塞大鼠的影响及HSP70的表达

目的 建立局灶性可重复性大鼠脑缺血动物模型，研究短暂性局部脑缺血后再灌注不同时间对大脑中动脉闭塞(MCAO)的影响。方法 应用改进的Longa's法局灶性脑缺血模型，建立阻断左侧大脑中动脉的局部脑缺血预处理模型。各组大鼠均经两次处理，预处理(PC)组大鼠经15min短暂预缺血，分别在再灌注6、12、24、72、168h后(n=15～16)，造成MCAO；脑梗塞组大鼠只在第二次处理造成大脑中动脉闭塞；短暂缺血组只在第一次处理时缺血15min。各组大鼠均在第二次处理后24h，检测以下指标：神经功能缺失评分；TTC染色测量梗塞范围；HE染色，观察组织结构变化；干湿法测量脑水含量；免疫组织化学染色观察HSP70的表达。结果 PC24h、PC72h和PC 168h组与脑梗塞组相比较，脑梗塞范围、脑水肿的严重程度、梗塞周边区脑组织的缺血性损伤明显减轻了；短暂缺血引起了轻微的神经细胞结构的改变并使缺血区HSP70表达增加，MCAO后24hHSP70蛋白在缺血周边区出现广泛表达。结论 短暂局部缺血预处理可以诱导脑梗塞后脑组织产生缺血耐受性，其保护作用出现在再灌注后1～7d；缺血预处理引起HSP70蛋白表达的改变与缺血耐受的产生有一定联系.     

经典的小鼠大脑中动脉闭塞再灌注模型的建立和评价

目的:建立经典的小鼠大脑中动脉闭塞再灌注模型。方法:以头端涂硅胶的尼龙线自左颈外动脉向颈内动脉插入至大脑中动脉起始部,阻断血流2h后拔出线栓再灌注。通过神经功能评分和氯化三苯基四氮唑(tetrazoliumchloride,TTC)染色对模型进行评价。结果:小鼠缺血2h后,出现自主活动时向右旋转等功能障碍表现,TTC染色显示出梗死范围。再灌后22hTTC改变加重,神经病学评分同前。结论:该模型可以控制缺血和再灌注时间,是研究脑栓塞病理生理等的经典动物模型。     

脑干梗死患者超早期动脉接触溶栓治疗的护理体会

椎-基底动脉系统，又称后循环，由椎动脉、基底动脉、大脑后动脉及其各级分支组成，主要分支供应脑干、小脑、枕叶、颞叶后部和丘脑等。后循环脑血流受损会引起脑干缺血，如果不及时恢复供血可导致脑干梗死。由于后循环解剖学和生理学的复杂性，后循环缺血梗死病情危重且难以治疗，患者常出现昏迷、四肢瘫痪以及急性呼吸循环衰竭症状，预后极差。     

亚低温对局灶性脑缺血再灌注大鼠脑皮质神经元凋亡及存活素、脑源性神经营养因子表达的影响

目的观察亚低温干预对局灶性脑缺血再灌注大鼠脑皮质神经元凋亡及存活累(Survivin)、脑源性神经营养因子(BDNF)表达的影响,探讨Survivin、BDNF在亚低温脑保护机制中的作用。方法采用线栓法制备成年雄性SD大鼠大脑中动脉闭塞(MCAO)局灶性脑缺血再灌注改良模型,将90只大鼠随机分为假手术组、常温缺血组和亚低温缺血组,缺血组分别于缺血3h再灌注3h、6h、12h、24h、48h、72h、7d处死,亚低温缺血组于缺血后10min实施全身亚低温持续3h。进行TUNEL染色及免疫组化染色,检测梗死灶周围皮质神经元凋亡数量和Sur-vivin、BDNF的表达水平。结果 (1)亚低温缺血组和常温缺血组于再灌注6h皮质区均出现TUNEL染色阳性细胞,72h达高峰,随后逐渐减少,两组内相邻时间点比较差异均有统计学意义(P<0.05);在相同时间点亚低温缺血组凋亡细胞数明显少于常温缺血组,两组间比较差异有统计学意义(P<0.05)。(2)亚低温缺血组于再灌注3hSurvivin、BDNF表达有所增加,BDNF于24h达高峰,Survivin于48h达高峰,随后表达逐渐降低,但7d时仍高于假手术组,常温缺血组表达趋势与之相似,两组各时间点Survivin、BDNF表达均高于假手术组,差异有统计学意义(P<0.05);除再灌注3h Survivin表达在亚低温缺血组与常温缺血组间无明显差异外,其余各时间点亚低温缺血组Sur-vivin、BDNF表达均高于常温缺血组,差异有统计学意义(P<0.05)。结论亚低温干预可抑制梗死灶周围脑皮质神经细胞凋亡,促进存活素及脑源性神经营养因子的表达,发挥脑保护作用。     

大鼠基底动脉闭塞对脑干血流影响的实验研究

目的：观察大鼠基底动脉闭塞后对脑干血流变化的影响。方法：两点凝闭基底动脉，应用激光多普勒技术测量基底动脉闭塞前及闭塞后30、60、120分钟血流值。结果：基底动脉闭塞后脑干局部血流较闭塞前显著降低。结论：两点闭塞基底动脉效果可靠，激光多普勒可用来观察局部血流动力学变化。     

椎基底动脉系缺血时植物神经作用的实验研究

目的 通过不同方法建立椎基镀动脉系缺血动物模型，对缺血病灶区超微结构进行研究，比较与血管伴行的交感神经损伤与否、病灶内的病理形成的差异，探讨交感神经在缺血时的作用机理。方法 通过电凝和直接栓塞兔小脑后下动脉，建立不同的椎基底动脉系缺血的模型，对模型进行动态的脑干诱发电位监测，并以光镜、透射电镜检查病灶内的病理变化，结果 病理检查显示电凝损害了闭塞部位的植物神经后，沿血管走行的对血管起支配作用的植物神经部分发生溃变，梗塞灶内充血性、缺血性梗塞同时存在，而栓塞组梗塞灶内毛细血管旁的交感神经纤维形态完整，梗塞均表现为缺血性，动态的脑干听觉诱发电位检查发现，由于支配血管的交感神经损害，发生了脑干的继发性损害，缺血性损害范围增大，预后恶化，结论 交感神经对脑血管的支配作用在缺血性中风的病理过程中起着重要的作用。它维持了正常情况下脑血管的张力，在 缺血、缺氧时能有效地增加脑血流，限制局灶性梗塞范围的扩大，对邻近的脑组织起着保护性作用。     

椎-基底动脉延长扩张症1例报告并文献复习

正椎-基底动脉延长扩张症(vertebrobasilar dolichoectasia,VBD)是指椎-基底动脉系统血管异常延长、扩张、迂曲改变的血管畸形,延长扩张的椎-基底动脉可因直接压迫颅神经或脑干而产生相应的临床症状,亦可导致阻塞性脑积水或椎基底动脉供血区缺血而引起不同的临床表现,故其临床症状     

脑缺血后适应对基质金属蛋白酶-9表达的影响

目的:探讨缺血后适应对大鼠脑缺血再灌注损伤的保护作用及与MMP-9的关系。方法:应用线栓法制做大鼠脑缺血再灌注损伤模型;对大鼠脑缺血再灌注1h和48h进行神经功能评分;48h后TTC染色测定脑梗死体积和脑水肿程度;4h、8h、24h、48h后免疫组化定位定量MMP-9水平。结果:缺血后适应组大鼠脑梗死体积、水肿程度、术后神经功能评分较对照组明显改善(P<0.05),各时间点后适应组大鼠基底节区MMP-9表达较对照组显著减少(P<0.05),梗死侧皮层MMP-9表达无显著改变。结论:缺血后适应能减少脑缺血后MMP-9的表达,缩小梗死体积,减轻脑水肿程度,改善术后神经功能。MMP-9下调可能是缺血后适应脑保护的分子机制之一。     

以脑干压迫症状为表现的椎基底动脉延长扩张症临床和影像学研究

目的 探讨椎基底动脉延长扩张症(vertebrobasilar dolichoectasia,VBD)的临床表现及诊断方法.方法 回顾2例典型椎基底动脉延长扩张症患者临床及影像学资料,并结合文献进行分析.结果 VBD具有时间顺序占位效应,面肌痉挛、低钾、三叉神经痛、眩晕发作、肢体偏瘫相继发生,VBD具有进展性.结论 VBD症状多样,具有时间顺序,面肌痉挛可能是较早出现的症状.部分后循环缺血(posterior circulation ischemia,PCI)症状可能仅仪是VBD脑干压迫的结果 ,而不是传统意义上的PCI.     

Basilar artery occlusion in rats

The basilar artery is one of the three major sources of blood supply to the circle of Willis. To investigate the effects of basilar artery occlusion, we surgically exposed and coagulated the basilar artery in 25 rats. Basilar artery occlusion at any single point between the foramen magnum and the circle of Willis in 11 rats did not produce histologically detectable infarcts in the brain at 12-24 hours. Two-point occlusions of the basilar artery in 12 rats produced variable infarcts between the occlusion sites but no ischemic lesions elsewhere. After either single- or double-point occlusions, the proximal basilar artery refilled within 2-3 minutes. When the basilar artery was occluded above and below the origins of the anterior inferior cerebellar arteries, the artery segments between the occlusion points initially collapsed but refilled within 2-3 minutes in two rats. Basilar artery occlusions invariably suppressed cortical somatosensory evoked potentials by greater than 50%. Regardless of whether a brain stem infarct developed, somatosensory evoked potential amplitudes recovered to greater than baseline levels by 4 hours in seven of 17 rats and returned to baseline levels by 24 hours in every rat tested. We conclude that the occluded basilar artery receives extensive retrograde collateral blood flow and that somatosensory evoked potentials are exquisitely sensitive to basilar artery occlusion but are insensitive to whether brain stem infarcts develop.     

A giant fusiform basilar aneurysm treated by bilateral vertebral artery occlusion.

OBJECTIVE AND IMPORTANCE: Fusiform aneurysms of the vertebrobasilar arteries that progressively enlarge causing symptomatic brainstem compression are dangerous and their treatment is difficult. A patient with such an aneurysm treated successfully with staged, microsurgical occlusions of the proximal vertebral arteries is described, and the literature pertaining to this rare condition is briefly reviewed. CLINICAL PRESENTATION: A 48-year-old man with a fusiform basilar trunk aneurysm of uncertain etiology presented initially with transient ischemic attacks (TIAs) of the posterior circulation that ceased with anticoagulation. Four years later he presented again with progressive ataxia, dysphagia and dysphonia due to considerable enlargement of the aneurysm causing brainstem compression. INTERVENTION: Staged microsurgical vertebral artery occlusions proximal to the aneurysm were performed. The second (left) vertebral artery was clipped only after the patient passed its temporary occlusion with an endovascular test balloon. The aneurysm subsequently thrombosed, the distal basilar artery kept patent by a single (left) posterior communicating artery. The patient's clinical condition improved markedly over a number of months as the aneurysm mass atrophied. CONCLUSION: Giant vertebrobasilar aneurysms are rare but treacherous lesions, sometimes justifying aggressive management. Carefully selected patients with progressive and severe symptoms due to brainstem compression may tolerate proximal vertebral artery occlusions, provided there is adequate collateral flow to the basilar termination and all of its perforating branches.     

Diffuse cerebral ischemia in the cat: III. Neuropathological sequelae of severe ischemia.

The neuropathological consequences of sever diffuse cerebral ischemia were investigated in an animal model in which postischemic alterations of regional brain blood flow and energy metabolism had been previously characterized. Pentobarbital-anesthetized cats received either 15 or 30 minutes of ischemia produced by basilar artery and bilateral carotid artery occlusions plus mild hypotension; this was followed by 60 to 90 minutes of normotensive recirculation. The brains were perfusion-fixed for light microscopy. Both insult durations resulted in unequivocal ischemic cell change affecting neurons of the cerebral neocortex, striatum, thalamus, and hippocampus and portions of the rostral brainstem. Animals with 30 minutes of prior ischemia differed from those with 15 minutes of ischemia in showing a more apparent regional accentuation of ischemic change in the parasagittal cortical gyri--the sites of previously documented focal postischemic heterogeneities of blood flow and metabolism. In other respects, however, the overall distribution and spectrum of severity of the ischemic alterations were similar for the two insult durations. These data support the view that significant permanent neuronal injury may result from a period of cerebral ischemia as brief as 15 minutes.     

Large vessel occlusions requiring repeated mechanical thrombectomy caused by silent myocardial infarction in a young adult

ObjectivesSilent myocardial ischemia, defined as objective evidence of myocardial ischemia without symptoms, is associated with ischemic stroke. Nevertheless, silent myocardial infarction is a rare cause of ischemic stroke, especially in young adults with no medical history.Materials and methodsHerein, we report a young adult patient with acute ischemic stroke treated with repeated mechanical thrombectomy for recurrent large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction.ResultsA 40-year-old man was transferred by ambulance to our hospital because of a generalized seizure. He was diagnosed with cerebral infarction and left middle cerebral artery occlusion. We performed intravenous thrombolysis and mechanical thrombectomy. Recanalization was achieved and his symptoms gradually improved. However, the day after treatment he developed bilateral cerebellar infarction and basilar artery occlusion. We performed a second mechanical thrombectomy and recanalization was achieved. Transthoracic echocardiography revealed a mobile left ventricular thrombus. Although he had no previous chest symptomatic episodes, cardiac examination confirmed myocardial infarction of unknown onset. He was diagnosed with acute ischemic stroke with large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction. Anticoagulation therapy reduced the amount of thrombus. At 1-year follow-up, he had not experienced any recurrences or symptoms.ConclusionsSilent myocardial infarction should be considered a cause of ischemic stroke in young adults, even without any vascular risk factors. Recurrent large vessel occlusion may occur in patients with left ventricular thrombus, and repeated mechanical thrombectomy should be considered for treatment.     

Clinical features of proven basilar artery occlusion

Our study describes the early symptoms and signs of 85 patients with either basilar artery occlusion or bilateral distal vertebral artery occlusion documented by selective angiography. The most common prodromal symptoms were vertigo, nausea, and headache, which occurred during the 2 weeks before the stroke. Angiographic findings of 49 patients were classified into proximal, middle, and distal basilar artery occlusions. Twenty-two of these patients had additional vertebral artery lesions. A fourth group was composed of 36 patients with bilateral distal vertebral artery occlusion without opacification of the basilar artery through a vertebral artery injection. Onset was sudden in 20 patients; sudden, but preceded by prodromal symptoms in 11 patients; and progressive in 54 patients. Patients with progressive strokes often had bilateral vertebral artery occlusions. Most patients with acute onset had occlusion of the middle and distal basilar artery. An embolic origin of basilar artery occlusion from an arteriosclerotic vertebral artery lesion was assumed to be an important mechanism. An embolus reaching the basilar artery may not necessarily reach the top of the artery, but may also become lodged more proximally.     

5-LOX和Caspase-1在大鼠脑缺血中的表达意义

目的研究大鼠脑缺血后5-脂氧合酶(5-lipoxygenase,5-LOX)和Caspase-1蛋白和基因的表达情况及其相关性。方法用线栓法制备大鼠脑缺血(MCAO)模型,用逆转录聚合酶链反应(RT-PCR)和免疫组化测定缺血脑组织6、12、24、48h不同时点脑皮质5-LOX和Caspase-1在基因和蛋白水平的表达。结果TTC脑片染色证实脑缺血模型建立成功,发现5-LOX和Caspase-1均在正常脑组织中少量表达,且随缺血时间延长表达量增高。结论大鼠脑缺血可诱导5-LOX和Caspase-1表达增高,二者可能参与缺血性脑损伤的形成。     

两次线栓法构建脑缺血耐受模型大鼠血脑屏障通透性改变与基质金属蛋白酶9的表达☆

背景：诸多研究证实,短暂性脑缺血预处理可诱导脑缺血耐受。然而,脑缺血耐受的内源性保护机制尚未明确。 目的：观察脑缺血预处理诱导脑缺血耐受大鼠再灌注不同时间窗血脑屏障通透性改变及基质金属蛋白酶9表达的变化。 方法：将Wistar大鼠随机分为3组,缺血预处理组采用线栓法阻塞大脑中动脉10 min建立局灶性缺血预处理模型,分别在缺血预处理后1,3,7,14,21 d进行再次缺血2 h;模型组不进行缺血预处理,假手术组不阻塞血管。于再灌注22 h进行神经功能检测,采用TTC染色测定脑梗死体积,通过测定渗出血管外的伊文思蓝含量来评价血脑屏障通透性的变化,免疫组织化学和原位杂交法检测基质金属蛋白酶9蛋白及mRNA的表达。 结果与结论：与模型组比较,缺血预处理组1,3,7 d亚组的神经功能评分、脑梗死体积、血脑屏障通透性、脑含水量以及基质金属蛋白酶9蛋白和mRNA表达均明显减小/降低(P < 0.05或P < 0.01),其中以3 d亚组降低最为明显。提示缺血预处理诱导了脑缺血耐受,预缺血诱导的血脑屏障通透性改变以及基质金属蛋白酶9表达减低在脑缺血耐受中发挥重要作用。