绿光光照诱导大鼠脑血栓模型后脑组织病理与行为学改变的研究

目的：为了评价自制绿光冷光源建立大鼠脑血栓模型的可靠性。方法：E要用光化学法制备大鼠大脑中动脉血栓模型,通过观察神经行为学、脑组织光镜及电镜病理特等指标的改变评价该模型。结果：模型组造模清醒后出现神经行为学改变,TTC染色脑冠状切面出明显的梗死灶,HE染色及透射电镜可见神经元细胞呈不同程度的缺血性改变。结论：在此冷光源条件下,建立的大鼠大脑中动脉血栓模型稳定可靠,其神经为行学、脑组织病理上接近临床。     

大鼠自体血栓结合线栓阻塞大脑中动脉制备脑缺血模型的建立与评价

目的建立和评价大鼠自体血栓结合线栓阻塞大脑中动脉（MCA）制备的脑缺血动物模型。方法大鼠随机分为假手术组（10只）、线栓组（12只）、血栓结合线栓组（12只）。线栓组大鼠用尼龙栓线阻塞MCA制备大脑中动脉闭塞（MCAO）模型。血栓结合线栓组由颈外动脉插入改良的内置尼龙套线聚乙烯导管，插管成功后栓线退出一定长度，血液在导管内自凝后拔出套线，经导管推入凝血酶，血栓形成后再次插入套线，根据套线标记的长度向前推进血栓，使之阻塞大鼠MCA制备MCAO模型。术后6h，观察大鼠神经症状评分；测定脑组织含水量、脑梗死面积，观察大鼠脑组织病理变化。结果线栓组和血栓结合线栓组均较假手术组大鼠的神经症状评分增高，脑组织含水量增加，脑梗死面积增大（P均〈0．01），脑组织出现明显的病理损伤；与线栓组比较，血栓结合线栓组大鼠的神经症状评分、脑组织含水量、脑梗死面积及脑组织病理损伤差异均无显著性（P均〉0．05）。结论自体血栓结合线栓阻塞大鼠MCA可引起神经功能损害、脑组织水肿，造成脑组织明显的病理损伤，该法制备的MCAO模型可使血栓阻塞在期望血管（MCA）并可进行脑缺血／再灌注研究，防止血栓模型制备过程中及区域动脉溶栓治疗后再出血等，具有阻塞位置确切、梗死范围恒定、模型易于操作及可重复性好等特点。     

大鼠短暂脑缺血术后行为学的评价

目的　观察大脑中动脉阻塞 (MCAO) 2h造成的短暂脑缺血大鼠 (MCAO大鼠 )行为学表现。方法　采用插线法阻塞成年SD大鼠大脑中动脉制作短暂脑缺血模型 ,分别对模型大鼠进行神经行为学、四肢协调性及学习记忆能力检查 ;术后第 14天处死大鼠取脑组织进行四氮唑红 (TTC)染色鉴定模型的成功与否。对照组不进行动脉阻塞。结果　术后 1h至第 14天 ,MCAO大鼠与对照组比较 ,在神经行为学、协调性及学习记忆能力等方面均有明显的缺失和障碍 (P <0 0 1)。结论　采用插线法制作的大鼠短暂脑缺血模型操作简单 ;术后动物行为学实验是 1种半定量分析 ,具有敏感、客观的特点 ,能够广泛应用于各种实验研究。     

Ⅶ型胶原酶诱导大鼠脑出血模型研究

目的:Ⅶ型胶原酶制作大鼠脑出血模型并评价。方法:Ⅶ型胶原酶立体定向注入大鼠尾壳核,于术后1、3、7d观察大鼠神经行为学、血肿体积及脑组织病理改变。结果:存活大鼠均有神经功能缺损,术后3d最明显;尾壳核有出血灶,术后3d血肿体积最大;血肿及周围脑组织存在典型脑出血后病理改变。结论:Ⅶ型胶原酶制作大鼠脑出血模型是理想的造模方法。     

大鼠大脑中动脉血栓栓塞脑缺血模型的实验研究

目的：建立病理生理过程与人类近似的脑缺血模型。方法：采用成组设计的随机对照研究,用大鼠自体血血栓注入大脑中动脉建立栓塞模型,观察缺血后6、12、24h大鼠的神经功能评分、脑含水量和梗死灶体积。结果：模型稳定、可靠、重复性好。结论：自体血血栓栓塞模型适用于缺血性脑血管病治疗及药物评价的实验。     

NRG1β/JNK信号通路在大鼠脑缺血再灌注损伤的作用机制研究

目的探究神经调节素1β(NRG1β)/JNK信号通路在大鼠脑缺血再灌注损伤的作用机制。方法选取40只6周龄SPF级SD大鼠,随机分为4组,空白对照组、模型组、神经调节素1β组、JNK信号通路抑制剂组。空白对照组不建模,其他三组采用改良线栓法制作大鼠大脑中动脉闭塞(MCAO)模型。造模成功后神经调节素1β组按照2μg/kg的注射比例给大鼠注射NRG1β,JNK信号通路抑制剂组将抑制剂用10%DMSO溶解稀释,向大鼠血管内注入5μl浓度为4 mg/kg的JNK信号通路抑制剂-SP600125。模型组和空白组使用等量的生理盐水处理。采用HE将大鼠脑组织细胞染色,观察缺血脑组织病理改变;采用原位末端标记法(TUNEL)检测缺血后神经细胞凋亡情况;采用改良神经功能缺损评分评价大鼠神经行为功能;检测大鼠脑组织含水量;采用Western blot法检测脑组织JNK表达水平。结果 HE染色结果显示,相比空白对照组,模型组大鼠脑细胞列紊乱、细胞固缩且被染色加深,坏死细胞较多;相比模型组,神经调节素1β组和JNK信号通路抑制剂组大鼠脑细胞显著改善。相比空白对照组,模型组大鼠脑细胞凋亡指数、神经功能缺损评分、大鼠脑组织含水量、p-JNK蛋白表达水平显著升高,且差异有统计学意义(P 0. 01);大鼠脑组织JNK蛋白表达水平无显著变化(P 0. 05);相比模型组,神经调节素1β组和NK信号通路抑制剂组大鼠细胞凋亡指数、神经功能缺损评分、大鼠脑组织含水量、p-JNK蛋白表达水平显著降低,且差异有统计学意义(P 0. 01);大鼠脑组织JNK蛋白表达水平无显著变化(P 0. 05)。结论经NRG1β可以通过抑制JNK信号通路,从而缓解大鼠脑缺血再灌注损伤。     

醒脑静注射液对脑缺血再灌注诱导的脑神经细胞凋亡防治作用的实验研究

目的 :观察醒脑静注射液对脑缺血再灌注诱导的脑神经细胞凋亡的防治作用 ,探讨其神经保护作用的机制。方法 :30只 Wistar大鼠 ,随机分为缺血再灌注模型组和醒脑静治疗组 ,每组各 15只。建立大鼠可逆性大脑中动脉梗死动物模型 ,分别观察 2组动物脑组织的干重与湿重比 (干重 /湿重 ) ,采用红四氮唑染色、原位细胞凋亡染色和透射电镜检测鼠脑组织的细胞凋亡情况。结果 :醒脑静治疗组较脑缺血再灌注模型组脑组织水肿减轻、梗死面积减小 ,神经细胞凋亡数目减少 ,病理损害明显减轻。结论 :醒脑静注射液可显著抑制由缺血再灌注诱导的脑神经细胞凋亡 ,从而起到一定程度的神经保护作用。     

光化学法诱导大鼠单侧海马梗死模型的实验研究

目的：观察不同浓度虎红联合冷光源诱导的大鼠单侧海马梗死模型，了解梗死后学习记忆功能及组织病理改变。方法：大鼠60只随机分为8组：单纯光照组，单纯光敏剂组及6组不同光敏剂浓度(30、40、50、60、70、80mg/kg)的模型组，不同光敏剂浓度的模型组给予静脉注射虎红，冷光源照射左侧海马CA1区，3d后观察其梗死面积、神经行为学及组织病理学改变，以评估模型的可行性。结果：50mg/kg以上的虎红经冷光源照射，可诱导大鼠海马梗死，且面积恒定，病理形态学改变明显，但大鼠单侧海马梗死后的神经行为学改变不明显。结论：虎红结合冷光源诱导的大鼠单侧海马梗死模型稳定性、重复性好，动物存活率高。     

茶氨酸对脑缺血损伤大鼠自由基代谢的影响

目的:从对自由基代谢影响方面探讨茶氨酸对脑缺血损伤的保护作用机制。方法:选用30只SD雄性大鼠,线栓阻塞大鼠大脑中动脉制备局灶性脑缺血模型,观察脑缺血损伤大鼠神经症状改变,测定脑组织含水量、脑组织病理及钙离子含量;观察其血清和脑组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量变化以及茶氨酸对上述变化的影响。结果:脑缺血组大鼠的神经症状评分、脑组织含水量及钙离子含量均显著增高,病理损伤明显,正常神经元细胞数目减少;茶氨酸可显著降低神经症状评分、脑组织含水量及钙离子含量,增加正常神经元细胞数目。脑缺血组大鼠的血清、脑组织SOD活性显著降低,茶氨酸组大鼠血清、脑组织SOD活性较脑缺血组显著增高;脑缺血组大鼠的血清、脑组织MDA含量显著增高,茶氨酸组脑组织MDA含量较脑缺血组下降明显。结论:茶氨酸对大鼠脑缺血损伤具有显著的保护作用,可能与调节脑缺血损伤引起的自由基代谢失调有关。     

局灶性脑缺血鼠大脑半球含水量及病理变化的实验研究

目的：探讨鼠一侧大脑中动脉栓塞／再灌流（MCA／OR）后大脑半球脑水肿形成及病理变化的病生机制，方法：线栓法制作一侧MCA－OR大鼠模型；干湿重法测定双侧大脑半球脑含水量；HE染色观察脑病理变化。结果：一侧MCAOR后双侧大脑顶叶含水量均有增加，出现不同程度病理改变，病灶侧重于非病灶侧。结论：一侧大脑中动脉栓塞／再灌流后。不仅同侧大脑半球产生脑水肿和病理变化，对侧大脑半球对称部位亦有脑含水量增加和脑组织解剖结构变化。其确切机制有待于进一步研究。     

兔急性脑梗死介入治疗动物模型的建立

INTRODUCTIONItisimportanttoestablishananimalmodelthatisaccordtopatho-physiologicalcharactersandfitsforstudyofclinicaltreatment.Herewestudiedthetechniquetoestablisharabbitmodelofacutecerebralinfarctionbyselectiveembolismofmiddlecerebralarterythroughfemoralarterialcannulation.MATERIALSANDMETHODSMaterialsExperimentanimals:24Zelanianrabbits(providedbyexperimentalanimalCenterofLanzhouMedicalCollege),weighted2.1kgto2.5kg,weredividedrandomly:6infalseoperatedgroup,18inoperativegroup.3wer…     

Establishment of rabbit model of cerebral infarction for interventional treatment

AIM:To establish a model of cerebral infarction in order to study the interventional treatment.METHODS:An improved 3.0F SP Cobra catheter was introduced to the internal carotid artery by puncturing the femoral artery.After intemal carotid arteriography thrombus was injected to embolize its MCA.3 hours later,clinic observe and computed tomography was examined to analyze results.RESULTS:Clinic observation confirmed that the rabbit had some nerve defect symptoms and CT exam proved cerebral infarction.CONCLUSION;This technique is convenient for application and the model can meet the standard of study of clinical interventional treatment.     

硬化大脑中动脉及豆纹支管壁弹性结构改变及意义

本文用光镜、电镜观察了正常和硬化大脑中动脉及其豆纹支管壁弹性结构的形态。结果显示，硬化大脑中动脉内弹力膜断裂，且以外层断裂明显，波纹状外观消失；而豆纹支内弹力膜结构完整，波纹状外观清晰可见。平滑肌萎缩、变性，胶原纤维增多。提示硬化大脑中动脉破裂出血是内弹力膜破坏，平滑肌萎缩，管壁脆性增加所致；而豆纹动脉是根部存在＂中膜缺损＂，此外受血流冲击引起破裂的可能性大。     

Antithrombotic effects of FK419, a novel nonpeptide platelet GPIIb/IIIa antagonist, in a guinea pig photochemically induced middle cerebral artery thrombosis model: comparison with ozagrel and argatroban

Platelet activation and subsequent aggregation play a key role in the pathogenesis of ischemic brain damage. Recent studies revealed that enhanced platelet activation is also observed after ischemia, suggesting that secondary thrombus formation might participate in the development of cerebral infarction. The binding of platelet glycoprotein GPIIb/IIIa (integrin alpha(IIb)beta3) to fibrinogen is the final common pathway in platelet aggregation. Therefore, GPIIb/IIIa antagonists might be useful in acute ischemic stroke as well as in the secondary prevention of ischemic stroke. In the present study, we evaluated the effect of three compounds, FK419 ((S)-2-acetylamino-3-[(R)-[1-[3-(piperidin-4-yl) propionyl] piperidin-3-ylcarbonyl] amino] propionic acid trihydrate), a novel nonpeptide GPIIb/IIIa antagonist, ozagrel, a selective thromboxane A(2) synthase inhibitor, and argatroban, a thrombin inhibitor, on middle cerebral artery (MCA) patency and ischemic brain damage using photochemically induced MCA thrombosis model in guinea pigs. FK419, ozagrel, or argatroban was administered 5 min after the termination of photoirradiation. FK419 dose-dependently improved MCA patency by decreasing the total occlusion time, time to continuous reperfusion, and the number of cyclic flow reductions, at doses that inhibited ADP-induced platelet aggregation ex vivo. In contrast, ozagrel only improved total occlusion time, and argatroban showed no improvement in MCA patency. FK419 also reduced ischemic brain damage in a dose-dependent fashion, whereas ozagrel and argatroban did not. Finally, FK419 ameliorated neurological deficits, whereas ozagrel and argatroban did not. These results indicate that FK419, a GPIIb/IIIa antagonist, ameliorates ischemic brain damage by improving MCA patency after occlusion and that FK419 is a promising candidate for the treatment of acute ischemic stroke.     

MyosinIIa contractility is required for maintenance of platelet structure during spreading on collagen and contributes to thrombus stability

BACKGROUND: MyosinIIs are adenosine triphosphate-driven molecular motors that form part of a cell's contractile machinery. They are activated by phosphorylation of their light chains, by either activation of myosin light chain (MLC) kinase or inhibition of MLC phosphatase via Rho kinase (ROCK). MyosinIIa phosphorylation underlies platelet rounding and stress fiber formation. OBJECTIVE: To identify the functional significance of myosinIIa in platelet spreading and thrombus formation on collagen using inhibitors of ROCK (Y27632) and myosinII (blebbistatin). RESULTS: Stress fiber formation on collagen is inhibited by both Y27632 and blebbistatin. A substantial proportion of spread platelets generate internal holes or splits on collagen, presumably because of a reduction in contractile strength. Platelet integrity, however, is maintained. In an in vitro model, thrombus embolization on collagen is increased in the presence of Y27632 and blebbistatin at intermediate shear, leading to a reduction in platelet aggregate growth. Moreover, Y27632 causes a marked reduction in thrombus formation in an in vivo laser-injury model. CONCLUSIONS: MyosinIIa contractility is required for maintenance of platelet structure during spreading on collagen and contributes to thrombus stability.     

Early middle cerebral artery stenosis following stent-assisted thrombectomy

Stent-assisted thrombectomy (SAT) is an extensively used endovascular treatment method for stroke in which the thrombectomy stents come into direct contact with the vascular intimal surface and entrap the thrombus causing the arterial occlusion. Although there are a few studies that demonstrate that the vessel wall changes in the arteries where stroke intervention is performed, we observed progressive stenosis in early follow-up imaging studies in a case. We present a middle cerebral artery (MCA) stroke patient who had four repetitive stent passes during SAT and developed distal MCA stenosis 2 months after SAT at the control magnetic resonance angiography (MRA). Inclusion of early follow-up MRA studies would be helpful in defining the silent vascular changes in patients who have undergone repetitive SAT.     

A pilot study: influence of visual cue color on freezing of gait in persons with Parkinson's disease

Purpose.?To investigate the effect of red and green light beams on gait and freezing of gait (FOG) in persons with Parkinson's disease (PD).

Methods.?Seven persons with PD who experienced FOG participated in the study. Gait and turning performances were studied while walking with canes with red, green, and no light beams while ‘off’ and ‘on’ anti-Parkinsonian medications. Gait speed, cadence, and stride were recorded. Time and number of freezing episodes were recorded during a 50-foot walk and a 360° turn.

Results.?During ‘off’ medication, compared to no light, stride length improved when using the green light, but not the red. During the 50-foot walk, freezing episodes were reduced when using the green light compared to both the red and no light. During the 360° turn, time, number of steps and number of freezing episodes were reduced using the green light compared to the red and no light. During ‘on’ medication, gait speed and stride length improved more with the green light compared to the red. Neither color showed any effect on cadence during either medication state.

Conclusion.?A green light improved gait and alleviate FOG in persons with PD better than a red light or no light.     

Intracranial hemodynamics during intravenous infusion of glyceryl trinitrate

The mechanisms of glyceryl trinitrate (GTN)-induced headache are not fully elucidated. In this study we administered GTN 0.5 microg/kg/min i.v. for 20 min in six healthy volunteers. Before, during and 60 min after the infusion, we investigated regional cerebral blood flow (rCBF), cerebral blood volume (CBV), both estimated with SPECT, and blood flow velocity (BFV) in the middle cerebral artery (MCA), measured with transcranial Doppler. Headache was scored on a numerical verbal rating (0-10) scale. rCBF was unchanged, CBV was slightly increased (13%) during GTN infusion, whereas BFV decreased both during (20%) and 60 min (15%) after GTN. Headache was short-lived and maximal during infusion. This discrepancy of time-effect curves for the effect of GTN on headache and dilatation of MCA indicates that MCA is most likely not the primary source of pain in GTN-induced headache. The time-effect curves for the effect of GTN on headache and on dilation of MCA differed markedly. This indicates that MCA is most likely not the primary source of pain in GTN-induced headache.     

经胸彩色多普勒冠状动脉血流显像技术对冠状动脉左前降支心肌桥的初步研究

目的 利用经胸冠状动脉血流显像技术研究左前降支（LAD）心肌桥患者的壁冠状动脉血流频谱特征以及硝酸甘油对血流频谱的影响;探讨应用经胸冠状动脉血流显像技术诊断心肌桥的可行性.方法 取32例冠状动脉造影检出的心肌桥患者作为研究对象,其中31例心肌桥位于LAD中段,1例位于远段, 静息及舌下喷服硝酸甘油后观察壁冠状动脉及其近、远端彩色多普勒及频谱多普勒特点,比较壁冠状动脉与其近、远端血流参数及诱发前后壁冠状动脉血流参数.结果 硝酸甘油诱发前后LAD中段彩色多普勒总显示率87.1%.静息状态12例患者壁冠状动脉段出现特征性的＂拇指征＂频谱,列为静息阳性组,诱发后出现＂拇指征＂频谱的10例患者列为诱发阳性组.诱发前彩色多普勒检出1例壁冠状动脉起始处舒张期花色血流,诱发后增加显示6例,其中1例出现收缩期反向蓝色血流,多普勒检查示诱发前后拇指征频谱与其近、远端比较舒张期峰值流速、舒张期平均流速、加速度差异有统计学意义;诱发前后＂拇指征＂频谱比较舒张期峰值流速、舒张期平均流速、加速度差异有统计学意义,壁冠状动脉受压时间差异无统计学意义.诱发后2例测及收缩期反向波频谱.结论 经胸冠状动脉血流显像技术是诊断心肌桥的一种新方法,应用硝酸甘油可提高心肌桥的检出率.     

下肢静脉超声图像与凝血纤溶指标关系的探讨

目的 探讨下肢静脉超声图像与反映凝血纤溶机制相关指标之间的关系。方法 根据43例下肢静脉腔内血流不同的声像图表现,分为四组:(1)血栓组;(2)粗颗粒组;(3)细光点组;(4)无回声组。并将各组反映凝血纤溶机制的相关指标:D-二聚体、纤维蛋白原(FIB)、血浆凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)进行统计学分析。 结果 血栓组与粗颗粒组比较,所有指标P>0.05,无显著性差异。细光点组与无回声组比较,所有指标P>0.05,无显著性差异。血栓组分别与细光点组、无回声组D-二聚体比较,所有P<0.01,均有高度显著性差异。粗颗粒组分别与细光点组、无回声组D-二聚体比较,所有P<0.01,也有高度显著性差异。结论粗颗粒组的下肢静脉内虽未见明显血栓形成,但与血栓组一样,血液也处于高凝状态,有形成血栓的危险。细光点组与无回声组一样,凝血纤溶系统处于动态平衡状态,声像图的差异可能是个体透声差异所致。