Name: 2-vessel occlusion/hypotension: a rat model of global brain ischemia
Uploaded: 2013-06-22T13:00:00
Description: Watch this Scientific Journal Video about 2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia at JoVE.com

1。准备所有的动物实验必须符合机构的指导方针，并接收由各自的动物保健委员会批准开始前。这里提出的所有程序已通过韦恩州立大学的机构动物护理和使用委员会和遵循的准则所提出的道德对待动物实验室动物护理和使用指南，向美国政府原则利用脊椎动物用于测试，研究，培训和护理。在手术开始之前，准备必要的手术材料和手术后恢复笼。本程序是一个生存手术，因...

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B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Death+by+design:+apoptosis,+necrosis+and+autophagy.">Death by design: apoptosis, necrosis and autophagy.</a> Current Opinion in Cell Biology. 16, 663-669 (2004).</li><li>Kirino, T. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Delayed+neuronal+death+in+the+gerbil+hippocampus+following+ischemia.">Delayed neuronal death in the gerbil hippocampus following ischemia.</a> Brain Research. 239, 57-69 (1982).</li><li>Yager, J. Y., Brucklacher, R. M., Vannucci, R. 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M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Apoptosis+and+c-Jun+in+the+thalamus+of+the+rat+following+cortical+infarction.">Apoptosis and c-Jun in the thalamus of the rat following cortical infarction.</a> Neuroreport. 7, 425-428 (1996).</li><li>Watanabe, H., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Protein+synthesis+inhibitor+transiently+reduces+neuronal+death+in+the+thalamus+of+spontaneously+hypertensive+rats+following+cortical+infarction.">Protein synthesis inhibitor transiently reduces neuronal death in the thalamus of spontaneously hypertensive rats following cortical infarction.</a> Neuroscience Letters. 233, 25-28 (1997).</li><li>Wei, L., Ying, D. J., Cui, L., Langsdorf, J., Yu, S. P. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Necrosis,+apoptosis+and+hybrid+death+in+the+cortex+and+thalamus+after+barrel+cortex+ischemia+in+rats.">Necrosis, apoptosis and hybrid death in the cortex and thalamus after barrel cortex ischemia in rats.</a> Brain Research. 1022, 54-61 (2004).</li><li>Zong, W. X., Thompson, C. B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Necrotic+death+as+a+cell+fate.">Necrotic death as a cell fate.</a> Genes &amp; Development. 20, 1-15 (2006).</li><li>Ito, U., Spatz, M., Walker, J. T., Klatzo, I. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Experimental+cerebral+ischemia+in+mongolian+gerbils.+I.+Light+microscopic+observations.">Experimental cerebral ischemia in mongolian gerbils. I. Light microscopic observations.</a> Acta Neuropathologica. 32, 209-223 (1975).</li><li>Saver, J. L., Albers, G. W., Dunn, B., Johnston, K. C., Fisher, M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Stroke+Therapy+Academic+Industry+Roundtable+(STAIR)+recommendations+for+extended+window+acute+stroke+therapy+trials.">Stroke Therapy Academic Industry Roundtable (STAIR) recommendations for extended window acute stroke therapy trials.</a> Stroke; a Journal of Cerebral Circulation. 40, 2594-2600 (2009).</li><li>Busto, R., Dietrich, W. D., Globus, M. Y., Ginsberg, M. D. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+importance+of+brain+temperature+in+cerebral+ischemic+injury.">The importance of brain temperature in cerebral ischemic injury.</a> Stroke; a Journal of Cerebral Circulation. 20, 1113-1114 (1989).</li><li>Voll, C. L., Auer, R. N. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Postischemic+seizures+and+necrotizing+ischemic+brain+damage:+neuroprotective+effect+of+postischemic+diazepam+and+insulin.">Postischemic seizures and necrotizing ischemic brain damage: neuroprotective effect of postischemic diazepam and insulin.</a> Neurology. 41, 423-428 (1991).</li><li>Yamaguchi, M., Calvert, J. W., Kusaka, G., Zhang, J. H. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=One-stage+anterior+approach+for+four-vessel+occlusion+in+rat.">One-stage anterior approach for four-vessel occlusion in rat.</a> Stroke; a Journal of Cerebral Circulation. 36, 2212-2214 (2005).</li><li>Gionet, T. X., Warner, D. S., Verhaegen, M., Thomas, J. D., Todd, M. 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这里描述的模型产生的缺血性损伤到大脑，可发生心脏骤停，复苏的结果，提供了类似的伤害在人类身上发现的。这种方法生产全脑缺血多种协议之一。我们利用这个协议，也是最重要的，其相对较低的死亡率，恢复快，可重复的结果。心跳骤停/复苏模型可以说是临床上最相关的模型，但是技术上最难不断重现。 4VO全脑缺血模型是另一种常用的协议，有价值的事实，所有四个促成血管闭塞缺血?...

脑损伤，心脏骤停和中风的后果是死亡和长期残疾的首要原因。虽然成功心肺复苏的心脏骤停的受害者至少有60％的患者随后死在医院恢复自主循环，每年大约70,000名患者在美国7,8由于广泛的脑损伤，只有3-10％复苏的患者可以恢复他们以前的生活方式9,10。显然，了解脑损伤的机制，导致全脑缺血后设计治疗干预措施，以最大限度地减少神经创伤是非常重要的。 利用多种方法，可以模拟脑缺血。最常见的脑缺血产生的啮齿类动物的大脑，大脑中动脉闭塞的主要血管，从而产生局部缺血性中风11,12。虽然临床上重要的，局灶性脑缺血是不准确的方法来研究脑损伤所产生心脏骤停/复苏。这项临床范式建模必须整个大脑缺血后血流放归。要密切模仿这种临床表现，研究者通过实验诱发心跳骤停，心肺复苏和除颤13,14复苏。这个模型是临床相关性，但不可预知的复苏时间可以增加变化，可能使数据分析难以解释。此外，这款机型具有高死亡率相关联，进一步提高动物数量需要测试一个假设。调查更重现性好，一致性和生存能力侮辱的全脑缺血和/或再灌注损伤的脑反应可能会是首选。 全脑缺血可诱发大脑中的血流全身，同时保留了一些。这降低死亡率，同时允许侦查n的组织损伤的机制在大脑中2。要产生全球性的脑缺血，有必要中断或大大限制流量在所有四个大脑，颈内动脉和椎动脉的血管供应。这些船只供应大脑的血液流经血管结构叫做威利斯，形成一个吻合口环圈。这种血管的架构，使大脑能够保留灌注近端血管闭塞事件。因此，诱导完全缺血的大脑，血液流动必须通过所有供款船只发生。颈内动脉闭塞，可以通过使用微创腹侧颈切下来，动脉瘤夹应用所需期间。通过椎动脉血流中断可以是困难的，因为它们在横向的脊柱椎间孔incased。调查人员已经解决了这个通过electrocauterizing椎动脉24-48小时前颈闭塞和脑缺血（4VO模型）15。在这种方法中，Smith 等人开发了一种方法，通过减少全脑缺血诱导全身平均动脉压（MAP）至40毫米汞柱，以减少通过椎动脉灌注血流量丢失或大大降低到一个点。再加上颈动脉闭塞时，这种方法产生的整个前脑缺血造成的脑损伤的图案，密切模仿，心脏骤停幸存者。在此方法的进一步改进中，我们在座的模型需要在30毫米汞柱±1mHg紧MAP调节在整个8分钟的缺血。我们发现，这种改变提高了重现性脑损伤的影响该模型，Smith 等人的原始设计的技术，同时保持低的死亡率。 精确的表型的细胞死亡和整体组织损伤程度所造成的这里提出的模型是直接依赖于缺血持续时间16。 8分钟的缺血之后，CA1区神经元表现出延迟的细胞死亡，表明在再灌注阶段15,17的治疗干预，有一个时间窗口。在再灌注的发作，神经元迅速恢复功能，没有直接的细胞死亡是检测18。然而，这侮辱导致诱导细胞死亡的级联（凋亡）从线粒体释放凋亡蛋白，包括细胞色素C，4-6小时再灌注3,19之间达到高潮。 6至24小时再灌注，海马CA1区神经元的细胞消亡，凋亡的细胞死亡程序执行了19。应该指出的是负责缺血性损伤的细胞死亡表型是极具争议。早期的研究表明坏死是主要的细胞死亡表型，20,21，而其他人报告apoptOSIS的主要机制22,23。总体而言，目前的证据表明，细胞死亡的频谱范围从经典的细胞凋亡坏死的细胞死亡表型。性细胞死亡的具体模式是依赖于许多因素，各表型的贡献程度取决于侮的严重程度，除其他因素外24,25。再灌注24小时，死亡的细胞具有细胞核固缩，简明细胞质聚集细胞内容物有明确的证据，并失去功能的线粒体形态。死细胞进一步细分，由免疫细胞如巨噬细胞和/或小胶质细胞吞噬，清除从海马CA1区区域。通过再灌注4-7天，去除死细胞，所有剩下的炎症细胞和胶质细胞激活17,26。因此，7天的最佳时间再灌注海马CA1区神经元死亡的，可以量化的，使用简单，非特异性细胞污渍少量甲酚紫或复习续 - 伊红计数基于形态学纳入标准。留在这个晚期再灌注间隔可以算作存活细胞的细胞，从而提供了一个索引的脑损伤。 如果这个模型将被用来测试治疗干预，因此建议，实验设计遵循的楼梯标准（中风治疗学术产业圆桌会议）27。设计和进行研究时，应遵循这些准则，但这里不讨论。

<table border="1">
 <tbody>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Material Name</td>
 </tr>
 <tr>
 <td>5-0 VICRYL suture, reverse cutting </td>
 <td>Ethicon</td>
 <td>J391H</td>
 <td></td>
 </tr>
 <tr>
 <td>Scalpel, No.10</td>
 <td>Swann-Morton</td>
 <td>6601</td>
 <td></td>
 </tr>
 <tr>
 <td>Gauze Sponges</td>
 <td>Fisher</td>
 <td>22-362-178</td>
 <td></td>
 </tr>
 <tr>
 <td>18G x 1 &frac12; in needle</td>
 <td>BD</td>
 <td>305201</td>
 <td></td>
 </tr>
 <tr>
 <td>23G x 1 in needle</td>
 <td>BD</td>
 <td>305145</td>
 <td></td>
 </tr>
 <tr>
 <td>26 G x 3/8 in needle</td>
 <td>BD</td>
 <td>305110</td>
 <td></td>
 </tr>
 <tr>
 <td>18 G x 1 &frac14; catheter</td>
 <td>EXEL</td>
 <td>26735</td>
 <td></td>
 </tr>
 <tr>
 <td>1 ml syringe</td>
 <td>BD</td>
 <td>309659</td>
 <td></td>
 </tr>
 <tr>
 <td>10 ml syringe</td>
 <td>BD</td>
 <td>309604</td>
 <td></td>
 </tr>
 <tr>
 <td>60 ml syringe</td>
 <td>BD</td>
 <td>309653</td>
 <td></td>
 </tr>
 <tr>
 <td>Surgilube</td>
 <td>Henry Schein</td>
 <td>1152666</td>
 <td></td>
 </tr>
 <tr>
 <td>.9% Saline, plastic IV bag</td>
 <td>Henry Schein</td>
 <td>1537468</td>
 <td></td>
 </tr>
 <tr>
 <td>Suture 3-0 Silk</td>
 <td>Henry Schein</td>
 <td>1007842</td>
 <td></td>
 </tr>
 <tr>
 <td>Puralube Ophthalmic Ointment</td>
 <td>Henry Schein</td>
 <td>3390017</td>
 <td></td>
 </tr>
 <tr>
 <td>Betadine</td>
 <td>Henry Schein</td>
 <td>6903564</td>
 <td></td>
 </tr>
 <tr>
 <td>Sterile Towel Drape</td>
 <td>Moore Medical</td>
 <td>14170</td>
 <td></td>
 </tr>
 <tr>
 <td>Polyethylene Tubing, 50</td>
 <td>Intramedic</td>
 <td>427411</td>
 <td></td>
 </tr>
 <tr>
 <td>Stopcock, 3 way</td>
 <td>Smiths medical</td>
 <td>MX9311L</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Drug Name</td>
 </tr>
 <tr>
 <td>AERRANE (isoflurane)</td>
 <td>Henry Schein</td>
 <td>2091966</td>
 <td></td>
 </tr>
 <tr>
 <td>Mapap Liquid (Tylenol)</td>
 <td>Major Pharmaceuticals</td>
 <td>1556</td>
 <td></td>
 </tr>
 <tr>
 <td>Kedavet (ketamine)</td>
 <td>Ketathesia Butney</td>
 <td>NDC 50989-996-06</td>
 <td></td>
 </tr>
 <tr>
 <td>Butorphic (butorphanol)</td>
 <td>Lloyd Labs</td>
 <td>4881</td>
 <td></td>
 </tr>
 <tr>
 <td>Heparin</td>
 <td>APP Pharmaceuticals</td>
 <td>504011</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Chemical Name </td>
 </tr>
 <tr>
 <td>Paraformaldehyde prills</td>
 <td>Elecron Microscopy Sci.</td>
 <td>19202</td>
 <td></td>
 </tr>
 <tr>
 <td>2-methylbutane</td>
 <td>Sigma</td>
 <td>270342</td>
 <td></td>
 </tr>
 <tr>
 <td>Cresyl Violet Acetate</td>
 <td>Sigma</td>
 <td>C5042</td>
 <td></td>
 </tr>
 <tr>
 <td>Sucrose</td>
 <td>Sigma</td>
 <td>S9378</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Software</td>
 </tr>
 <tr>
 <td>ImageJ</td>
 <td>NIH</td>
 <td></td>
 <td></td>
 </tr>
 </tbody>
</table>

2-vessel occlusion/hypotension: a rat model of global brain ischemia

其次是复苏的心脏骤停，结果往往是戏剧性的脑损伤引起的大脑缺血和再灌注的。全球脑缺血产生损害特定的大脑区域是高度敏感的缺血1所示。海马神经元中有较高的灵敏度相比，其他的细胞群，具体的缺血损伤，海马CA1区是特别容易受到缺血/再灌注2。 治疗干预，或参与脑损伤的机制研究，需要设计一个模型，产生类似的临床状况和重现的方式损害。双侧颈动脉血管闭塞低血压（2VOH）的可逆的脑缺血，产生一个模型，模拟心脏骤停，复苏过程中可能发生的脑血管事件。我们描述了一个模型修改史密斯等人 。 （1984）2首次提出在其目前的形式，Sanderson 等 （2008）3，产生重复性损伤选择性脆弱的大脑区域3-6。该模型的可靠性取决于全身血压的精确控制在应用性低血压，缺血时间，接近的温度控制，一个特定的麻醉方案，手术后护理和勤奋。有8分钟的缺血性损伤产生进展超过6至24小时再灌注过程中海马CA1区神经元细胞死亡，而较脆弱的大脑区域都未能幸免。这种渐进性细胞死亡是很容易量化7-14天再灌注后，此时，一个近乎完整的CA1区神经元的损失是显而易见的。 除了这个脑损伤模型中，我们提出了一个简单而透彻，方法CA1区损伤量化的方法。重要的是，量化可以通过使用一个简单的安装在摄像机上的显微镜，达免费ImageJ的研究院（NIH）的软件插件，省却成本过高的体视软件程序进行损失评估和电动显微阶段。

全脑缺血/再灌注模型2VOH导致神经元死亡的海马CA1区。 图2表示的伤害所产生的8分钟全脑缺血再灌注后14天内处理。 图2A和2B比较海马假大脑缺血后，用甲酚紫染色。 图2A显示了表现形态正常，包括一个完整的CA1假手术大鼠海马齿状回，CA2和CA3 图2B表明海马缺血/再灌注，影响最小形态。选择性脆弱的海马CA1区神经元，不生存缺血/再灌?...

Watch this Scientific Journal Video about 2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia at JoVE.com

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

双侧颈动脉闭塞，加上全身性低血压生产全脑缺血大鼠海马损坏，导致重复性严重。受试动物损害与脑损伤预测的模式，它们方便地恢复率和死亡率相对较低。

2血管闭塞/低血压：全脑缺血模型大鼠

Cardiac arrest followed by resuscitation often results in dramatic brain damage caused by ischemia and subsequent reperfusion of the brain. Global brain ...

Research

JoVE Journal

Medicine

MRI-guided Disruption of the Blood-brain Barrier using Transcranial Focused Ultrasound in a Rat Model

MRI引导下的破坏血脑屏障在大鼠模型经颅聚焦超声

Focused ultrasound (FUS) disruption of the blood-brain barrier (BBB) is an increasingly investigated technique for circumventing the BBB1-5. The BBB is a ...

科研

医学

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

闭胸鼠心肌缺血再灌注模型

Surgical trauma by thoracotomy in open-chest models of coronary ligation induces an immune response which modifies different mechanisms involved in ...

Rat Model of Blood-brain Barrier Disruption to Allow Targeted Neurovascular Therapeutics

允许有针对性的大鼠模型血 - 脑屏障破坏神经血管治疗

Endothelial cells with tight junctions along with the basement membrane and astrocyte end feet surround cerebral blood vessels to form the blood-brain ...

In situ Transverse Rectus Abdominis Myocutaneous Flap: A Rat Model of Myocutaneous Ischemia Reperfusion Injury

In situ Transverse Rectus Abdominis Myocutaneous Flap: A Rat Model of Myocutaneous Ischemia Reperfusion Injury

在原位横向腹直肌肌皮瓣：肌缺血再灌注损伤模型大鼠

Free tissue transfer is the gold standard of reconstructive surgery to repair complex defects not amenable to local options or those requiring composite ...

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

缺氧缺糖再给氧作为<em&gt;在体外</em&gt;缺血再灌注损伤模型的研究血脑屏障功能障碍

Ischemia-Reperfusion (IR) injury is known to contribute significantly to the morbidity and mortality associated with ischemic strokes. Ischemic ...

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

基于短暂性脑缺氧缺血性血栓性中风模型

Stroke research has endured many setbacks in translating neuroprotective therapies into clinical practice. In contrast, the real-world therapy (tPA ...

Reproducible Motor Deficit Following Aortic Occlusion in a Rat Model Of Spinal Cord Ischemia

主动脉阻塞后脊髓缺血大鼠模型中的可再生电机缺陷

Spinal cord ischemia is a fatal complication following thoracoabdominal aortic aneurysm surgery. Researchers can investigate the strategies for preventing ...

A Chronic Cardiac Ischemia Model in Swine Using an Ameroid Constrictor

应用 Ameroid 的猪慢性心肌缺血模型

Cardiovascular disease remains the number one cause of mortality in the United States. There are numerous approaches to treating these diseases, but ...

Isometric Contractility Measurement of the Mouse Mesenteric Artery Using Wire Myography

用线 Myography 测定小鼠肠系膜动脉的等轴收缩力

The wire myograph technique is used to assess the contractility of vascular smooth muscles in response to depolarization, GPCR agonists/inhibitors and ...

Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia

评估下肢缺血的Murine模型的治疗血管生成

Critical limb ischemia (CLI) is a serious condition that entails a high risk of lower limb amputation. Despite revascularization being the gold-standard ...