我们要感谢的胸外科基础研究和教育项目的资金支持。

1。术前准备和麻醉<ol><li>一定要在整个过程中观察无菌技术。奠定了所有仪器。 </li><li>打开前麻醉诱导温度控制床，以便它可以加热至适当的温度（36.5℃）。功率激光多普勒血流灌注监视器上，以便它可以诱导过程中启动。 </li><li>将鼠标放置在感应室。 <ol><li>仔细监视鼠标的感应过程中的呼吸频率。 </li><li>只要呼吸速率已目视减缓，从感应腔移开鼠标。 </li><li>执行脚趾捏来评估麻醉剂是否足够。 </li></ol></li><li>用鼠标正常麻醉，把鼠标放置在仰卧位。 </li><li>将脸变成鼻锥和固定所有四肢加热表。 <ol><li>要特别注意确保四肢固定在解剖位置，没有deviati对一侧。如果鼠标位置不当，这是难以避免的胸骨切开术中胸廓内动脉横断。 </li></ol></li><li>用推剪或市售脱毛膏，从中线胸部取出头发和左下肢腹面。 <ol><li>如果使用脱毛霜，避免留下到位霜大于30秒，碱烧伤可能发生。 </li></ol></li><li>滴定挥发性麻醉剂蒸发器浓度，以维持足够的麻醉。 <ol><li>预计蒸发器部分是使用异氟醚与高流量氧气 1-5％之间。 </li><li>挥发性麻醉剂蒸发浓度应滴定至在手术刺激维持麻醉，同时保持自然呼吸。 </li></ol></li></ol> 2。直肠探头激光多普勒安置<ol><li>将润滑直肠探头插入鼠标的直肠。在安全的地方，歌剧院阿婷床。 </li><li>调节加热床为36.5°C的目标直肠温度</li><li>做小切口在小鼠股动脉解剖和皮肤远离皮下组织。 </li><li>将激光多普勒探头在股动脉。 </li><li>调整探头位置，直到灌流监视器寄存器大于800灌注单位。 <ol><li>稳定到位，安全探头。 不当抵押探头可以有虚假的低灌注测量。 </li></ol></li></ol> 3。主动脉弓/锁骨下动脉夹层<ol><li>做2厘米的皮肤切口上方的胸骨切迹，轻轻地剖析肌肤远离皮下组织。 </li><li>解剖游离颌下腺。 <ol><li>如果发生出血，温和的压力可以用棉签被应用。 </li><li>通过中线在股骨头缺血性平面划分颌下腺。 </li></ol></li><li>轻轻提起胸骨用钳子和使用SCISSORS使1厘米中线胸骨切开术，通过胸骨中线。 从中线的任何偏差可能会导致内乳动脉出血这将是难以控制的。 </li><li>将每边5-0回缩缝合在胸骨边缘和缩回横向胸骨缝合固定于操作床上。 避免将回缩缝线太横向，以防止气胸。 </li><li>用钝性剥离免费带状肌沿气管。左侧肩带肌肉可以用剪刀来划分，以提高曝光。 </li><li>解剖释放胸腺从周围的组织。继续钝性分离，直到大血管被可视化。要特别小心，以防止进入胸膜腔。 </li><li>将血管夹在主动脉弓及左锁骨下动脉。 </li><li>验证远端流量已经适当地打乱。这将被看作是在灌注单位减少&gt; 90％。 <ol><li>继续闭塞德斯黎红色为4-8分钟。 </li></ol></li><li>去除血管钳和胸部闭合前核实止血。 </li></ol> 4。闭合胸骨和皮肤<ol><li>除去在鼠标的左侧回缩缝合。 </li><li>关闭胸骨与正确的回缩缝合。 <ol><li>一个单一的胸骨缝合（使用之前放置回缩针）是足够的胸骨闭合。配售另一针是不必要的，增加了气胸和出血的风险。 </li></ol></li><li>关闭皮肤与运行5-0针。 </li></ol> 5。恢复和术后评估<ol><li>传输鼠标恢复笼。笼应放在一个加热垫，以增加回收室的环境温度和减少热量损失到环境中。 </li><li>密切监测鼠标的迹象呼吸窘迫或癫痫发作。每个管理机构的指引镇痛。 Euthanize老鼠如果立即扣押或呼吸窘迫观察。 <ol><li> CO 2室安乐死是我们的首选方法。颈椎脱位是另一种选择，如果二氧化碳是不可用。 </li><li>完全恢复，可以预计在1-2小时，这取决于挥发性麻醉剂和浓度使用的长度。 </li></ol></li><li>返回鼠标正常笼。放置食物和水的地方在笼子的地板上。 </li><li>使用巴索鼠标量表步态8在12小时的时间间隔评估神经功能状态。 </li></ol>

<ol>
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F. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Spinal+cord+infarction:+etiology+and+outcome.">Spinal cord infarction: etiology and outcome.</a> Neurology. 47, 321-330 (1996).</li><li>Kakinohana, M., 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=Delayed+paraplegia+after+spinal+cord+ischemic+injury+requires+caspase-3+activation+in+mice.">Delayed paraplegia after spinal cord ischemic injury requires caspase-3 activation in mice.</a> Stroke. 42 (8), 2302-2307 (2011).</li><li>Wang, Z., Yang, W., Britz, G. W., Lombard, F. W., Warner, D. 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作者宣称没有竞争的财务权益。

截瘫继发于脊髓缺血再灌注损伤是知之甚少病状9的复合物的结果。虽然这是胸腹主动脉瘤手术后最常见的，各种其他辱骂如主动脉夹层，创伤，栓塞现象，血管炎和系统性低血压10可导致截瘫。为了获得进一步的了解这个伤害，并为未来的目标，以消除这种损伤，动物模型已经成为必然。 患者患有这种并发症展览要么是立即或延迟瘫痪。这种模式和其他人充分平行麻痹11的双峰分布临床可见。而中度缺血（4分）产生延迟性瘫痪，长期缺血（8分）导致立即和永久性瘫痪。 该模型具有的优势相比，那些需要人ATERAL开胸12,13。胸骨正中曝光叶胸膜腔完整，并消除了对气管插管或重新建立在胸膜腔的负压。临床上，胸骨与在更短的术后疼痛较外侧开胸相关，并可能减少术后镇痛药的需求。 这种模式是不是没有限制的。与其他车型，鼠手术有一个学习曲线，良好的手术技术是势在必行。小鼠可以迅速就范，如果清扫不小心进行。术中死亡率的最常见的原因是出血或气胸。为了避免潜在的致命性出血的胸骨必须进行中线。如果胸骨是否过于横向内乳动脉和随后出血的交易可能会发生。此外，降主动脉和锁骨下动脉夹层粗糙会导致出血会difficulT或无法控制。气胸是另一种潜在的致命并发症。这通常发生在放置回缩缝线或主动脉夹层中。如果回缩缝线是太到位横向或主动脉弓没有解剖小心气胸可能发生，而且普遍是致命的。 进一步的步骤需要被用来保证可重复性。常温是至关重要的。在手术过程中小鼠保持接近36.5°C越好。即使是轻度低温已被证明在有脊髓和中风模型14,15显著神经保护作用。此外，激光多普勒测量应密切监测，并与小鼠远端流量减少只有90％应包括进行比较。主动脉或锁骨下动脉闭塞不全可导致更高远流和结果是高度可变的。 总之，L的小鼠模型奥尔下肢瘫痪呈现可以很容易地通过，因此具有高重复性的结果。这种模式的应用程序可以与学习直接和延迟瘫痪的手段提供的调查。此外，采用这种模式可能证明是有益的，以打击这种破坏性的并发症。

下肢瘫痪的不断复杂化胸腹干预。这次受伤，被称为脊髓缺血再灌注损伤（SCIR），导致瘫痪的高危患者1的高达20％。外科手术辅助系统，例如左心脏搭桥，腰椎cerbrospinal流体水渠，低温停循环和肋间动脉再植减少这种并发症2的发病率，但是，太多的患者继续受到影响。 在临床上，脊髓缺血再灌注损伤被看作是立即或延迟瘫痪以下干预3。然而，我们的这种损伤的认识已经扼杀了机械缺乏细节。其结果是，几个选项可用来衰减一旦发生损伤。 因此，我们已委托一个小动物，鼠，模型脊髓缺血和再灌注损伤更好地表征其发病机制。大多数研究迄今已经使用更大的动物模型来描述这种损伤，即大鼠4，兔5，和猪6款车型。然而，这些是由它们的成本，复杂性，可变的再现性，并且，最重要的是，缺乏对遗传操作可行技术的限制。最可靠的这些公布的动物模型包括兔腹主动脉的肾下交叉夹紧。然而，人类的脊髓前神经元最经常得到他们的血管供应的更近端分支7。在这些模型的脊髓可变血管解剖增加了难度在过渡其结果投入临床使用。 这个手稿提出了一个模型，立即或延迟截瘫以下胸主动脉阻塞是临床相关且易于使用。通过曝光迷你sternoto主动脉弓我是创伤小，能引起高度重复性的结果，最少的发病率和死亡率。虽然这种模式在并非没有挑战和技术的细微差别，这些都可以通过仔细解剖和组织处理克服生产的后肢瘫痪了一个模型，可以很容易地实现。

<table><tbody><tr><td>VMS Anesthesia Machine</td><td>MDS Matrx</td><td></td><td></td></tr><tr><td>Isoflurane</td><td>Vet One</td><td>13985-528-60</td><td>2.0% through nose cone&amp;nbsp;</td></tr><tr><td>Induction Chamber</td><td>Vet Equip</td><td>941444</td><td></td></tr><tr><td>Heating Bed</td><td>Vestavia Scientific</td><td></td><td></td></tr><tr><td>Lazer Doppler Monitor</td><td>Moor Instruments</td><td>VMS-LDF1</td><td></td></tr><tr><td>5-0 Suture, Polyester</td><td>Surgidac</td><td>VD-551</td><td>Taper Needle</td></tr><tr><td>Microdissecting Clips</td><td>Biomedical Research Instruments</td><td>14-1030, 14-1060</td><td></td></tr><tr><td>Surgical Instruments</td><td>Fine Surgical Instruments</td><td></td><td>Forceps, needle holder</td></tr></tbody></table>

reproducable paraplegia by thoracic aortic occlusion in a murine model of spinal cord ischemia-reperfusion

背景 下肢瘫痪的不断复杂主动脉干预。的基本病理认识的缺乏阻碍了进步，以减少发生这种损伤。目前的模型表明重现性下肢瘫痪下面的胸主动脉闭塞。 方法 成年雄性C57BL6小鼠用异氟烷麻醉。通过cervicosternal切口主动脉被曝光。胸降主动脉和左锁骨下动脉被认定不进入胸膜腔。这些动脉的骨架，其次是立即关闭（深）或闭塞4分钟（中度缺血）或8分（长期缺血）。在胸骨和皮肤被关闭，鼠标被转移到气候变暖床上进行恢复。以下恢复，在12小时的时间间隔获得的功能分析，直到48小时。 业绩 小鼠接受假手术均未见观察后肢赤字。老鼠受到中度缺血4分钟有最小功能缺损在12小时之后的进展在48小时才能完成瘫痪。小鼠长期遭受缺血产生了立竿见影的麻痹，没有观察后肢运动在术后的任何一点。没有观察到术中或术后死亡率。 结论 重现性下肢瘫痪是否立即或延迟可在小鼠模型来实现。此外，通过采用胸骨正中切开，并小心剥离，高生存率和重现性得以实现。

小鼠进行假手术（3例）或主动脉闭塞4（N = 3）到8分钟（N = 3）。术后小鼠由巴索鼠标分数（ 图1）进行分级。小鼠接受假手术有没有明显的功能障碍在任何时候术后。老鼠受到中度缺血（4分）有接近正常的后肢功能在12小时渐进功能下降由48小时来完成瘫痪。小鼠在长时间缺血组（8分钟）有完全麻痹手术后没有任何可收回功能（图2）。 <img alt="图1" fo:content-width="5in" fo:src="/files/ftp_upload/50910/50910fig1highres.jpg" src="/files/ftp_upload/50910/50910fig1.jpg" /> 图1。巴索分数为后肢运动功能8。对于后肢神经功能障碍从0（无功能）分级，9（正常FUNCTI评分系统上） <a href="https://www-jove-com.remotexs.ntu.edu.sg/files/ftp_upload/50910/50910fig1highres.jpg" target="_blank">点击此处查看大图。</a> <img alt="图2" fo:content-width="5in" fo:src="/files/ftp_upload/50910/50910fig2highres.jpg" src="/files/ftp_upload/50910/50910fig2.jpg" /> 图2术后后肢功能。使用巴索鼠标规模在12小时的时间间隔，直到术后48小时神经功能缺损的严重程度进行分级。 <a href="https://www-jove-com.remotexs.ntu.edu.sg/files/ftp_upload/50910/50910fig2highres.jpg" target="_blank">点击这里查看大图。</a>

Watch this Scientific Journal Video about Reproducable Paraplegia by Thoracic Aortic Occlusion in a Murine Model of Spinal Cord Ischemia-reperfusion at JoVE.com

Reproducable Paraplegia by Thoracic Aortic Occlusion in a Murine Model of Spinal Cord Ischemia-reperfusion

脊髓缺血再灌注损伤的机理认识的缺乏阻碍了进一步的附属物，以防止截瘫以下高风险的主动脉操作。因此，动物模型的开发是必不可少的。这个手稿展示了可重复的下肢瘫痪继小鼠模型主动脉闭塞。

可重放截瘫胸主动脉阻断脊髓缺血再灌注的小鼠模型

Background
Lower extremity paralysis continues to complicate aortic interventions. The lack of understanding of the underlying pathology has hindered ...

reproducable-paraplegia-thoracic-aortic-occlusion-murine-model-spinal

Nanyang Technological University

Research

JoVE Journal

Medicine

12.0K 次观看.  University of Colorado. 脊髓缺血再灌注损伤的机理认识的缺乏阻碍了进一步的附属物，以防止截瘫以下高风险的主动脉操作。因此，动物模型的开发是必不可少的。这个手稿展示了可重复的下肢瘫痪继小鼠模型主动脉闭塞。 

视频: Reproducable Paraplegia by Thoracic Aortic Occlusion in a Murine Model of Spinal Cord Ischemia-reperfusion

Murine Model of Hindlimb Ischemia 

In the United States, peripheral arterial disease (PAD) affects about 10 million individuals, and is also prevalent worldwide. Medical therapies for symptomatic relief are limited. Surgical or endovascular interventions are useful for some individuals, but long-term results are often disappointing. As a result, there is a need for developing new therapies to treat PAD. The murine hindlimb ischemia preparation is a model of PAD, and is useful for testing new therapies. When compared to other models of tissue ischemia such as coronary or cerebral artery ligation, femoral artery ligation provides for a simpler model of ischemic tissue. Other advantages of this model are the ease of access to the femoral artery and low mortality rate. 
In this video, we demonstrate the methodology for the murine model of unilateral hindimb ischemia. The specific materials and procedures for creating and evaluating the model will be described, including the assessment of limb perfusion by laser Doppler imaging. This protocol can also be utilized for the transplantation and non-invasive tracking of cells, which is demonstrated by Huang et al.1.

Murine Model of Hindlimb Ischemia

The surgical procedure for induction of unilateral hindlimb ischemia is demonstrated, with confirmation of ischemia by laser Doppler perfusion imaging.

肢体缺血小鼠模型

In the United States, peripheral arterial disease (PAD) affects about 10 million individuals, and is also prevalent worldwide.  Medical therapies for ...

科研

生物学

A Murine Model of Cervical Spinal Cord Injury to Study Post-lesional Respiratory Neuroplasticity

A cervical spinal cord injury induces permanent paralysis, and often leads to respiratory distress. To date, no efficient therapeutics have been developed to improve/ameliorate the respiratory failure following high cervical spinal cord injury (SCI). Here we propose a murine pre-clinical model of high SCI at the cervical 2 (C2) metameric level to study diverse post-lesional respiratory neuroplasticity. The technique consists of a surgical partial injury at the C2 level, which will induce a hemiparalysis of the diaphragm due to a deafferentation of the phrenic motoneurons from the respiratory centers located in the brainstem. The contralateral side of the injury remains intact and allows the animal recovery. Unlike other SCIs which affect the locomotor function (at the thoracic and lumbar level), the respiratory function does not require animal motivation and the quantification of the deficit/recovery can be easily performed (diaphragm and phrenic nerve recordings, whole body ventilation). This pre-clinical C2 SCI model is a powerful, useful, and reliable pre-clinical model to study various respiratory and non-respiratory neuroplasticity events at different levels (molecular to physiology) and to test diverse putative therapeutic strategies which might improve the respiration in SCI patients.

Respiratory failure is the leading cause of death following a cervical spinal cord injury. Having a reproducible, quantifiable, and reliable pre-clinical animal model of respiratory failure induced by a partial cervical injury will help to understand the subsequent respiratory and non-respiratory neuroplasticity and allow testing putative repair strategies.

颈脊髓损伤的小鼠模型研究后皮损呼吸神经可塑性

A cervical spinal cord injury induces permanent paralysis, and often leads to respiratory distress. To date, no efficient therapeutics have been developed ...

医学

A Murine Model of Myocardial Ischemia-reperfusion Injury through Ligation of the Left Anterior Descending Artery

Acute or chronic myocardial infarction (MI) are cardiovascular events resulting in high morbidity and mortality. Establishing the pathological mechanisms at work during MI and developing effective therapeutic approaches requires methodology to reproducibly simulate the clinical incidence and reflect the pathophysiological changes associated with MI. Here, we describe a surgical method to induce MI in mouse models that can be used for short-term ischemia-reperfusion (I/R) injury as well as permanent ligation. The major advantage of this method is to facilitate location of the left anterior descending artery (LAD) to allow for accurate ligation of this artery to induce ischemia in the left ventricle of the mouse heart. Accurate positioning of the ligature on the LAD increases reproducibility of infarct size and thus produces more reliable results. Greater precision in placement of the ligature will improve the standard surgical approaches to simulate MI in mice, thus reducing the number of experimental animals necessary for statistically relevant studies and improving our understanding of the mechanisms producing cardiac dysfunction following MI. This mouse model of MI is also useful for the preclinical testing of treatments targeting myocardial damage following MI.

We introduce a surgical method to induce experimental ischemia/reperfusion (I/R) injury to simulate myocardial infarction (MI) in mouse models that allows for more clarity in positioning of the ligation on the left anterior descending artery (LAD) to increase the reproducibility of MI experiments in mice.

心肌缺血再灌注损伤的通过左前降支结扎小鼠模型

Acute or chronic myocardial infarction (MI) are cardiovascular events resulting in high morbidity and mortality. Establishing the pathological mechanisms ...

Photothrombosis-induced Focal Ischemia as a Model of Spinal Cord Injury in Mice

Spinal cord injury (SCI) is a devastating clinical condition causing permanent changes in sensorimotor and autonomic functions of the spinal cord (SC) below the site of injury. The secondary ischemia that develops following the initial mechanical insult is a serious complication of the SCI and severely impairs the function and viability of surviving neuronal and non-neuronal cells in the SC. In addition, ischemia is also responsible for the growth of lesion during chronic phase of injury and interferes with the cellular repair and healing processes. Thus there is a need to develop a spinal cord ischemia model for studying the mechanisms of ischemia-induced pathology. Focal ischemia induced by photothrombosis (PT) is a minimally invasive and very well established procedure used to investigate the pathology of ischemia-induced cell death in the brain. Here, we describe the use of PT to induce an ischemic lesion in the spinal cord of mice. Following retro-orbital sinus injection of Rose Bengal, the posterior spinal vein and other capillaries on the dorsal surface of SC were irradiated with a green light resulting in the formation of a thrombus and thus ischemia in the affected region. Results from histology and immunochemistry studies show that PT-induced ischemia caused spinal cord infarction, loss of neurons and reactive gliosis. Using this technique a highly reproducible and relatively easy model of SCI in mice can be achieved that would serve the purpose of scientific investigations into the mechanisms of ischemia induced cell death as well as the efficacy of neuroprotective drugs. This model will also allow exploration of the pathological changes that occur following SCI in live mice like axonal degeneration and regeneration, neuronal and astrocytic Ca2+ signaling using two-photon microscopy.

Photothrombosis is a minimally invasive and highly reproducible procedure to induce focal ischemia in the spinal cord and serves as a model of spinal cord injury in mice.

Photothrombosis引起的局部脑缺血脊髓损伤的小鼠模型

Spinal cord injury (SCI) is a devastating clinical condition causing permanent changes in sensorimotor and autonomic functions of the spinal cord (SC) ...

A Neonatal Mouse Spinal Cord Compression Injury Model

Spinal cord injury (SCI) typically causes devastating neurological deficits, particularly through damage to fibers descending from the brain to the spinal cord. A major current area of research is focused on the mechanisms of adaptive plasticity that underlie spontaneous or induced functional recovery following SCI. Spontaneous functional recovery is reported to be greater early in life, raising interesting questions about how adaptive plasticity changes as the spinal cord develops. To facilitate investigation of this dynamic, we have developed a SCI model in the neonatal mouse. The model has relevance for pediatric SCI, which is too little studied. Because neural plasticity in the adult involves some of the same mechanisms as neural plasticity in early life1, this model may potentially have some relevance also for adult SCI. Here we describe the entire procedure for generating a reproducible spinal cord compression (SCC) injury in the neonatal mouse as early as postnatal (P) day 1. SCC is achieved by performing a laminectomy at a given spinal level (here described at thoracic levels 9-11) and then using a modified Yasargil aneurysm mini-clip to rapidly compress and decompress the spinal cord. As previously described, the injured neonatal mice can be tested for behavioral deficits or sacrificed for ex vivo physiological analysis of synaptic connectivity using electrophysiological and high-throughput optical recording techniques1. Earlier and ongoing studies using behavioral and physiological assessment have demonstrated a dramatic, acute impairment of hindlimb motility followed by a complete functional recovery within 2 weeks, and the first evidence of changes in functional circuitry at the level of identified descending synaptic connections1.

This article describes a method for generating a reproducible spinal cord compression injury (SCI) in the neonatal mouse. The model provides an advantageous platform for studying mechanisms of adaptive plasticity that underlie spontaneous functional recovery.

新生儿小鼠脊髓压迫损伤模型

Spinal cord injury (SCI) typically causes devastating neurological deficits, particularly through damage to fibers descending from the brain to the spinal ...

Murine Model of Intestinal Ischemia-reperfusion Injury

Intestinal ischemia is a life-threatening condition associated with a broad range of clinical conditions including atherosclerosis, thrombosis, hypotension, necrotizing enterocolitis, bowel transplantation, trauma and chronic inflammation. Intestinal ischemia-reperfusion (IR) injury is a consequence of acute mesenteric ischemia, caused by inadequate blood flow through the mesenteric vessels, resulting in intestinal damage. Reperfusion following ischemia can further exacerbate damage of the intestine. The mechanisms of IR injury are complex and poorly understood. Therefore, experimental small animal models are critical for understanding the pathophysiology of IR injury and the development of novel therapies.
Here we describe a mouse model of acute intestinal IR injury that provides reproducible injury of the small intestine without mortality. This is achieved by inducing ischemia in the region of the distal ileum by temporally occluding the peripheral and terminal collateral branches of the superior mesenteric artery for 60 min using microvascular clips. Reperfusion for 1 hr, or 2 hr after injury results in reproducible injury of the intestine examined by histological analysis. Proper position of the microvascular clips is critical for the procedure. Therefore the video clip provides a detailed visual step-by-step description of this technique. This model of intestinal IR injury can be utilized to study the cellular and molecular mechanisms of injury and regeneration.

Here we describe the detailed procedure of intestinal ischemia-reperfusion in mice which results in reproducible injury without mortality to encourage the standardization of this technique across the field. This model of intestinal ischemia-reperfusion injury can be utilized to study the cellular and molecular mechanisms of injury and regeneration.

肠缺血再灌注损伤的小鼠模型

Intestinal ischemia is a life-threatening condition associated with a broad range of clinical conditions including atherosclerosis, thrombosis, ...

Reproducible Arterial Denudation Injury by Infrarenal Abdominal Aortic Clamping in a Murine Model

Percutaneous vascular interventions uniformly result in arterial denudation injuries that subsequently lead to thrombosis and restenosis. These complications can be attributed to impairments in re-endothelialization within the wound margins. Yet, the cellular and molecular mechanisms of re-endothelialization remain to be defined. While several animal models to study re-endothelialization after arterial denudation are available, few are performed in the mouse because of surgical limitations. This undermines the opportunity to exploit transgenic mouse lines and investigate the contribution of specific genes to the process of re-endothelialization. Here, we present a step-by-step protocol for creating a highly reproducible murine model of arterial denudation injury in the infrarenal abdominal aorta using external vascular clamping. Immunocytochemical staining of injured aortas for fibrinogen and &#946;-catenin demonstrate the exposure of a pro-thrombotic surface and the border of intact endothelium, respectively. The method presented here has the advantages of speed, excellent overall survival rate, and relative technical ease, creating a uniquely practical tool for imposing arterial denudation injury in transgenic mouse models. Using this method, investigators may elucidate the mechanisms of re-endothelialization under normal or pathological conditions.

Understanding the cellular and molecular mechanisms of re-endothelialization following arterial denudation injury is of paramount importance in preventing thrombosis and restenosis of arteries. Here we describe a protocol for reproducible arterial denudation injury of the infrarenal abdominal aorta. The procedure was developed to investigate the underlying mechanisms that regulate endothelial regeneration using mouse models.

重复性的动脉剥脱损伤腹主动脉阻断在小鼠模型

Percutaneous vascular interventions uniformly result in arterial denudation injuries that subsequently lead to thrombosis and restenosis. These ...

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

Spinal cord ischemia is a fatal complication following thoracoabdominal aortic aneurysm surgery. Researchers can investigate the strategies for preventing and treating this complication using experimental models of spinal cord ischemia. The model described here demonstrates varying degrees of paraplegia that relate to the length of occlusion following thoracic aortic occlusion in a rat spinal cord ischemia model.
A 2-Fr. balloon-tipped catheter was advanced through the femoral artery into the descending thoracic aorta until the catheter tip was placed at the left subclavian artery in anesthetized male Sprague-Dawley rats. Spinal cord ischemia was induced by inflating the catheter balloon. After a set period of occlusion (9, 10, or 11 min), the balloon was deflated. Neurologic assessment was performed using the motor deficit index at 24 h after surgery, and the spinal cord was harvested for histopathological examination.
Rats that underwent 9 min of aortic occlusion showed mild and reversible motor impairment in the hind limb. Rats subjected to 10 min of aortic occlusion presented with moderate but reversible motor impairment. Rats subjected to 11 min of aortic occlusion displayed complete and persistent paralysis. The motor neurons in the spinal cord sections were more preserved in rats subjected to shorter duration of aortic occlusion.
Researchers can achieve a reproducible hind limb motor deficit following thoracic aortic occlusion using this spinal cord ischemia model.

This study demonstrates the technique to make a minimally invasive and easily reproducible model of spinal cord ischemia in rats. Various degrees of hind limb motor deficit can be produced by controlling the aortic occlusion time.

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 ...

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion

In this study, a middle cerebral artery (MCA) occlusion mouse model is employed to study cerebral ischemia-reperfusion. A reproducible and reliable mouse model is useful for investigating the pathophysiology of cerebral ischemia-reperfusion and determining potential therapeutic strategies for patients with stroke. Variations in the anatomy of the circle of Willis of C57BL/6 mice affects their infarct volume after cerebral-ischemia-induced injury. Studies have indicated that distal MCA occlusion (MCAO) can overcome this problem and result in a stable infarct size. In this study, we establish a two-vessel occlusion mouse model of cerebral ischemia-reperfusion through the interruption of the blood flow to the right MCA. We distally ligate the right MCA and right common carotid artery (CCA) and restore blood flow after a certain period of ischemia. This ischemia-reperfusion injury induces an infarct of stable size and a behavioral deficit. Peripheral immune cells infiltrate the ischemic brain within the 24 h infiltration period. Additionally, the neuronal loss in the cortical area is less for a longer reperfusion duration. Therefore, this two-vessel occlusion model is suitable for investigating the immune response and neuronal recovery during the reperfusion period after cerebral ischemia.

A mouse model of cerebral ischemia-reperfusion is established to investigate the pathophysiology of stroke. We distally ligate the right middle cerebral artery and right common carotid artery and restore blood flow after 10 or 40 min of ischemia.

脑缺血再灌注的双血管闭塞小鼠模型

In this study, a middle cerebral artery (MCA) occlusion mouse model is employed to study cerebral ischemia-reperfusion. A reproducible and reliable mouse ...

Induction of Complete Transection-Type Spinal Cord Injury in Mice

Spinal cord injury (SCI) largely leads to irreversible and permanent loss of function, most commonly as a result of trauma. Several treatment options, such as cell transplantation methods, are being researched to overcome the debilitating disabilities arising from SCI. Most pre-clinical animal trials are conducted in rodent models of SCI. While rat models of SCI have been widely used, mouse models have received less attention, even though mouse models can have significant advantages over rat models. The small size of mice equates to lower animal maintenance costs than for rats, and the availability of numerous transgenic mouse models is advantageous for many types of studies. Inducing repeatable and precise injury in the animals is the primary challenge for SCI research, which in small rodents requires high-precision surgery. The transection-type injury model has been a commonly used injury model over the last decade for transplantation-based therapeutic research, however a standardized method for inducing a complete transection-type injury in mice does not exist. We have developed a surgical protocol for inducing a complete transection type injury in C57BL/6 mice at thoracic vertebral level 10 (T10). The procedure uses a small tip drill instead of rongeurs to precisely remove the lamina, after which a thin blade with rounded cutting edge is used to induce the spinal cord transection. This method leads to reproducible transection-type injury in small rodents with minimal collateral muscle and bone damage and therefore minimizes confounding factors, specifically where behavioral functional outcomes are analyzed.

This protocol describes how to create a precise laminectomy for induction of stable transection-type spinal cord injury in the mouse model, with minimal collateral damage for spinal cord injury research.

小鼠完全转型脊髓损伤的诱导

Spinal cord injury (SCI) largely leads to irreversible and permanent loss of function, most commonly as a result of trauma. Several treatment options, ...