The authors would like to acknowledge Dr. Wanchun Tang MD, MCCM, FCCP, FAHA and Jena Cahoon of the Weil Institute of Critical Care Medicine in Rancho Mirage, CA. for their contributions to the resuscitation protocol outline and for having helped train the rodent surgeon (LL). The preparation of this article was in part supported by a gift in memory of US Navy Retired SKC Robert W. Ply by Ms. Monica Ply for research in heart disease and Parkinson&#8217;s disease and by a discretionary fund from the Department of Medicine at Rosalind Franklin University of Medicine and Science.

注:本协议在医学和科学的罗莎琳德·富兰克林大学被批准的机构动物护理和使用委员会。所有的程序均符合美国国家研究委员会公布实验动物与指南的护理和使用 。 1.实验装置和麻醉<ol><li>用数据采集系统（压力，温度，活塞位移，心电图[心电图]，二氧化碳浓度监测仪等 ）被捕捉的各种信号的执行校准。 </li><li>消毒器械和导管（ 例如 ，在高压釜的仪器和环氧乙烷灭菌的导管）和运营穿长衫，戴口罩，帽子，无菌手套，如果实验涉及的生存术。清洁的外科器械和导管，但没有必要是无菌非存活手术。 </li><li>制备如下所述和在网络中所描绘的导管古尔1大鼠0.45公斤和0.55 kg的体重。 <ol><li>标记的2F T型热电偶导管，尺寸0.6毫米外径（2F），在3,5和8厘米的尖端永久标记，用于前进到胸主动脉。使用这种导管以测量温度和心输出量。 </li><li>切的聚乙烯管，尺寸0.46毫米ID和0.91 mm外径（PE25）≈长度25cm，一个用于前进到胸主动脉，另一个用于前进到右心房。 </li><li>切割每个PE25导管末端的端部，以在一90°角被插入到容器中。 注:斜面提示，在45°角可以用PE管材时，会引起血管穿孔。然而，斜面尖端可以修剪下来用砂纸以降低其清晰度。 </li><li>附加一个26号阴路厄存根适配器到每个PE25导管的近端。 </li><li>马克主动脉导管在3,5，和8厘米，右心房导管3，5，8，10，并从尖端12公分。使用AORTIC导管以测量主动脉压和血液取样。使用右心房导管测量右心房压力。 </li><li>附上每个鲁尔存根适配器到装有3通旋塞阀一个压力传感器。 </li><li>切3F聚氨酯小儿静脉置管，大小0.6毫米ID和1.0毫米外径（3F）的尖端，以45°角晋升到右心房。 </li><li>纪念3F颈外静脉导管在4厘米的一角。使用这种导管导丝前进进入右心室电感应的VF与随后的选项以使用它用于药物递送和血液取样。附加一个3通旋塞阀到导管。 注:标记就导管是外科医生的指导导管是先进的。 3厘米的导管的标记通过股血管的警报中高级从开始到曲线向上朝着胸部区域的血管生成的潜在性的区域的外科医生。该8厘米三月对主动脉导管和热电偶导管KS指示针尖在胸降主动脉。在右心房导管12厘米标记表示前端是在右心房。临时标记是导游的导管推进。在右颈外导管的4厘米标记表示尖端是在右心房。 </li><li>素各导管与含有肝素的10国际单位/毫升的盐水（以确保其通畅），并打开相应的旋塞到闭合位置。 </li><li>切5F氟化乙烯丙烯插管，大小1.1毫米ID和1.6毫米外径（5F）安装在stylette，是≈8厘米长创造了钝尖。使用此套管晋升入气管期间和心脏复苏后，将其尖端≈2厘米距隆突为正压通气。 注:套管的金属stylette需要以145°角≈3厘米从前端被弯曲在前进，以帮助进入气管。 </li></ol></li><li>准备大鼠的手术器械。 <ol><li>麻醉大鼠腹腔注射戊巴比妥钠（45毫克/千克）。如果需要的话，给予额外的剂量（10毫克/千克）静脉内，每30分钟以维持麻醉的手术平面（建立血管通路后）。 注:大多数研究使用男性退休饲养员SD大鼠。 </li><li>夹在那里电击将交付外科领域和地区的头发;其中包括背侧胸部区域，左和右腹股沟，颈部和前表面胸廓。 </li><li>施用0.02毫克/千克（1毫升/公斤）丁丙诺啡皮下镇痛。 </li><li>由胶带前面固定在外科板仰卧位置大鼠后肢在从中线成45°角。 </li><li>用优碘擦洗擦洗切口区域，随后用70％乙醇3次。 </li><li>适用的抗菌眼药膏的薄膜的角膜。 </li><li>插入直肠热敏电阻≈4厘米进入直肠和安全的热敏电阻手术板上。 </li><li>使用整个实验白炽灯的加热灯之间保持36.5℃，37.5℃的体温。 </li><li>地方心电图针皮下的右上肢，左上肢，和右后肢，并记录在整个实验的心电图。 </li></ol></li></ol> 2.血管插管 2.1）左股动脉用于推进T型热电偶导管插入胸降主动脉<ol><li>使左侧腹股沟区有2厘米的切口，在90°角相对于它的一小树林。 </li><li>通过使用一对止血的周围结缔组织的钝器解剖暴露股血管和神经。 </li><li>暴露血管周围使用弯曲微解剖钳血管鞘。 注:避免穿刺或者容器或NERVE。 </li><li>旅行与股动脉，静脉和神经底下微解剖钳和支持他们以90°角相对艘。随着两艘船和支持神经，使用另一种对弯曲微解剖钳开始从神经和静脉动脉分离。 注:分离从下方平行做血管，尽量减少损伤的血管和神经的风险。 </li><li>重新定位支撑钳;释放好意思只支持静脉和动脉。 </li><li>线程的动脉和静脉之间的钳子，并将它们分离到的≈1cm的长度。 </li><li>从支持镊子轻轻松开隔离静脉，并保持只支持动脉。 </li><li>插入两个3-0丝编织非吸收性连笔字和远端位置1和一个近端≈1厘米分开。 </li><li>拧紧远端结扎，而动脉用外科医生的结＆＃仍支持160;其次为两个单结。拧紧近端结扎与一个松散的外科医生的结。 </li><li>使用一对邻近所述远端结扎微解剖剪的容器上的一个小切口，在60°角相对于容器中的切割约其横截面面积的四分之一。 注:小滴血摆脱切断信号管腔达到。 </li><li>滴落肝素生理盐水到容器，以允许在导管的平滑插入。 注意:一到两滴的1％利多卡因溶液，也可用于防止容器中的痉挛。 </li><li>插入一个22号针头-其尖端已经定制弯曲成70°角，用砂纸（ 即介绍人）减弱-到血管开放，同时轻轻拉远端结扎与止血稳定器。 </li><li>抬起导引轻轻以暴露腔和引导导引下的T型热电偶导管，除去它一旦导管尖端已被插入。 </li><li>固定在原位导管用一只手同时容纳另一方面在一个舒适的位置来推进导管。 </li><li>关闭支承镊子和移动向远侧导管前进。 注意:如果任何遇到阻力，同时推进导管;停下来，拉了回来，并插入以替代角度。 </li><li>推进导管，直到8厘米标记到其前端位置到胸降主动脉。 </li><li>通过拧紧所述近端结扎并增加两个附加的单结固定导管的容器中。 注:安全结得足够紧，以防止导管周围和无意的位移出血;然而，足够松，如果需要重新定位，使来回运动。 </li><li>取出镊子和止血钳轻轻地。 </li></ol> 2.2）左股静脉用于推进PE25导管插入右心房<ol><li>电梯吨他股动脉已经通过在结扎轻轻拉起并暴露在相邻股静脉插管与T型热电偶导管。 </li><li>静脉下旅行使用镊子，并打开他们撑起静脉。 </li><li>按照步骤2.1.8至2.1.18但推进PE25导管（而不是T型热电偶）到12厘米标记来定位靠近右心房的小费。 </li><li>血液检查可以通过导管被撤回，以确认其腔内通畅位置和冲洗导管用0.2ml肝素盐水。 </li><li>关闭手术切口用一个外科医生的结。 </li></ol> 2.3）右股动脉用于推进PE25导管插入胸降主动脉<ol><li>按照步骤2.1.1至2.1.18但推进PE25导管到8厘米标记到其前端位置到胸降主动脉。 </li><li>重复步骤2.2.4和2.2.5。 </li></ol> 2。4）右颈外静脉用于推进3F聚氨酯儿科静脉导管插入右心房<ol><li>使1.5厘米长的切口开始在颈部，1cm到气管的右侧，结束正下方的甲状腺的基础。 注意:避免伤害或暴露甲状腺。 </li><li>轻轻解剖使用一对止血的以暴露颈外静脉周围的结缔组织。 </li><li>静脉下旅行使用镊子，并打开他们撑起静脉。 </li><li>对于静脉插管重复步骤2.1.8至2.1.18，但推进3F导管到4厘米标记定位其尖端在右心房。 </li><li>重复步骤2.2.4。 </li><li>盖住导管与上述活栓的3路，并把它的关闭位置。 </li></ol> 3.气管插管 3.1）气管曝光<ol><li>扩大先前进行颈部切口朝向使用止血中线。 </li><li>迪斯<html> ECT使用钝器技术的cleidocephalic肌肉的胸骨舌骨，sternothyroid和乳突部分暴露气管并保持暴露出用纸巾止血吊具和镊子。 </li></ol> 3.2），气管插管<ol><li>拉出舌头伸展气道。推进5F导管（ 即气管插管）安装在stylette。紧紧握住套管，同时与尖朝上，并事先寻求进入上呼吸道，声带和气管推进。 </li><li>跨可视化气管插管，因为它的进步指导到适当的位置。 </li><li>除去从套管的stylette并附加一个红外的CO 2分析仪适配器套管的远端。 </li><li>通过识别特征capnographic波形确认成功气管插管; 即呼气时气道的二氧化碳增加，吸气时下降。 </li></ol>ove_title"&gt; 4。确认基线稳定性<ol><li>完成手术器械和各种导管，插管的连接，并且经由它们相应的换能器和信号调节器的ECG导致的数据采集系统，并确认基于心输出量和血压meaurements和代谢稳定性（最好）通过测量血液的血流动力学稳定性气体和乳酸水平。 注:心输出量是通过加入200μl丸剂注射的0.9％NaCl在室温下到右心房后通过热电偶记录在胸降主动脉热稀释曲线的计算机分析测定。 </li><li>定义为感兴趣的各种参数的具体基准参考值;这可能会发生变化队伍的大鼠品系，性别和体重。代表性实验使用本文描述的大鼠模型基线和复苏后的参考值列于表1中 。</li></ol> 5.实验协议 5.1）诱导心室颤动（VF） <ol><li>插入在大鼠的腹壁连接到一个60赫兹的负极的针皮下，交流电（AC）发电机（0至12 mA）的。避免提前超出皮下组织针进入腹腔，以避免不慎损伤内部器官。 </li><li>附加一个预弯曲0.38毫米OD的一端和40厘米长的导向线（经由有线连接）连接到交流发电机的正极。确保极性接反;否则音频可能不被诱导。 </li><li>除去活栓从在右颈外静脉插入3F聚氨酯导管3路并推进导丝约7厘米寻求进入右心室同时监测心电图和主动脉压力的柔软尖端。 注:导向线的正确位置将被建议由异位ventricular次的心电图和主动脉压观察。 </li><li>打开60赫兹交流发电机，并逐渐增加的电流，同时监测动脉压。 注:将2.0毫安的电流通常是足以诱导VF但变化取决于相对于右心室导丝的位置。可能需要稍微调整尖端位置以诱导VF在较低电流水平。 </li><li>通过记录（1）停止主动脉脉动和主动脉压力的指数衰减至≈20毫米汞柱≈5秒，（2）在所述ECG外观无组织的电活动的内，如图2确认诱导室颤。 </li><li>保持3分钟减少第一分钟到大约一半的水平以诱导VF所需后的强度的当前不间断。 </li><li> 3分钟和文档音频继续，而不需要施加电流后把当前的关闭。 注:小心灵自发除颤定短路长度由此纤维性颤动前方的前缘到达其尾端在不应期解除折返。仅在一段心肌缺血后; 即 ，3分钟，足以减慢传导，以允许折返是VF变成自持， 如图2。 </li><li>与上述活栓的3路取出导丝，再盖颈静脉导管，取出接地针，并允许音频继续自发为协议的欲望的持续时间根据公布开始复苏的干预（ 即 ，4〜15分钟，然后研究）。 </li></ol> 5.2）胸外按压和正压通气注:胸部压缩机本出版物中是一个特制的气动和电控活塞装置。呼吸机是一种可商购的装置。 <ol><li>使用未经处理的VF的时间行动说明Below;尽管它们可诱导的VF之前进行。 </li><li>纪念胸口处2.8厘米和4.2厘米剑突的基地。发起胸部按压的最佳地区这两个标记之间通常发现。 </li><li>涂抹导电凝胶除颤桨和滑动老鼠的胸部下方，固定桨手术板上。 </li><li>放置两个胸前标志略微触及胸部的胸压缩机的活塞。 </li><li>设置在压缩机以提供每分钟200按压并设置初始活塞位移为0毫米。 注:压缩率是适合于小动物用的350分钟的自发心脏速率-1，但它可以变化为尚未定义的最佳压缩率的大鼠模型。 </li><li>在25分钟内设置换气-1递送6毫升/ kg的潮气量的1.0的非同步和吸入氧的一小部分（氧合指数2）胸部Ç来说，压缩。 </li><li>附加呼吸管将气管套管离开（在Y适配器连接的吸气和呼气四肢结束）介于红外线的CO 2分析仪适配器。 </li><li>打开呼吸机上，并通过逐渐增加的压缩深度从0至10mm的第一分钟期间开始胸部按压。移动略微活塞侧向和rostrocaudal寻求找到产生最高主动脉舒张压一个位置（即，按压之间的压力），用于一个给定的压缩深度。 注:在压缩深度的逐渐增加是唯一的复苏研究所大多数研究者开始与最大压缩深度。 </li><li>继续第二分钟期间增加压缩深度，直到目标主动脉舒张压的实现。 注:24毫米汞柱或更高的目标主动脉舒张压产生20毫米汞柱或更高的冠状动脉灌注压减去后右房舒张压;对应于这种大鼠模型4 resuscitability门槛。目标主动脉舒张压 - 这可能超出resuscitability门槛 - 是基于研究目的的调查来决定。然而，这是不可取的，超过17毫米的按压深度，避免伤到胸壁和胸腔内器官。 </li><li>保持胸部按压所需时间试图除颤之前。 注:六分钟胸外按压似乎心肌创造有利条件成功除颤26将所需的最低。然而，随着持续时间，胸部按压下降的血流动力学和药效大多数研究使用的持续时间为6至10分钟。 </li></ol> 5.3）除颤<ol><li>使用市售的双相波除颤器有能力进行内部除颤与出发为5J传递能量，配备有桨叶定制，以大鼠。 </li><li>涂抹导电凝胶除颤桨。 </li><li>立即完成胸外按压的预定时间之前收取的除颤器。 </li><li>中断胸外按压，并确认心脏仍然在VF检查心电图。 </li><li>提供高达每5焦耳交叉于胸前的隔壁5秒钟的时间间隔2电击如果VF存在，观察是否有回报的电有组织心电图主动脉脉冲和平均动脉压≥25毫米汞柱。 </li><li>恢复胸部按压为30秒或60秒（取决于特定协议）如果平均动脉压是&lt;25毫米汞柱，无论电气节奏。 </li><li>从5.3.4重复步骤5.3.6多达5倍队伍的具体协议，但不断升级的除颤能量到7焦耳如果初始5焦耳的冲击不终止音频。图3描绘了除颤亲母育酚用在复苏研究所和图4示出在相除颤一个代表性实验。 </li><li>提供电击只有当VF存在;否则，继续胸外按压前没有电击，并假设的心脏是无脉性电活动或心搏停止。 </li><li>确定在完成除颤压缩循环（ 图3）的复苏结果。 </li></ol> 5.4）后复苏<ol><li>从25分钟提高通风量-1〜60分钟-1自主循环恢复后自主循环15分钟后，降低2氧合指数从1.0到0.5。 </li><li>提供电击，在最后的冲击相同的能量，如果VF复发。但是，通常VF自发逆转窦性心律几秒钟之内。 注:VF复发可能发生的再灌注心律失常的一部分，不久自主循环恢复后，但很少超过15分钟。 </li><li>根据由研究者决定特定复苏后协议观察动物;通常180〜240分急性试验没有安乐死前，麻醉恢复期。一个典型的急性实验的时间线示于图5。 </li><li>急性实验进行剖检记录导管损伤位置和内脏，可以使实验无效。 </li><li>删除所有导管，结扎血管，并关闭创面金属夹，并按照生存实验下面列出的步骤。 </li><li>拔管的动物，只要它是能够自主呼吸。 </li><li>返回动物到一个干净的笼从麻醉中通过完整而求告无门自行扶正从背斜卧证明后恢复。 </li><li>喷出温热的0.9％NaCl（1毫升/ 100克体重）腹膜内以降低低温以及d的风险ehydration。 </li><li>辖美洛昔康（2毫克/千克）镇痛的剂量，随后用1毫克/千克剂量皮下每天长达72小时一次后皮下注射4小时皮下剂量。 </li><li>房子仅在动物与富集长达48小时的安全回收和利用的术后护理和监测机构的标准作业程序。 </li></ol>

The authors have nothing to disclose.

在协议中的关键步骤 有在该协议的关键步骤。当掌握了，准备和协议进行如下简洁如下所述。外科手术的准备是迅速的，迅速推进导管通过小切口触发最小或没有血管痉挛和定位所述导管尖端的意图，随后成功气管插管后的单一或几个尝试（多个）;因此，完成了制备在≈90分钟，从最初的戊巴比妥剂量诱导的VF带内的参考值的基线测量（ 表1）。 VF是在每?...

接近36万个人在美国1和许多世界各地的2患心脏骤停每年一个小插曲。试图恢复生活不仅要求心脏活动重新建立但重要器官的损害预防，尽量减少或逆转。当前心肺复苏技术得到的约30％的初始复苏速率然而，出院生存率只有5％1。心肌功能障碍，神经功能障碍，全身炎症，并发疾病，或其出现复苏后账户是谁，尽管流通的初始收益死亡的患者大比例的组合。因此，迫切需要的基本病理生理学和新颖复苏的方法更好的理解，以增加初始复苏和随后的存活与完整器官功能的速率。 动物模式心脏骤停的LS提供见解心脏骤停和复苏的病理生理机制，并提供构思和测试新的干预措施，才可以在人类3进行测试切实可行的手段发挥新的复苏疗法的发展具有重要作用。这里所描述的关胸心肺复苏的大鼠模型（CPR）等方面发挥了重要作用。在后期教授马克斯·哈里·韦伊医学博士的实验室和她的合作者4 -该模型在1988年开发的艾琳·冯·足底-研究员当时在健康科学大学（更名为医学和科学的罗莎琳德·富兰克林大学在2004年），并已广泛应用于复苏的领域主要由威尔教授和他们的学员的同伴。 该模型模拟心脏骤停复苏与用传统CPR技术未遂的情节，因此包括INDUCT离子心室纤颤（VF）通过提供到右心室心内膜和提供封闭胸CPR的电流由一个气动驱动的活塞装置，同时伴随地输送正压通气与富氧气体。终止VF是由胸交付电击来完成。大鼠模型撞击在大型动物（ 例如 ，猪）和模型在较小的动物研制开发的模型之间的平衡（ 例如 ，小鼠），允许新的研究概念在良好标准化，重复性好，高效的方式访问探索健壮库存相关的测量。该模型是在研究，探索新概念和研究混杂因素的影响进行研究的大动物模型更昂贵过，但更大的影响平移初期阶段尤其有用。 一个Medline检索所有同行评议的文章作为报告有VF为心脏骤停的机制，某种形式的胸外复苏imilar大鼠模型共使用模型69个原始研究发现，因为它在1988年第4年首次出版，研究领域包括复苏5-17病理生理方面，影响的结果18-30因素，药物干预研究血管加压剂31-43，缓冲剂的作用44，正性肌力药45，代理旨在心肌或脑保护46-70，并且还间质干细胞71-73的影响。 在这篇文章中描述的模型和协议，目前正在使用的复苏研究所。然而，有多个机会来"定制"的基础上提供给个人的调查和研究的目标的能力模型。

<table><tbody><tr><td>Sodium pentobarbital</td><td>Sigma Aldrich</td><td>P3761</td><td>http://www.sigmaaldrich.com/catalog/product/sigma/p3761?lang=en&amp;amp;region=US</td></tr><tr><td>Rectal thermistor</td><td>BIOPAC Systems, INC</td><td>TSD202A</td><td>http://www.biopac.com/fast-response-thermistor</td></tr><tr><td>Needle electrode biopolar concentric 25 mm TP</td><td>BIOPAC Systems, INC</td><td>EL451</td><td>http://www.biopac.com/needle-electrode-concentric-25mm</td></tr><tr><td>PE25 polyethylene tubing&amp;nbsp;</td><td>Solomon Scientific</td><td>BPE-T25</td><td>http://www.solsci.com/products/polyethylene-pe-tubing</td></tr><tr><td>26GA female luer stub adapter</td><td>Access Technologies</td><td>LSA-26</td><td>http://www.norfolkaccess.com/needles.html</td></tr><tr><td>Stopcocks with luer connections; 3-way; male lock, non-sterile</td><td>Cole-Parmer</td><td>UX-30600-02</td><td>http://www.coleparmer.com/Product/Large_bore_3_way&lt;br/&gt; _male_lock_stopcocks&lt;br/&gt; _10_pack_Non_sterile/EW-30600-23</td></tr><tr><td>TruWave disposable pressure transducer</td><td>Edwards Lifesciences</td><td>PX600I&amp;nbsp;</td><td>http://www.edwards.com/products/pressuremonitoring/Pages/truwavemodels.aspx?truwave=1</td></tr><tr><td>Type-T thermocouple</td><td>Physitemp Instruments</td><td>IT-18</td><td>http://www.physitemp.com/products/probesandwire/flexprobes.html</td></tr><tr><td>Central venous pediatric catheter&amp;nbsp;</td><td>Cook Medical&amp;nbsp;</td><td>C-PUM-301J</td><td>https://www.cookmedical.com/product/-/catalog/display?ds=cc_pum1lp_webds</td></tr><tr><td>Abbocath-T subclavian I.V. catheter (14 g x 5 1/2&quot;)</td><td>Hospira</td><td>453527</td><td>http://www.hospira.com/products_and_services/iv_sets/045350427</td></tr><tr><td>Novametrix Medical Systems, Infrared CO2 monitor</td><td>Soma Technology, Inc.</td><td>7100 CO2SMO&amp;nbsp;</td><td>http://www.somatechnology.com/MedicalProducts/novametrix_respironics_co2smo_&lt;br/&gt; 7100.asp</td></tr><tr><td>Harvard Model 683 small animal ventilator</td><td>Harvard Apparatus</td><td>555282</td><td>http://www.harvardapparatus.com/webapp/wcs/stores/servlet/haisku2_10001_11051_44453_-1_&lt;br/&gt; HAI_ProductDetail_N_37322_37323</td></tr><tr><td>Double-flexible tipped wire guides</td><td>Cook Medical&amp;nbsp;</td><td>C-DOC-15-40-0-2</td><td>https://www.cookmedical.com/product/-/catalog/display?ds=cc_doc_webds</td></tr><tr><td>High accuracy AC LVDT displacement sensor</td><td>Omega Engineering</td><td>LD320-25</td><td>http://www.omega.com/pptst/LD320.html</td></tr><tr><td>HeartStart XL defibrillator/monitor</td><td>Phillips Medical Systems</td><td>M4735A</td><td>http://www.healthcare.philips.com/main/products/resuscitation/products/xl/</td></tr><tr><td>Graefe micro dissection forceps 4 inches</td><td>Roboz&amp;nbsp;</td><td>RS-5135</td><td>http://shopping.roboz.com/Surgical-Instrument-Online-Shopping?search=RS-5135</td></tr><tr><td>Graefe micro dissection forceps 4 inches with teeth</td><td>Roboz&amp;nbsp;</td><td>RS-5157</td><td>http://shopping.roboz.com/Surgical-Instrument-Online-Shopping?search=RS-5157</td></tr><tr><td>Extra fine micro dissection scissors 4 inches</td><td>Roboz&amp;nbsp;</td><td>RS-5882</td><td>http://shopping.roboz.com/micro-scissors-micro-forceps-groups/micro-dissecting-scissors/Micro-Dissecting-Scissors-4-Straight-Sharp-Sharp</td></tr><tr><td>Heiss tissue retractor</td><td>Fine Science Tools&amp;nbsp;</td><td>17011-10</td><td>http://www.finescience.com/Special-Pages/Products.aspx?ProductId=321&amp;amp;CategoryId=134&amp;amp;&lt;br/&gt; lang=en-US</td></tr><tr><td>Crile curve tip hemostats</td><td>Fine Science Tools&amp;nbsp;</td><td>13005-14</td><td>http://www.finescience.com/Special-Pages/Products.aspx?ProductId=372</td></tr><tr><td>Visistat skin stapler&amp;nbsp;</td><td>Teleflex Incorporated</td><td>528135</td><td>http://www.teleflexsurgicalcatalog.com/weck/products/9936</td></tr><tr><td>Braided silk suture, 3-0</td><td>Harvard Apparatus</td><td>517706</td><td>http://www.harvardapparatus.com/webapp/wcs/stores/servlet/haisku2_10001_11051_43051_-1_&lt;br/&gt; HAI_ProductDetail_N_37916_37936</td></tr><tr><td>Betadine solution</td><td>Butler Schein</td><td>3660</td><td>https://www.henryscheinvet.com/</td></tr><tr><td>Sterile saline, 250 ml bags</td><td>Fisher</td><td>50-700-069</td><td>http://www.fishersci.com/ecomm/servlet/itemdetail?catnum=50700069&amp;amp;storeId=10652</td></tr><tr><td>Heparin sodium injection, USP</td><td>Fresenius Kabi</td><td>504201</td><td>http://fkusa-products-catalog.com/files/assets/basic-html/page25.html</td></tr><tr><td>Loxicom (meloxicam)</td><td>Butler Schein</td><td>045-321</td><td>https://www.henryscheinvet.com/</td></tr><tr><td>Thermodilution cardiac output computer for small animals</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Resuscitation Institute using National Instruments hardware and LabVIEW software</td></tr><tr><td>Analog-to-digital data acquisition and analysis system</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Resuscitation Institute using National Instruments hardware and LabVIEW software</td></tr><tr><td>Pneumatically-driven and electronically controlled piston device for chest compression in small animals</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Weil Institute of Critical Care Medicine</td></tr><tr><td>60 Hz alternating current generator</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Weil Institute of Critical Care Medicine</td></tr></tbody></table>

a rat model of ventricular fibrillation and resuscitation by conventional closed-chest technique

A rat model of electrically-induced ventricular fibrillation followed by cardiac resuscitation using a closed chest technique that incorporates the basic components of cardiopulmonary resuscitation in humans is herein described. The model was developed in 1988 and has been used in approximately 70 peer-reviewed publications examining a myriad of resuscitation aspects including its physiology and pathophysiology, determinants of resuscitability, pharmacologic interventions, and even the effects of cell therapies. The model featured in this presentation includes: (1) vascular catheterization to measure aortic and right atrial pressures, to measure cardiac output by thermodilution, and to electrically induce ventricular fibrillation; and (2) tracheal intubation for positive pressure ventilation with oxygen enriched gas and assessment of the end-tidal CO2. A typical sequence of intervention entails: (1) electrical induction of ventricular fibrillation, (2) chest compression using a mechanical piston device concomitantly with positive pressure ventilation delivering oxygen-enriched gas, (3) electrical shocks to terminate ventricular fibrillation and reestablish cardiac activity, (4) assessment of post-resuscitation hemodynamic and metabolic function, and (5) assessment of survival and recovery of organ function. A robust inventory of measurements is available that includes &#8211; but is not limited to &#8211; hemodynamic, metabolic, and tissue measurements. The model has been highly effective in developing new resuscitation concepts and examining novel therapeutic interventions before their testing in larger and translationally more relevant animal models of cardiac arrest and resuscitation.

此处所描述的大鼠模型最近使用期间胸部按压和复苏后61来比较对心肌和血液动力学功能的肌膜钠-氢交换亚型1（NHE-1）的2抑制剂的影响。据此前报道，NHE-1抑制剂通过限制钠引起的胞浆和线粒体钙超载减轻心肌再灌注损伤，从而有助于在胸外按压保持左室扩张，减轻复苏后心功能不全12。在这项研究中，NHE-1抑制剂cariporide（1毫克/千克），它已被广泛地研究，在过去，是使用较新?...

Watch this Scientific Journal Video about A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique at JoVE.com

A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique

This article describes a rat model of electrically-induced ventricular fibrillation and resuscitation by chest compression, ventilation, and delivery of electrical shocks that simulates an episode of sudden cardiac arrest and conventional cardiopulmonary resuscitation. The model enables gathering insights on the pathophysiology of cardiac arrest and exploration of new resuscitation strategies.

室颤由传统的封闭胸技术大鼠模型和复苏

A rat model of electrically-induced ventricular fibrillation followed by cardiac resuscitation using a closed chest technique that incorporates the basic ...

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15.8K 次观看.  Rosalind Franklin University of Medicine and Science. This article describes a rat model of electrically-induced ventricular fibrillation and resuscitation by chest compression, ventilation, and delivery of electrical shocks that simulates an episode of sudden cardiac arrest and conventional cardiopulmonary resuscitation. The model enables gathering insights on the pathophysiology of cardiac arrest and exploration of new resuscitation strategies.

视频: A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique

Normothermic Cardiac Arrest and Cardiopulmonary Resuscitation: A Mouse Model of Ischemia-Reperfusion Injury

Acute Kidney Injury (AKI) is a common, highly lethal, complication of critical illness which has a high mortality1-4 and which is most 
frequently caused by whole-body hypoperfusion.5,6 Successful reproduction of whole-body hypoperfusion in rodent models has been fraught with 
difficulty.7-9,9,10 Models which employ focal ischemia have repeatedly demonstrated results which do not translate to the clinical setting, and larger 
animal models which allow for whole body hypoperfusion lack access to the full toolset of genetic manipulation possible in the mouse.11,12 However, in recent 
years a mouse model of cardiac arrest and cardiopulmonary resuscitation has emerged which can be adapted to model AKI.13 This model reliably reproduces 
physiologic, functional, anatomic, and histologic outcomes seen in clinical AKI, is rapidly repeatable, and offers all of the significant advantages of a murine surgical 
model, including access to genetic manipulative techniques, low cost relative to large animals, and ease of use. Our group has developed extensive experience 
with use of this model to assess a number of organ-specific outcomes in AKI.14,15

A powerful model for perioperative and critical care related acute kidney injury is presented. Using whole body hypoperfusion induced by cardiac arrest it is possible to nearly replicate the histologic and functional changes of clinical AKI.

常温心脏骤停和心肺复苏术：缺血再灌注损伤的小鼠模型

Acute Kidney Injury (AKI) is a common, highly lethal, complication of critical illness which has a high mortality1-4 and which is most 
frequently caused ...

科研

医学

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

Surgical trauma by thoracotomy in open-chest models of coronary ligation induces an immune response which modifies different mechanisms involved in ischemia and reperfusion. Immune response includes cytokine expression and release or secretion of endogenous ligands of innate immune receptors. Activation of innate immunity can potentially modulate infarct size. We have modified an existing murine closed-chest model using hanging weights which could be useful for studying myocardial pre- and postconditioning and the role of innate immunity in myocardial ischemia and reperfusion. This model allows animals to recover from surgical trauma before onset of myocardial ischemia.
Volatile anesthetics have been intensely studied and their preconditioning effect for the ischemic heart is well known. However, this protective effect precludes its use in open chest models of coronary artery ligation. Thus, another advantage could be the use of the well controllable volatile anesthetics for instrumentation in a chronic closed-chest model, since their preconditioning effect lasts up to 72 hours. Chronic heart diseases with intermittent ischemia and multiple hit models are other possible applications of this model.
For the chronic closed-chest model, intubated and ventilated mice undergo a lateral blunt thoracotomy via the 4th intercostal space. Following identification of the left anterior descending a ligature is passed underneath the vessel and both suture ends are threaded through an occluder. Then, both suture ends are passed through the chest wall, knotted to form a loop and left in the subcutaneous tissue. After chest closure and recovery for 5 days, mice are anesthetized again, chest skin is reopened and hanging weights are hooked up to the loop under ECG control.
At the end of the ischemia/reperfusion protocol, hearts can be stained with TTC for infarct size assessment or undergo perfusion fixation to allow morphometric studies in addition to histology and immunohistochemistry.

Surgical trauma induces an inflammatory response. Cytokines and endogenous ligands are known to modulate myocardial infarct size following ischemia and reperfusion. We present a modified closed-chest model of murine ischemia and reperfusion using hanging weights to minimize effects of thoracotomy.

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 ...

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

To date, many pharmacological agents used to treat or prevent arrhythmias in open-heart cases create undesired systemic side effects. For example, antiarrhythmic drugs administered intravenously can produce drops in systemic pressure in the already compromised cardiac patient. While performing open-heart procedures, surgeons will often either create a small port or form a pericardial cradle to create suitable fields for operation. This access yields opportunities for target pharmacological delivery (antiarrhythmic or ischemic preconditioning agents) directly to the myocardial tissue without undesired side effects.
We have developed a swine model for testing pharmacological agents for target delivery within the pericardial fluid. While fully anesthetized, each animal was instrumented with a Swan-Ganz catheter as well as left and right ventricle pressure catheters, and pacing leads were placed in the right atrial appendage and the right ventricle. A medial sternotomy was then performed and a pericardial access cradle was created; a plunge pacing lead was placed in the left atrial appendage and a bipolar pacing lead was placed in the left ventricle. Utilizing a programmer and a cardiac mapping system, the refractory period of the atrioventricular node (AVN), atria and ventricles was determined. In addition, atrial fibrillation (AF) induction was produced utilizing a Grass stimulator and time in AF was observed. These measurements were performed prior to treatment, as well as 30 min&#160;and 60 min&#160;after pericardial treatment. Additional time points were added for selected studies. The heart was then cardiopleged and reanimated in a four chamber working mode. Pressure measurements and function were recorded for 1 hr after reanimation. This treatment strategy model allowed us to observe the effects of pharmacological agents that may decrease the incidence of cardiac arrhythmias and/or ischemic damage, during and after open-heart surgery.

We have developed a swine model for the target delivery of pharmacological agents within the pericardial space/fluid. Using this approach, the relative benefits of administered agents on induced atrial fibrillation, relative refractory periods and/or ischemic protection can be investigated.

药理试验药物的疗效在心包目标交付模型在猪

To date, many pharmacological agents used to treat or prevent arrhythmias in open-heart cases create undesired systemic side effects. For example, ...

Pre-clinical Model of Cardiac Donation after Circulatory Death

Cardiac transplantation demand is on the rise; nevertheless, organ availability is limited due to a paucity of suitable donors. Organ donation after circulatory death (DCD) is a solution to address this limited availability, but due to a period of prolonged warm ischemia and the risk of tissue injury, its routine use in cardiac transplantation is seldom seen. In this manuscript we provide a detailed protocol closely mimicking current clinical practices in the context of DCD with continuous monitoring of heart function, allowing for the evaluation of novel cardioprotective strategies and interventions to decrease ischemia-reperfusion injury.
In this model, the DCD protocol is initiated in anesthetized Lewis rats by stopping ventilation to induce circulatory death. When systolic blood pressure drops below 30 mmHg, the warm ischemic time is initiated. After a pre-set warm ischemic period, hearts are flushed with a normothermic cardioplegic solution, procured, and mounted onto a Langendorff ex vivo heart perfusion system. Following 10 min of initial reperfusion and stabilization, cardiac reconditioning is continuously evaluated for 60 min using intraventricular pressure monitoring. A heart injury is assessed by measuring cardiac troponin T and the infarct size is quantified by histological staining. The warm ischemic time can be modulated and tailored to develop the desired amount of structural and functional damage. This simple protocol allows for the evaluation of different cardioprotective conditioning strategies introduced at the moment of cardioplegia, initial reperfusion and/or during ex vivo perfusion. Findings obtained from this protocol can be reproduced in large models, facilitating clinical translation.

This protocol shows a simple and flexible approach for the evaluation of new conditioning agents or strategies to increase the feasibility of cardiac donation after circulatory death.

循环死亡后心脏捐献的临床前模型

Cardiac transplantation demand is on the rise; nevertheless, organ availability is limited due to a paucity of suitable donors. Organ donation after ...

Standardized Model of Ventricular Fibrillation and Advanced Cardiac Life Support in Swine

Cardiopulmonary resuscitation after cardiac arrest, independent of its origin, is a regularly encountered medical emergency in hospitals as well as preclinical settings. Prospective randomized trials in human subjects are difficult to design and ethically ambiguous, which results in a lack of evidence-based therapies. The model presented in this report represents one of the most common causes of cardiac arrests, ventricular fibrillation, in a standardized setting in a large animal model. This allows for reproducible observations and various therapeutic interventions under clinically accurate conditions, hence facilitating the generation of better evidence and eventually the potential for improved medical treatment.

Cardiopulmonary resuscitation and defibrillation are the only effective therapeutic options during cardiac arrest caused by ventricular fibrillation. This model presents a standardized regimen to induce, assess, and treat this physiological state in a porcine model, thus providing a clinical approach with various opportunities for data collection and analysis.

猪心室颤动和高级心脏生命支持标准化模型

Cardiopulmonary resuscitation after cardiac arrest, independent of its origin, is a regularly encountered medical emergency in hospitals as well as ...

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence suggests that thrombolytic therapy or primary percutaneous coronary intervention (PPCI) does not prevent reperfusion injury. There is still no ideal animal model for MIRI. This study aims to improve the MIRI model in rats to make surgery easier and more feasible. A unique method for establishing MIRI is developed by using a soft tube during a key step of the ischemic period. To explore this method, thirty rats were randomly divided into three groups: sham group (n = 10); experimental model group (n = 10); and existing model group (n = 10). Findings of triphenyltetrazolium chloride staining, electrocardiography, and percent survival are compared to determine the accuracies and survival rates of the operations. Based on the study results, it has been concluded that the improved surgery method is associated with a higher survival rate, elevated ST-T segment, and larger infarct size, which is expected to mimic the pathology of MIRI better.

Myocardial ischemia-reperfusion model of rat heart is improved by using a self-made retractor, polyvinyl chloride tube, and a unique knotting method. Electrocardiogram, triphenyltetrazolium chloride and histological staining, and percent survival analysis results showed that the improved model group has higher success and survival rates than the already existing model group.

心肌缺血再灌注损伤的改进啮齿动物模型

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence ...

Transthoracic Echocardiography to Assess Post-Resuscitation Left Ventricular Dysfunction After Acute Myocardial Infarction and Cardiac Arrest in Pigs

One of the main causes of out-of-hospital cardiac arrest is acute myocardial infarction (AMI). After successful resuscitation from cardiac arrest, approximately 70% of patients die before hospital discharge due to post-resuscitation myocardial and cerebral dysfunction. In experimental models, myocardial dysfunction after cardiac arrest, characterized by an impairment in both left ventricular (LV) systolic and diastolic function, has been described as reversible but very little data are available in cardiac arrest models associated with AMI in pigs. Transthoracic echocardiography is the first-line diagnostic test for the assessment of myocardial dysfunction, structural changes and/or AMI extension. In this pig model of ischemic cardiac arrest, echocardiography was done at baseline and 2-4 and 96 hours after resuscitation. In the acute phase, the examinations are done in anesthetized, mechanically ventilated pigs (weight 39.8 &#177; 0.6 kg) and ECG is recorded continuously. Mono- and bi-dimensional, Doppler and tissue Doppler recordings are acquired. Aortic and left atrium diameter, end-systolic and end-diastolic left ventricular wall thicknesses, end-diastolic and end-systolic diameters and shortening fraction (SF) are measured. Apical 2-, 3-, 4-, and 5-chamber views are acquired, LV volumes and ejection fraction are calculated. Segmental wall motion analysis is done to detect the localization and estimate the extent of myocardial infarction. Pulsed Wave Doppler echocardiography is used to record trans-mitral flow velocities from a 4-apical chamber view and trans-aortic flow from a 5-chamber view to calculate LV cardiac output (CO) and stroke volume (SV). Tissue Doppler Imaging (TDI) of LV lateral and septal mitral anulus is recorded (TDI septal and lateral s&#39;, e&#39;, a&#39; velocities). All the recordings and measurements are done according to the recommendations of the American and European Societies of Echocardiography Guidelines.

Transthoracic echocardiography is the first-line diagnostic test for post-resuscitation left ventricular dysfunction and structural changes in a pig model of cardiac arrest.

经胸超声心动图评估猪急性心肌梗死和心脏骤停后复苏后左心室功能障碍

One of the main causes of out-of-hospital cardiac arrest is acute myocardial infarction (AMI). After successful resuscitation from cardiac arrest, ...

A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts

Ventricular fibrillation (VF) is a fatal arrhythmia with a high incidence in cardiac patients, but VF arrest under perfusion is a neglected method of intraoperative arrest in the field of cardiac surgery. With recent advances in cardiac surgery, the demand for prolonged VF studies under perfusion has increased. However, the field lacks simple, reliable, and reproducible animal models of chronic ventricular fibrillation. This protocol induces long-term VF through alternating current (AC) electrical stimulation of the epicardium. Different conditions were used to induce VF, including continuous stimulation with a low or high voltage to induce long-term VF and stimulation for 5 min with a low or high voltage to induce spontaneous long-term VF. The success rates of the different conditions, as well as the rates of myocardial injury and recovery of cardiac function, were compared. The results showed that continuous low-voltage stimulation induced long-term VF and that 5 min of low-voltage stimulation induced spontaneous long-term VF with mild myocardial injury and a high rate of recovery of cardiac function. However, the low-voltage, continuously stimulated long-term VF model had a higher success rate. High-voltage stimulation provided a higher rate of VF induction but showed a low defibrillation success rate, poor recovery of cardiac function, and severe myocardial injury. On the basis of these results, continuous low-voltage epicardial AC stimulation is recommended for its high success rate, stability, reliability, reproducibility, low impact on cardiac function, and mild myocardial injury.

This protocol presents a model of long-term ventricular fibrillation in rat hearts induced by continuous stimulation with low-voltage alternating current. This model has a high success rate, is stable, reliable, and reproducible, has a low impact on cardiac function, and causes only mild myocardial injury.

孤立大鼠心脏长期心室颤动模型

Ventricular fibrillation (VF) is a fatal arrhythmia with a high incidence in cardiac patients, but VF arrest under perfusion is a neglected method of ...

Chronic Ovine Model of Right Ventricular Failure and Functional Tricuspid Regurgitation

The pathophysiology of severe functional tricuspid regurgitation (FTR) associated with right ventricular dysfunction is poorly understood, leading to suboptimal clinical results. We set out to establish a chronic ovine model of FTR and right heart failure to investigate the mechanisms of FTR. Twenty adult male sheep (6-12 months old, 62 &#177; 7 kg) underwent a left thoracotomy and baseline echocardiography. A pulmonary artery band (PAB) was placed and cinched around the main pulmonary artery (PA) to at least double the systolic pulmonary artery pressure (SPAP), inducing right ventricular (RV) pressure overload and signs of RV dilatation. PAB acutely increased the SPAP from 21 &#177; 2 mmHg to 62 &#177; 2 mmHg. The animals were followed for 8 weeks, symptoms of heart failure were treated with diuretics, and surveillance echocardiography was used to assess for pleural and abdominal fluid collection. Three animals died during the follow-up period due to stroke, hemorrhage, and acute heart failure. After 2 months, a median sternotomy and epicardial echocardiography were performed. Of the surviving 17 animals, 3 developed mild tricuspid regurgitation, 3 developed moderate tricuspid regurgitation, and 11 developed severe tricuspid regurgitation. Eight weeks of pulmonary artery banding resulted in a stable chronic ovine model of right ventricular dysfunction and significant FTR. This large animal platform can be used to further investigate the structural and molecular basis of RV failure and functional tricuspid regurgitation.

Right ventricular failure and functional tricuspid regurgitation are associated with left-sided heart disease and pulmonary hypertension, which contribute significantly to morbidity and mortality in patients. Establishing a chronic ovine model to study right ventricular failure and functional tricuspid regurgitation will help in understanding their mechanisms, progression, and possible treatments.

右心室衰竭和功能性三尖瓣反流的慢性绵羊模型

The pathophysiology of severe functional tricuspid regurgitation (FTR) associated with right ventricular dysfunction is poorly understood, leading to ...

心脏骤停后动物模型体外心肺复苏

Pediatric Animal Model of Extracorporeal Cardiopulmonary Resuscitation After Prolonged Circulatory Arrest

Congenital heart disease (CHD) is the most prevalent congenital malformation, with about one million births impacted worldwide per year. Comprehensive investigation of this disease requires appropriate and validated animal models. Piglets are commonly used for translational research due to their analogous anatomy and physiology. This work aimed to describe and validate a neonatal piglet model of cardiopulmonary bypass (CPB) with circulatory and cardiac arrest (CA) as a tool for studying severe brain damage and other complications of cardiac surgery. In addition to including a list of materials, this work provides a roadmap for other investigators to plan and execute this protocol. After experienced practitioners performed several trials, the representative results of the model demonstrated a 92% success rate, with failures attributed to small piglet size and variant vessel anatomy. Furthermore, the model allowed practitioners to select from a wide variety of experimental conditions, including varying times in CA, temperature alterations, and pharmacologic interventions. In summary, this method uses materials readily available in most hospital settings, is reliable and reproducible, and can be widely employed to enhance translational research in children undergoing heart surgery.

作者聚焦：使用新生儿仔猪模型模拟儿科心脏手术

This protocol describes a neonatal porcine model of cardiopulmonary bypass (CPB), with circulatory and cardiac arrest as a tool for studying severe brain damage and other complications secondary to CPB.

长时间循环停止后体外心肺复苏的小儿动物模型

Congenital heart disease (CHD) is the most prevalent congenital malformation, with about one million births impacted worldwide per year. Comprehensive ...