作者感谢克里斯蒂娜 Pahrmann 的技术援助。
. 得到了最大凯基金会的支持。李政道获得了其他 kr 基金会 (2012_EKES 04) 和德意志 Forschungsgemeinschaft (DE2133/2-1 _。从德意志 Forschungsgemeinschaft (DFG) 获得了研究补助金;SCHR992/3-1, SCHR992/4-1)。

动物接受了人道护理, 符合《实验室动物原则指南》, 由实验室动物资源研究所编写, 并由国家卫生研究所出版。所有动物协议由负责任的地方当局批准 ("Amt Gesundheit 和 Verbraucherschutz, Hansestadt (办公室为健康和消费者保护) 汉堡")。
1. 导管制备
注: 有关导管的信息, 请参阅材料表。
<ol><li>从导管架上取导管。</li>
	<li>将丝从管腔中通过远端端口拉出。</li>
	<li>在导管远端放置一滴氰胶。 注意: 戴上乳胶或腈手套。</li>
	<li>将丝置于导管的 RX 口, 并将其通过管腔推进至远端端口。之后, 把丝向后轻轻地留出一个5毫米的空间到最后。</li>
	<li>等待5分钟, 使胶粘剂干燥。</li>
	<li>移动丝, 它应该是固定的。如果它仍然是移动的, 重复步骤 1.3-1.6。</li>
	<li>用1.5 毫升0.9% 盐水填充3毫升注射器, 并将其连接到气球充气端口。</li>
	<li>推动注射器柱塞测试气球膨胀。在注射器里留下0.6 毫升盐水</li>
</ol>2. 鼠标准备
<ol><li>在14周的年龄获得雄性小鼠, 体重约30克。 注: 我们用动物实验动物研究所获得。我们在这里用 C57BL/6J</li>
	<li>使用诱导室麻醉 2.0-2.5% isofurane (500 毫升/分钟氧气流量) 的鼠标。</li>
	<li>将鼠标放在加热垫上, 并用口罩覆盖鼠标的嘴和鼻子来维持麻醉。通过捏后腿和尾部检查是否有足够的麻醉深度, 以验证是否没有反应。</li>
	<li>用理发剪掉腹部的毛发。</li>
	<li>伸展后腿, 用胶带固定好自己的位置。</li>
	<li>用聚维酮碘消毒腹部面积, 其次为80% 乙醇。重复此步骤两次。</li>
	<li>使用手术的悬垂, 以确保外科网站不会受到污染。打开皮肤和肌肉层沿式阿尔巴与剪刀 (或手术刀), 以揭露腹部器官。</li>
	<li>放置在0.9% 盐水滋润手套和包装的肠道, 以保持他们的湿润。</li>
	<li>用两个好的镊子来除去腹主动脉上方的脂肪组织。</li>
	<li>使用胰岛素注射器 (30G), 注入250µL 肝素溶液 (50 U/毫升) 进入下腔静脉 (下静脉) 和等待3分钟, 其系统性分布。肝素在手术中会抑制止血, 防止不受欢迎的凝血。</li>
	<li>使用两个镊子, 解剖下主动脉下到它的分岔和其传出分支血管。</li>
	<li>结扎的侧血管, 预计将放置在固定的地区, 与高温 cauterizer。</li>
	<li>通过在肾动脉下直接夹紧下主动脉来阻止血液流动。</li>
	<li>在主动脉分岔的远端位置放置第二夹钳。</li>
	<li>用剪刀在容器的夹钳中点进行一个小的水平切口。 注: 切口尺寸应相当于容器周长的1/3。</li>
	<li>将注射器与 (30G) 针插入切口, 用250µL 肝素溶液冲洗主动脉 (50 U/毫升)。</li>
	<li>使用10-0 缝线, 在切口的两侧放置一个单一的结。</li>
	<li>通过将血管扩张插入切口并略微展开血管来扩张主动脉。重复扩张2到3次。</li>
	<li>用0.9% 盐水滋润气囊导管。</li>
	<li>将扁平气囊导管插入主动脉, 向主动脉上的近端钳推进。</li>
	<li>当到达近端钳, 小心打开近端钳和充气气球, 以防止血液泄漏, 通过注射〜0.6 毫升盐水。 注: 充气气球与容器的比例为 1.5: 1。</li>
	<li>推进导管逆行约2厘米。</li>
	<li>将膨胀的导管拉回, 同时通过释放注射器使气球略微收缩。</li>
	<li>当导管到达主动脉切口时, 重新连接近端钳。将气球完全放气并将其取出。</li>
	<li>使用30G 注射器冲洗主动脉与250µL 肝素溶液 (50 U/毫升)。</li>
	<li>用10-0 缝合线关闭主动脉切口。在每个侧面的地方间断针, 其次是一个或两个针在腹侧。</li>
	<li>打开远端钳。在出血的情况下, 再次关闭钳, 并放置额外的针。</li>
	<li>仔细打开近端钳。</li>
	<li>将两个拭子放在缝合线上以支持它并止血。</li>
	<li>将可吸收止血放在缝合线上以维持它。 注: 从切口远端可见主动脉搏动。</li>
	<li>把肠子放回腹部</li>
	<li>用无菌0.9% 盐水冲洗腹腔, 已预热至37° c。</li>
	<li>关闭腹部肌肉层使用6-0 运行缝合线。</li>
	<li>关闭皮肤与5-0 运行缝合线。</li>
	<li>注射4-5 毫克/千克卡洛芬皮下, 让鼠标醒来。监测动物, 直到它已经获得意识, 保持胸骨卧床。把动物单独关在笼子里, 直到完全恢复。</li>
	<li>添加乃到饮用水 (50 mg/100 毫升) 作为止痛药3天, 并监测动物的日常。通常老鼠喜欢甜味的乃, 并在手术后立即开始饮用。如果首选, 可持续释放的注射剂可以使用, 而不是乃。 注: 该模型的观察期为28天。</li>
</ol>3. 组织病理学
<ol><li>28天后, 通过准备步骤2.2 到2.9 中描述的小鼠来收获气球损伤的主动脉。</li>
	<li>使用剪刀去除气球受伤的主动脉 (在分岔和0.3 毫米之间的肾血管) 和安乐的老鼠通过切割出它的心脏。</li>
	<li>用0.9% 氯化钠冲洗容器的流明。</li>
	<li>在4% 甲醛 (粉煤灰) 过夜和脱水它在增加乙醇浓度, 从70% 乙醇为2小时, 80% 乙醇为1小时, 95% 乙醇为2小时, 100% 乙醇为5小时。然后, 在二甲苯中孵育样品2小时3次, 然后用石蜡浸润样品。 注: 与其用0.9% 氯化钠冲洗收获的容器, 倒不如用4% 的煤灰冲水。 注意: 粉煤灰和二甲苯是有毒的, 应特别小心处理。</li>
	<li>将样品嵌入石蜡切片, 用切片切割成5µm 厚度的薄片。</li>
	<li>用二甲苯 Deparaffinize 3 次, 5 分钟。</li>
	<li>用减少的乙醇系列水化组织切片。开始与100% 乙醇2次5分钟, 其次是3分钟的 95%, 80% 和70% 乙醇。</li>
	<li>用马尾松的三染色对幻灯片进行着色, 如18所述。</li>
	<li>脱水染色幻灯片100% 乙醇2次, 每10分钟。用二甲苯清除2次, 每次10分钟, 装入安装介质。</li>
	<li>用明亮的野外显微镜查看幻灯片。使用一个5x 放大倍数的镜头和一个数字孔径为0.12 的概述图片或一个镜头与20x 放大的数字孔径为 0.35, 详细观察。</li>
</ol>4. 免疫荧光显微镜
<ol><li>用减少的乙醇系列水化组织切片。开始与100% 乙醇2次5分钟, 其次是3分钟的 95%, 80% 和70% 乙醇。</li>
	<li>在20分钟的蒸笼中, 通过加热抗原检索溶液中的玻片来进行抗原检索。</li>
	<li>让幻灯片冷却到室温。</li>
	<li>用磷酸盐缓冲盐水 (PBS) 冲洗三次后, 在切片上应用抗原阻滞溶液30分钟。</li>
	<li>冲洗幻灯片三次, 5 分钟与 PBS。</li>
	<li>在初级抗体稀释剂中稀释初级抗体的孵育部分。 注意: 每种抗体应分别选择合适的浓度和孵育时间。</li>
	<li>清洗幻灯片三次, 5 分钟与 PBS, 以消除未绑定的抗体。</li>
	<li>在二次抗体稀释剂中稀释的预共轭二级抗体孵育部分。 注意: 每种抗体应分别选择合适的浓度和孵育时间。</li>
	<li>通过冲洗5分钟三次的幻灯片来去除未绑定的抗体。</li>
	<li>Counterstain 细胞核使用 4 ', 6-diamidino-2-吲 (DAPI) 15 分钟;最后的 DAPI 浓度应为 350 nM。</li>
	<li>在免疫荧光兼容安装解决方案中安装幻灯片。 注: 使用错误的安装解决方案可以掩盖荧光信号。</li>
	<li>用荧光显微镜查看幻灯片。使用一个数字光圈为1.3 的40x 放大镜头。</li>
</ol>

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作者没有什么可透露的。

本文介绍了小鼠模型研究 myointimal 增生的发展, 并允许探索的基础病理过程和测试新药或治疗方案。
该协议最关键的步骤是主动脉的剥蚀。在这一步中应特别注意, 过度的剥蚀会导致动脉瘤形成和模型衰竭。另一方面, 如果剥蚀的执行不够, 太少的 myointima 将发展。因此, 剥蚀台阶的强度对该动物模型的结果和成功至关重要。
关于外科手术, 这是至关重要的?...

冠状动脉和外周动脉狭窄对患者的发病率和死亡率有很大的影响1。一个潜在的病理机制是 myointima 增生 (MH), 其特点是增加增殖, 迁移, 并合成细胞外基质蛋白从血管平滑肌细胞 (SMC)2。SMC 位于容器的介质层, 并在对腔表面进行刺激后迁移。刺激信号包括生长因子、细胞因子、细胞接触、脂质、细胞外基质成分、机械剪切和拉伸力3、4、5、6。血管壁损伤, 病理或医源性, 导致内皮细胞和平滑肌细胞损伤, 刺激炎症反应, 从而导致 MH7。
目前有不同的动物模型可用于研究动脉损伤和 myointima 增生。像猪或狗这样的大型动物, 具有与人类分享相似的动脉和冠状动脉解剖的优势, 特别适合研究血管成形技术、过程和设备的调查8。然而, 猪模型有更高的缺点血栓9,10, 而狗只对船只伤害有轻微的反应11。此外, 所有大型动物模型都需要特殊的住房、设备和工作人员, 这些都与高昂的费用联系在一起, 而且并不总是在一个机构中提供。小动物模型包括老鼠和老鼠。与大鼠相比, 小鼠具有成本低且存在各种敲出模型的优点。本视频中描述的模型可以与以西方饮食喂养的载脂蛋白小鼠相结合, 以密切模仿动脉粥样硬化血管成形术的临床设置12。既往模型通过钢丝损伤诱发血管损伤13, 液体脱水的14, 春季15, 或袖扣伤16。由于损伤的性质将极大地影响 MH 的发展和构成, 使用气囊导管诱导血管损伤是模拟临床环境的最佳方法。
本文介绍了一种用气囊导管诱导小鼠 MH 的新方法。使用带 RX 端口 (图 1A) 的气囊导管 (1.2 mm x 6 mm) 可使内膜层的刮擦, 同时还能诱导血管的 overdistension。这两个因素都是 MH 发展的重要诱因。此模型的观察时间为28天17。

<table>
	<tbody>
		<tr>
			<td>10-0 Ethilon suture</td>
			<td>Ethicon</td>
			<td>2814G</td>
			<td></td>
		</tr>
		<tr>
			<td>3 mL Syringe</td>
			<td>BD Medical</td>
			<td>309658</td>
			<td></td>
		</tr>
		<tr>
			<td>37% HCl</td>
			<td>Sigma-Aldrich</td>
			<td>H1758</td>
			<td></td>
		</tr>
		<tr>
			<td>5-0 prolene suture</td>
			<td>Ethicon</td>
			<td>EH7229H</td>
			<td></td>
		</tr>
		<tr>
			<td>6-0 prolene suture</td>
			<td>Ethicon</td>
			<td>8706H</td>
			<td></td>
		</tr>
		<tr>
			<td>Acid Fuchsin</td>
			<td>Sigma-Aldrich</td>
			<td>F8129-25G</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>Antigen retrieval solution</td>
			<td>Dako</td>
			<td>S1699</td>
			<td></td>
		</tr>
		<tr>
			<td>Azophloxin</td>
			<td>Waldeck</td>
			<td>1B-103</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>Bepanthen Eye and Nose ointment</td>
			<td>Bayer</td>
			<td>1578675</td>
			<td>Eye ointment</td>
		</tr>
		<tr>
			<td>Betadine Solution</td>
			<td>Betadine Purdue Pharma</td>
			<td>NDC:67618-152</td>
			<td></td>
		</tr>
		<tr>
			<td>C57BL/6J</td>
			<td>Charles River</td>
			<td>Stock number 000664</td>
			<td></td>
		</tr>
		<tr>
			<td>Clamp applicator</td>
			<td>Fine Science Tools</td>
			<td>18056-14</td>
			<td></td>
		</tr>
		<tr>
			<td>Collagen 3</td>
			<td>abcam</td>
			<td>ab7778</td>
			<td>Antibody</td>
		</tr>
		<tr>
			<td>DAPI</td>
			<td>Thermo Fischer</td>
			<td>D1306</td>
			<td></td>
		</tr>
		<tr>
			<td>Donkey anti-Goat IgG AF555</td>
			<td>Invitrogen</td>
			<td>A21432</td>
			<td>Secondary antibody</td>
		</tr>
		<tr>
			<td>Donkey anti-Rabbit IgG AF488</td>
			<td>Invitrogen</td>
			<td>A21206</td>
			<td>Secondary antibody</td>
		</tr>
		<tr>
			<td>Donkey anti-Rabbit IgG AF488</td>
			<td>Invitrogen</td>
			<td>A11055</td>
			<td>Secondary antibody</td>
		</tr>
		<tr>
			<td>Donkey anti-Rabbit IgG AF555</td>
			<td>Invitrogen</td>
			<td>A31572</td>
			<td>Secondary antibody</td>
		</tr>
		<tr>
			<td>Ethanol 70%</td>
			<td>Th. Geyer</td>
			<td>2270</td>
			<td></td>
		</tr>
		<tr>
			<td>Ethanol 96%</td>
			<td>Th. Geyer</td>
			<td>2295</td>
			<td></td>
		</tr>
		<tr>
			<td>Ethanol absolute</td>
			<td>Th. Geyer</td>
			<td>2246</td>
			<td></td>
		</tr>
		<tr>
			<td>FAP</td>
			<td>abcam</td>
			<td>ab28246</td>
			<td>Antibody</td>
		</tr>
		<tr>
			<td>Forceps fine</td>
			<td>Fine Science Tools</td>
			<td>11251-20</td>
			<td></td>
		</tr>
		<tr>
			<td>Forceps standard</td>
			<td>Fine Science Tools</td>
			<td>11023-10</td>
			<td></td>
		</tr>
		<tr>
			<td>Glacial Acetic Acid</td>
			<td>Sigma-Aldrich</td>
			<td>537020</td>
			<td></td>
		</tr>
		<tr>
			<td>Hair clipper</td>
			<td>WAHL</td>
			<td>8786-451A ARCO SE</td>
			<td></td>
		</tr>
		<tr>
			<td>Heparin</td>
			<td>Rotexmedica</td>
			<td>PZN 3862340</td>
			<td>25.000 I.E./mL</td>
		</tr>
		<tr>
			<td>High temperature cautery kit</td>
			<td>Bovie</td>
			<td>18010-00</td>
			<td></td>
		</tr>
		<tr>
			<td>Image-iT FX Signal Enhancer</td>
			<td>Invitrogen</td>
			<td>I36933</td>
			<td>Blocking solution</td>
		</tr>
		<tr>
			<td>Light Green SF</td>
			<td>Waldeck</td>
			<td>1B-211</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>Microsurgical clamp</td>
			<td>Fine Science Tools</td>
			<td>18055-04</td>
			<td>Micro-Serrefine - 4mm</td>
		</tr>
		<tr>
			<td>MINI TREK Coronary Dilatation Catheter 1.20 mm x 6 mm / Rapid-Exchange</td>
			<td>Abbott</td>
			<td>1012268-06U</td>
			<td></td>
		</tr>
		<tr>
			<td>Molybdatophosphoric acid hydrate</td>
			<td>Merck</td>
			<td>1.00532.0100</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>NaCl 0,9%</td>
			<td>B.Braun</td>
			<td>PZN 06063042 Art. Nr.: 3570160</td>
			<td></td>
		</tr>
		<tr>
			<td>Needle holder</td>
			<td>Fine Science Tools</td>
			<td>12075-14</td>
			<td></td>
		</tr>
		<tr>
			<td>Novaminsulfon</td>
			<td>Ratiopharm</td>
			<td>PZN 03530402</td>
			<td>Metamizole</td>
		</tr>
		<tr>
			<td>Orange G</td>
			<td>Waldeck</td>
			<td>1B-221</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>Paraffin</td>
			<td>Leica biosystems</td>
			<td>REF 39602004</td>
			<td></td>
		</tr>
		<tr>
			<td>PBS pH 7,4</td>
			<td>Gibco</td>
			<td>10010023</td>
			<td></td>
		</tr>
		<tr>
			<td>PFA 4%</td>
			<td>Electron Microscopy Sciences</td>
			<td>#157135S</td>
			<td></td>
		</tr>
		<tr>
			<td>Ponceau S solution</td>
			<td>Serva Electrophoresis</td>
			<td>33427</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>Primary antibody diluent</td>
			<td>Dako</td>
			<td>S3022</td>
			<td></td>
		</tr>
		<tr>
			<td>Prolong Gold Mounting solution</td>
			<td>Thermo Fischer</td>
			<td>P36930</td>
			<td>Mounting solution for immunofluorescence stained slides</td>
		</tr>
		<tr>
			<td>Replaceable Fine Tip</td>
			<td>Bovie</td>
			<td>H101</td>
			<td></td>
		</tr>
		<tr>
			<td>Resorcin-Fuchsin Weigert</td>
			<td>Waldeck</td>
			<td>2E-30</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>Rimadyl</td>
			<td>Pfizer</td>
			<td>400684.00.00</td>
			<td>Carprofen</td>
		</tr>
		<tr>
			<td>Scissors</td>
			<td>Fine Science Tools</td>
			<td>14028-10</td>
			<td></td>
		</tr>
		<tr>
			<td>Scissors Vannas-style</td>
			<td>Fine Science Tools</td>
			<td>15000-03</td>
			<td></td>
		</tr>
		<tr>
			<td>Secondary antibody diluent</td>
			<td>Dako</td>
			<td>S0809</td>
			<td></td>
		</tr>
		<tr>
			<td>Fast acting Adhesive MINIS 3x1g</td>
			<td>UHU</td>
			<td>45370</td>
			<td>Cyanoacrylate</td>
		</tr>
		<tr>
			<td>Slide Rack</td>
			<td>Ted Pella</td>
			<td>21057</td>
			<td></td>
		</tr>
		<tr>
			<td>SM22</td>
			<td>abcam</td>
			<td>ab10135</td>
			<td>Antibody</td>
		</tr>
		<tr>
			<td>SMA</td>
			<td>abcam</td>
			<td>ab21027</td>
			<td>Antibody</td>
		</tr>
		<tr>
			<td>Staining dish</td>
			<td>Ted Pella</td>
			<td>21075</td>
			<td></td>
		</tr>
		<tr>
			<td>Surgical microscope</td>
			<td>Leica</td>
			<td>M651</td>
			<td></td>
		</tr>
		<tr>
			<td>Tabotamp fibrillar</td>
			<td>Ethicon</td>
			<td>431962</td>
			<td>Absorbable hemostat</td>
		</tr>
		<tr>
			<td>Transpore Surgical Tape</td>
			<td>3M</td>
			<td>1527-1</td>
			<td></td>
		</tr>
		<tr>
			<td>U-100 Insulin syringe</td>
			<td>BD Medical</td>
			<td>324825</td>
			<td></td>
		</tr>
		<tr>
			<td>Vessel Dilator</td>
			<td>Fine Science Tools</td>
			<td>18603-14</td>
			<td></td>
		</tr>
		<tr>
			<td>Vitro-Clud</td>
			<td>Langenbrinck</td>
			<td>04-0001</td>
			<td></td>
		</tr>
		<tr>
			<td>Weigerts iron hematoxylin Kit</td>
			<td>Merck</td>
			<td>1.15973.0002</td>
			<td>Trichrome staining</td>
		</tr>
		<tr>
			<td>Xylene</td>
			<td>Th. Geyer</td>
			<td>3410</td>
			<td></td>
		</tr>
	</tbody>
</table>

balloon-based injury to induce myointimal hyperplasia in the mouse abdominal aorta

使用动物模型对更好地了解 MH 是至关重要的, 这是动脉狭窄的主要原因之一。在这篇文章中, 我们演示了一个小鼠气球剥脱模型, 这是与建立在大型动物的血管损伤模型比较。主动脉剥脱模型与球囊导管模拟临床设置, 并导致可比病理和生理变化。简单地, 在主动脉紫癜中进行水平切口后, 气球导管将插入容器中, 充气, 并引入逆行。气球的膨胀会导致血管内膜损伤和 overdistension。取出导管后, 主动脉切口将与单拆线闭合。本文所介绍的模型重现性好, 易于执行, 且能快速可靠地建立。它特别适用于评价昂贵的实验性治疗剂, 可以在经济的方式应用。利用不同的击倒-小鼠菌株, 可以评估不同基因对 MH 发育的影响。

球囊剥脱是研究小鼠 MH 发育的一个合适的模型。动物从手术中恢复良好, 并显示出良好的身体状况后手术。我们在50只小鼠中建立了这个模型, 由于手术的原因, 死亡率不到3%。图 1B-c显示关键的手术步骤。沿式阿尔巴进行皮肤切口后, 确定主动脉紫癜。放置显微外科钳 (图 1B)。做一个小切口在中间的主?...

Watch this Scientific Journal Video about Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta at JoVE.com

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

本文对小鼠主动脉球囊损伤后 myointimal 增生 (MH) 的发育进行了研究。

球囊损伤诱发小鼠腹主动脉 Myointimal 增生的研究

The use of animal models is essential for a better understanding of MH, one major cause for arterial stenosis.In this article, we demonstrate a murine ...

balloon-based-injury-to-induce-myointimal-hyperplasia-mouse-abdominal

Research

JoVE Journal

Medicine

9.5K 次观看.  University Heart Center. 本文对小鼠主动脉球囊损伤后 myointimal 增生 (MH) 的发育进行了研究。

视频: Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

The C-seal: A Biofragmentable Drain Protecting the Stapled Colorectal Anastomosis from Leakage

Colorectal anastomotic leakage (AL) is a serious complication in colorectal surgery leading to high morbidity and mortality rates1. The incidence of AL varies between 2.5 and 20% 2-5. Over the years, many strategies aimed at lowering the incidence of anastomotic leakage have been examined6, 7. 
The cause of AL is probably multifactorial. Etiological factors include insufficient arterial blood supply, tension on the anastomosis, hematoma and/or infection at the anastomotic site, and co-morbid factors of the patient as diabetes and atherosclerosis8. Furthermore, some anastomoses may be insufficient from the start due to technical failure.
Currently a new device is developed in our institute aimed at protecting the colorectal anastomosis and lowering the incidence of AL. This so called C-seal is a biofragmentable drain, which is stapled to the anastomosis with the circular stapler. It covers the luminal side of the colorectal anastomosis thereby preventing leakage.
The C-seal is a thin-walled tube-like drain, with an approximate diameter of 4 cm and an approximate length of 25 cm (figure 1). It is a tubular device composed of biodegradable polyurethane. Two flaps with adhesive tape are found at one end of the tube. These flaps are used to attach the C-seal to the anvil of the circular stapler, so that after the anastomosis is made the C-seal can be pulled through the anus. The C-seal remains in situ for at least 10 days. Thereafter it will lose strength and will degrade to be secreted from the body together with the gastrointestinal natural contents.
The C-seal does not prevent the formation of dehiscences. However, it prevents extravasation of faeces into the peritoneal cavity. This means that a gap at the anastomotic site does not lead to leakage.
Currently, a phase II study testing the C-seal in 35 patients undergoing (colo-)rectal resection with stapled anastomosis is recruiting. The C-seal can be used in both open procedures as well as laparoscopic procedures. The C-seal is only applied in stapled anastomoses within 15cm from the anal verge. In the video, application of the C-seal is shown in an open extended sigmoid resection in a patient suffering from diverticular disease with a stenotic colon.

The C-seal is a biofragmentable drain protecting the stapled colorectal anastomosis. In this video, details of the manufacturing, deployment and use are shown.

C密封:一个Biofragmentable漏漏电保护吻合结直肠吻合

Colorectal anastomotic leakage (AL) is a serious complication in colorectal surgery leading to high morbidity and mortality rates1. The incidence of AL ...

科研

医学

Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice

Murine models are extensively used to investigate acute injuries of different organs systems (1-34). Acute lung injury (ALI), which occurs with prolonged mechanical ventilation, contributes to morbidity and mortality of critical illness, and studies on novel genetic or pharmacological targets are areas of intense investigation (1-3, 5, 8, 26, 30, 33-36). ALI is defined by the acute onset of the disease, which leads to non-cardiac pulmonary edema and subsequent impairment of pulmonary gas exchange (36). We have developed a murine model of ALI by using a pressure-controlled ventilation to induce ventilator-induced lung injury (2). For this purpose, C57BL/6 mice are anesthetized and a tracheotomy is performed followed by induction of ALI via mechanical ventilation. Mice are ventilated in a pressure-controlled setting with an inspiratory peak pressure of 45 mbar over 1 - 3 hours. As outcome parameters, pulmonary edema (wet-to-dry ratio), bronchoalveolar fluid albumin content, bronchoalveolar fluid and pulmonary tissue myeloperoxidase content and pulmonary gas exchange are assessed (2). Using this technique we could show that it sufficiently induces acute lung inflammation and can distinguish between different treatment groups or genotypes (1-3, 5). Therefore this technique may be helpful for researchers who pursue molecular mechanisms involved in ALI using a genetic approach in mice with gene-targeted deletion.

A murine model for ventilator induced lung injury is an important tool to study an acute lung injury in vivo. Here, we report an easy applicable in situ model for acute lung injury using high-pressure mechanical ventilation to induce acute failure of the lung.

压力控制通气诱导小鼠急性肺损伤

Murine models are extensively used to investigate acute injuries of different organs systems (1-34). Acute lung injury (ALI), which occurs with prolonged ...

The CYP2D6 Animal Model: How to Induce Autoimmune Hepatitis in Mice

Autoimmune hepatitis is a rare but life threatening autoimmune disease of the liver of unknown etiology1,2. In the past many attempts have been made to generate an animal model that reflects the characteristics of the human disease 3-5. However, in various models the induction of disease was rather complex and often hepatitis was only transient3-5. Therefore, we have developed a straightforward mouse model that uses the major human autoantigen in type 2 autoimmune hepatitis (AIH-2), namely hCYP2D6, as a trigger6. Type 1 liver-kidney microsomal antibodies (LKM-1) antibodies recognizing hCYP2D6 are the hallmark of AIH-27,8. Delivery of hCYP2D6 into wildtype FVB or C57BL/6 mice was by an Adenovirus construct (Ad-2D6) that ensures a direct delivery of the triggering antigen to the liver. Thus, the ensuing local inflammation generates a fertile field9 for the subsequent development of autoimmunity. A combination of intravenous and intraperitoneal injection of Ad-2D6 is the most effective route to induce a long-lasting autoimmune damage to the liver (section 1). Here we provide a detailed protocol on how autoimmune liver disease is induced in the CYP2D6 model and how the different aspects of liver damage can be assessed. First, the serum levels of markers indicating hepatocyte destruction, such as aminotransferases, as well as the titers of hCYP2D6 antibodies are determined by sampling blood retroorbitaly (section 2). Second, the hCYP2D6-specific T cell response is characterized by collecting lymphocytes from the spleen and the liver. In order to obtain pure liver lymphocytes, the livers are perfused by PBS via the portal vein (section 3), digested in collagen and purified over a Percoll gradient (section 4). The frequency of hCYP2D6-specific T cells is analyzed by stimulation with hCYP2D6 peptides and identification of IFN&gamma;-producing cells by flow cytometry (section 5). Third, cellular infiltration and fibrosis is determined by immunohistochemistry of liver sections (section 6). Such analysis regimen has to be conducted at several times after initiation of the disease in order to prove the chronic nature of the model. The magnitude of the immune response characterized by the frequency and activity of hCYP2D6-specific T and/or B cells and the degree of the liver damage and fibrosis have to be assessed for a subsequent evaluation of possible treatments to prevent, delay or abrogate the autodestructive process of the liver.

Infection of mice with an Adenovirus expressing the major human autoantigen cytochrome P450 2D6 (hCYP2D6) recognized by sera of patients suffering from type 2 autoimmune hepatitis results in a persistent form of autoimmune-mediated liver disease characterized by extensive hepatitis, fibrosis and generation of a CYP2D6-specific immune response.

CYP2D6动物模型:如何诱导小鼠自身免疫性肝炎

Autoimmune hepatitis is a rare but life threatening autoimmune disease of the liver of unknown etiology1,2. In the past many attempts have been made to ...

The Measurement and Treatment of Suppression in Amblyopia

Amblyopia, a developmental disorder of the visual cortex, is one of the leading causes of visual dysfunction in the working age population. Current estimates put the prevalence of amblyopia at approximately 1-3%1-3, the majority of cases being monocular2. Amblyopia is most frequently caused by ocular misalignment (strabismus), blur induced by unequal refractive error (anisometropia), and in some cases by form deprivation.
Although amblyopia is initially caused by abnormal visual input in infancy, once established, the visual deficit often remains when normal visual input has been restored using surgery and/or refractive correction. This is because amblyopia is the result of abnormal visual cortex development rather than a problem with the amblyopic eye itself4,5 . Amblyopia is characterized by both monocular and binocular deficits6,7 which include impaired visual acuity and poor or absent stereopsis respectively. The visual dysfunction in amblyopia is often associated with a strong suppression of the inputs from the amblyopic eye under binocular viewing conditions8. Recent work has indicated that suppression may play a central role in both the monocular and binocular deficits associated with amblyopia9,10 .
Current clinical tests for suppression tend to verify the presence or absence of suppression rather than giving a quantitative measurement of the degree of suppression. Here we describe a technique for measuring amblyopic suppression with a compact, portable device11,12 . The device consists of a laptop computer connected to a pair of virtual reality goggles. The novelty of the technique lies in the way we present visual stimuli to measure suppression. Stimuli are shown to the amblyopic eye at high contrast while the contrast of the stimuli shown to the non-amblyopic eye are varied. Patients perform a simple signal/noise task that allows for a precise measurement of the strength of excitatory binocular interactions. The contrast offset at which neither eye has a performance advantage is a measure of the "balance point" and is a direct measure of suppression. This technique has been validated psychophysically both in control13,14 and patient6,9,11 populations.
In addition to measuring suppression this technique also forms the basis of a novel form of treatment to decrease suppression over time and improve binocular and often monocular function in adult patients with amblyopia12,15,16 . This new treatment approach can be deployed either on the goggle system described above or on a specially modified iPod touch device15.

Amblyopia is a developmental disorder of the visual cortex that is often accompanied by strong suppression of one eye. We present a new technique for measuring and treating interocular suppression in patients with amblyopia that can be deployed using virtual reality goggles or a portable iPod Touch device.

测量和制止在弱视治疗

Amblyopia, a developmental disorder of the visual cortex, is one of the leading causes of visual dysfunction in the working age population. Current ...

An Alkali-burn Injury Model of Corneal Neovascularization in the Mouse

Under normal conditions, the cornea is avascular, and this transparency is essential for maintaining good visual acuity. Neovascularization (NV) of the cornea, which can be caused by trauma, keratoplasty or infectious disease, breaks down the so called &lsquo;angiogenic privilege' of the cornea and forms the basis of multiple visual pathologies that may even lead to blindness. Although there are several treatment options available, the fundamental medical need presented by corneal neovascular pathologies remains unmet. In order to develop safe, effective, and targeted therapies, a reliable model of corneal NV and pharmacological intervention is required. Here, we describe an alkali-burn injury corneal neovascularization model in the mouse. This protocol provides a method for the application of a controlled alkali-burn injury to the cornea, administration of a pharmacological compound of interest, and visualization of the result. This method could prove instrumental for studying the mechanisms and opportunities for intervention in corneal NV and other neovascular disorders.

Neovascularization (NV) of the cornea can complicate multiple visual pathologies. Utilizing a controlled, alkali-burn injury model, a quantifiable level of corneal NV can be produced for mechanistic study of corneal NV and evaluation of potential therapies for neovascular disorders.

角膜新生血管在小鼠碱烧伤模型

Under normal conditions, the cornea is avascular, and this transparency is essential for maintaining good visual acuity. Neovascularization (NV) of the ...

Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models

Various in vivo laboratory rodent models for the induction of artery stenosis have been established to mimic diseases that include arterial plaque formation and stenosis, as observed for example in ischemic heart disease. Two highly reproducible mouse models&#160;&#8211;&#160;both resulting in artery stenosis but each underlying a different pathway of development&#160;&#8211; are introduced here. The models represent the two most common causes of artery stenosis; namely one mouse model for each myointimal hyperplasia, and atherosclerosis are shown. To induce myointimal hyperplasia, a balloon catheter injury of the abdominal aorta is performed. For the development of atherosclerotic plaque, the ApoE -/- mouse model in combination with western fatty diet is used. Different model-adapted options for the measurement and evaluation of the results are named and described in this manuscript. The introduction and comparison of these two models provides information for scientists to choose the appropriate artery stenosis model in accordance to the scientific question asked.

This video shows two models of intimal plaque development in murine arteries and emphasizes the differences in myointimal hyperplasia and atherosclerosis.

诱导肌内膜增生对战动脉粥样硬化小鼠:两种有效的模型介绍

Various in vivo laboratory rodent models for the induction of artery stenosis have been established to mimic diseases that include arterial plaque ...

Ischemic Tissue Injury in the Dorsal Skinfold Chamber of the Mouse: A Skin Flap Model to Investigate Acute Persistent Ischemia

Despite profound expertise and advanced surgical techniques, ischemia-induced complications ranging from wound breakdown to extensive tissue necrosis are still occurring, particularly in reconstructive flap surgery. Multiple experimental flap models have been developed to analyze underlying causes and mechanisms and to investigate treatment strategies to prevent ischemic complications. The limiting factor of most models is the lacking possibility to directly and repetitively visualize microvascular architecture and hemodynamics. The goal of the protocol was to present a well-established mouse model affiliating these before mentioned lacking elements. Harder et al. have developed a model of a musculocutaneous flap with a random perfusion pattern that undergoes acute persistent ischemia and results in ~50% necrosis after 10 days if kept untreated. With the aid of intravital epi-fluorescence microscopy, this chamber model allows repetitive visualization of morphology and hemodynamics in different regions of interest over time. Associated processes such as apoptosis, inflammation, microvascular leakage and angiogenesis can be investigated and correlated to immunohistochemical and molecular protein assays. To date, the model has proven feasibility and reproducibility in several published experimental studies investigating the effect of pre-, peri- and postconditioning of ischemically challenged tissue.

The window of the murine dorsal skinfold chamber presented visualizes a zone of acute persistent ischemia of a musculocutaneous flap. Intravital epi-fluorescence microscopy permits for direct and repetitive assessment of the microvasculature and quantification of hemodynamics. Morphologic and hemodynamic results can further be correlated with histological and molecular analyses.

在背皮褶商会鼠标的缺血性组织损伤:一个皮瓣模型，探讨急性缺血持续

Despite profound expertise and advanced surgical techniques, ischemia-induced complications ranging from wound breakdown to extensive tissue necrosis are ...

Creation of Abdominal Adhesions in Mice

Abdominal adhesions consist of fibrotic tissue that forms in the peritoneal space in response to an inflammatory insult, typically surgery or intraabdominal infection. The precise mechanisms underlying adhesion formation are poorly understood. Many compounds and physical barriers have been tested for their ability to prevent adhesions after surgery with varying levels of success. The mouse and rat are important models for the study of abdominal adhesions. Several different techniques for the creation of adhesions in the mouse and rat exist in the literature. Here we describe a protocol utilizing abrasion of the cecum with sandpaper and sutures placed in the right abdominal sidewall. The mouse is anesthetized and the abdomen is prepped. A midline laparotomy is created and the cecum is identified. Sandpaper is used to gently abrade the surface of the cecum. Next, several figure-of-eight sutures are placed into the peritoneum of the right abdominal sidewall. The abdominal cavity is irrigated, a small amount of starch is applied, and the incision is closed. We have found that this technique produces the most consistent adhesions with the lowest mortality rate.

Abdominal adhesions that form after surgery are a major cause of pain, infertility, and hospitalization and reoperation for small bowel obstruction. Our surgical procedure for creating abdominal adhesions in mice is a reliable tool to study the mechanisms underlying the formation of adhesions.

小鼠腹腔粘连的创建

Abdominal adhesions consist of fibrotic tissue that forms in the peritoneal space in response to an inflammatory insult, typically surgery or ...

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 ...

A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats

Heart failure is one of the leading causes of death worldwide. It is a complex clinical syndromethat includes fatigue, dyspnea, exercise intolerance, and fluid retention. Changes in myocardial structure, electrical conduction, and energy metabolism develop with heart failure, leading to contractile dysfunction, increased risk of arrhythmias, and sudden death. Hypertensive heart disease is one of the key contributing factors of cardiac remodeling associated with heart failure. The most commonly-used animal model mimicking hypertensive heart disease is created via surgical interventions, such as by narrowing the aorta. Abdominal aortic constriction is a useful experimental technique to induce a pressure overload, which leads to heart failure. The surgery can be easily performed, without the need for chest opening or mechanical ventilation. Abdominal aortic constriction-induced cardiac pathology progresses gradually, making this model relevant to clinical hypertensive heart failure. Cardiac injury and remodeling can be observed 10 weeks after the surgery. The method described here provides a simple and effective approach to produce a hypertensive heart disease animal model that is suitable for studying disease mechanisms and for testing novel therapeutics.

A rat model of abdominal aortic constriction that induces cardiac hypertrophy and remodeling is described. An efficient, highly-reproducible, and minimally-invasive method is used to provide a simple yet useful platform for research in myocardial hypertrophy and dysfunction.

心脏重构通过大鼠腹主动脉缩窄的模型

Heart failure is one of the leading causes of death worldwide. It is a complex clinical syndromethat includes fatigue, dyspnea, exercise intolerance, and ...