这项工作是由瑞士心血管基金会RT的资助。

该协议遵循苏黎世大学的人类研究伦理委员会的机构准则。 1.制备用于外科<ol><li>干净，以典型的方式准备了外科手术室。为了便于外科医生和灌注师之间的通信，心脏心肺机放置到患者的左侧，相对于该外科医生。 </li><li>麻醉诱导前60分钟 - 由5毫克咪达唑仑，30的口服给药前用药患者。 </li><li>让患者根据标准的指导方针，与直接动脉和麻醉师中心静脉压访问进行监控。 1.5毫克/千克丙泊酚，1 - - 2微克/千克芬太尼，和0.6毫克/公斤使用罗库溴铵0.5的初始静脉注射诱导麻醉。 </li><li>执行气管插管，并通过100的静脉内输注维持麻醉 - 150微克/ kg / min的丙泊酚，0.015 - 0.0381克/ kg / min的芬太尼和0.6 - 1.2微克/ kg / min的罗库溴铵需要。 </li><li>在仰卧位安装的病人，悬垂她/他在无菌的方式，使胸部，腹部，腹股沟免费手术视野。 </li></ol> 2.手术<ol><li>为了最小化由插管术野的拥挤，建立胸腔外的心肺旁路访问。 <ol><li>下面2厘米执行6厘米长的切口，并平行于右锁骨。准备右锁骨下动脉，从周围组织中释放它。得到的肝素/ kg的300 IU通过IV线。 </li><li>侧钳与库利Derra夹右锁骨下动脉。执行平行于其轴线的容器的10毫米长的动脉切口。 </li><li>使用运行6/0聚丙烯单丝缝线（ 例如，聚丙烯纺织纤维）缝8毫米涤纶移植物的端至端连接到动脉切口。插管用24星期五细长的单件动脉插管用于接枝rterial返回患者。 </li><li>在食管超声心动图的指导下，经皮导管插入右股静脉上的静脉引流导丝。 </li></ol></li><li>通过胸骨正中切口进入心脏。 <ol><li>纵向切开皮肤15厘米，开始胸骨上切迹下方1厘米。小心留在胸骨宽度的中间。 </li><li>看到了振荡锯胸骨。小心留在胸骨宽度的中间。 </li><li>切开心包在主动脉揭开了大规模扩张，曲折的右冠状动脉。 <ol><li>抓住与卡彭铁尔解剖钳心包。切断与梅岑鲍姆剪刀心包。继续切割心包到其反射线在使用电升主动脉。 </li></ol></li><li>启动体外循环和周解剖主动脉，从周围组织中解放出来，includ荷兰国际集团肺动脉，小心不要弄伤异常左冠状动脉。 <ol><li>轻推升主动脉用肺卷收器的左侧。抓住与卡彭铁尔解剖钳升主动脉后方软组织。 </li><li>从使用电周围组织分离升主动脉的后壁。尾部继续升主动脉后方。确保不损害升主动脉后方右肺动脉。 </li><li>抓住与卡彭铁尔解剖钳主肺动脉，轻轻将其推至左侧。从使用电灼主肺动脉分离升主动脉的左侧壁。 </li></ol></li><li>解剖与周围组织无主肺动脉。 <ol><li>拉向使用安装在一个夹具艾利斯花生纱布右侧升主动脉。 </li><li>直截了当地解剖主肺动脉后壁与安装在一个艾利斯夹持器的第二花生纱布。确保不损害主肺动脉背后的主力左冠状动脉。 </li><li>通过主肺动脉下剥离。轻轻打开剖分准备一个隧道血管循环的通道。 </li><li>打倒安装在卡彭铁尔解剖镊子血管循环，并将其放置在解剖的开放颌骨之间。关闭剥离的爪抓住容器循环。 </li><li>抓住升主动脉的外膜和拉被剥离持有的容器环环绕主肺动脉。 </li></ol></li><li>将左心室排气孔。 <ol><li>广场上有4/0聚​​丙烯单丝缝合右上肺静脉荷包。 </li><li>轻轻推动上腔静脉向左侧。 </li><li>请在与18刀片刀，右上肺静脉荷包中间一小截（参见材料李氏T）。 </li><li>轻轻扩张与LERICHE止血钳夹开幕。 </li><li>通过插入右上肺静脉和二尖瓣的通风口进入左心室卸载左心脏。与编织聚酯2/0结扎与聚涂层固定。 </li></ol></li><li>将逆行心脏停搏插管通过冠状窦。与编织聚酯2/0结扎用聚丁烯涂层固定。 </li><li>安装顺行停搏根。 <ol><li>广场上有4/0聚​​丙烯单丝缝合主，肺动脉荷包。 </li><li>请在与18刀片刀，主肺动脉荷包中间一小截（见材料清单）。 </li><li>轻轻扩张与LERICHE止血钳夹开幕。插入主肺动脉顺行停搏插管。与编织聚酯2/0结扎与聚涂层固定。 </li><li>放置PU在具有4/0聚​​丙烯单丝缝线的升主动脉RSE串。 </li><li>请在与18刀片刀，升主动脉荷包中间一小截。 </li><li>轻轻扩张与LERICHE止血钳夹开幕。 </li><li>插入一个顺行停搏插管入升主动脉。与编织聚酯2/0结扎与聚涂层固定。切断与梅岑鲍姆剪刀结扎。验证在主肺动脉及升主动脉顺行停搏插管的正确位置。 </li></ol></li></ol></li><li>准备打开主动脉。 <ol><li>夹闭主动脉远端为尽可能。通过主动脉和肺动脉同时交付顺行冷血停搏。 </li><li>取下主动脉和肺动脉插管并重复冷血停跳液逆行每20分钟。 </li><li>横切主动脉。 <ol><li>抓住作为cending左去除心脏停搏插管继开口的每一侧与卡彭解剖钳主动脉。放大有18刃刀开幕。 </li><li>完成与梅岑鲍姆剪刀主动脉横断。验证不存在于主动脉左窦主动脉内的左冠状动脉口的。 </li></ol></li><li>横切主肺动脉。 <ol><li>抓住左去除心脏停搏插管继开口的每一侧与卡彭解剖钳主肺动脉。放大有18刃刀开幕。 </li><li>完成与梅岑鲍姆剪刀主肺动脉横断。确认左冠状动脉口的存在，从向右的窦肺动脉110始发。 </li></ol></li><li>从肺动脉的右向窦1分离左冠状动脉口。 <ol><li>抓住近端肺主ARtery与卡彭铁尔解剖钳。使用梅岑鲍姆剪刀，从与肺根壁的慷慨周围补丁肺动脉右向窦1分离左冠状动脉口，小心不要伤害肺动脉瓣。 </li><li>调动主力左冠状动脉高达分叉。 </li></ol></li></ol></li><li>准备左冠状动脉开口重新植入。 <ol><li>抓住与卡彭铁尔解剖钳升主动脉近端。 </li><li>用直刀主动脉左窦2创建一个新口。离开主动脉根壁的10毫米左右缘向左窦2和主动脉的右冠状窦之间的连合的新口，以及朝向主动脉环。 </li><li>主要的左冠状动脉口端至端连接到新口在使用运行6/0聚丙烯单丝缝线的主动脉的左侧窦2。在D启动吻合主力左冠状动脉口的eepest点，并允许它上来就吻合的右侧。通过运行缝合线的左侧，以满足另一端完成吻合。 </li><li>为了拉动缝合时对组织舒缓紧张情绪，每次把主动脉和主左冠状动脉口在一起。 </li></ol></li><li>修复在肺动脉根缺陷。 <ol><li>使用非自体治疗心包补片。 </li><li>自体心包补片连接在使用一个运行6/0聚丙烯单丝缝线的肺动脉的右向窦1的最深点。 </li><li>第一运行起来左边，然后缝合线的右端到缺陷的中间高度在肺动脉的右向窦1。离开所述缝合线的两个端部在张力下。 </li></ol></li><li>重建大血管的连续性。 <ol><li>重新连接主动脉近端到其远端部分与端至端吻合术使用运行5/0聚丙烯单丝缝线。在最深点开始吻合，允许它上来就吻合的右侧。通过运行缝合线的左侧，以满足另一端完成吻合。 </li><li>去空气中的主动脉。取出主动脉阻断。启动复温病人。 </li><li>为了缩短缺血时间，进行近端和跳动的心脏肺动脉远端部分的重新连接。把泵吸盘到远端肺动脉以改善视力手术视野的。 </li><li>在正在运行的方式继续已被停在缺陷的中间高度肺动脉的右向窦1完成后及吻合的左侧方面的6/0聚丙烯缝线的左端。 </li><li>在正在运行的方式继续已被停在中间高度的6/0聚丙烯缝线的右端缺陷在肺动脉的右向窦1完成后和吻合的右方面。领带缝线的两端来完成连接。 </li></ol></li></ol>

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作者什么都没有透露。

这个协议描述了ALCAPA的直接再植入到主动脉与主左冠状动脉从根据道奇-哈塔米分类10中的肺动脉的右向窦起源成年患者的详细技术。心肌保护策略和肺动脉重建都清楚地证明。这个技术的主要关键步骤是通过左冠状动脉的慷慨动员表示实现无张力的吻合术。 长时间去饱和冠状动脉灌注容忍到成年期在少数个人。谁生存本到成年的临床表现的光谱，从没有症?...

从肺动脉（ALCAPA）左冠状动脉异常起源是一种罕见的先天性异常通常被视为分离的病变1。 ALCAPA的发生率估计为1 300000活产，0.24％和先天性心脏病2,3的0.46％之间，包括这是小儿心肌缺血和梗死的最常见的原因之一，如果不及时治疗，导致死亡率生活4的第一年90％。只有10 - 15％的婴儿存活由于大主导右冠状动脉（RCA）提供广泛的intercoronary络4的迅猛发展到成年。在新生儿期，高肺血管阻力和所得肺动脉（PA）的压力下确保顺行流从PA保持到异常左冠状动脉。由于pulmonarÿ血管阻力逐渐减小，顺行流向左冠状动脉降低。这最终导致流动的逆转，和左到右分流到PA，从而导致"冠状动脉偷5"。因此，左心室（LV）心肌灌注取决于intercoronary络从RCA 5,6。 冠状偷现象和逆行左侧冠状动脉血流提供慢性心内膜下缺血，这可能导致左心功能不全，缺血性二尖瓣反流，和由急性心肌缺血7沉淀恶性室性心律失常的基板。在成人患者的子集，在介绍的平均年龄为41岁，性别分布朝向女性患者的移位（女到男比:2:1）8。在此患者群体中，14％是无症状; 66％用本心绞痛，呼吸困难，心悸，或疲劳的症状;和现在有危及生命的症状，包括室性心律失常，晕厥和心源性猝死8 17％。危及生命的表现，平均年龄为33岁，心脏性猝死31岁8。因此，手术矫正高度只要作出诊断建议，不论年龄或intercoronary抵押1,9的程度。 根据异常左冠状动脉起源的ALCAPA进入主动脉的直接再植入是多种生理声音修复技术重建双冠状动脉灌注系统。最常见地，从ALCAPA右侧肺窦（PA的窦1），其面向主动脉窦其中主左冠状动脉通常起源（主动脉窦2）10 &lt;起飞/ SUP&gt;。这冠状动脉解剖是最适合于直接再注入技术。本报告的目的是描述，详细，对于成人患者在ALCAPA左冠状动脉的直接再植入技术。后面直接再注入的理由是优势-双冠状动脉的生理重建灌注它提供了一个在异常左冠状动脉与冠状动脉旁路移植11，12，13结合的结扎。

<table border="1" fo:keep-together.within-page="1" fo:keep-with-next.within-page="always">
	<tbody>
		<tr>
			<td>Heart surgery infrastructure:</td>
			<td></td>
			<td></td>
		</tr>
		<tr>
			<td>Heart Lung Machine</td>
			<td>Stockert</td>
			<td>SIII</td>
		</tr>
		<tr>
			<td>EOPA 24Fr. arterial cannula</td>
			<td>Medtronic</td>
			<td>77624</td>
		</tr>
		<tr>
			<td>Quickdraw 25Fr. femoral venous cannula</td>
			<td>Edwards</td>
			<td>QD25</td>
		</tr>
		<tr>
			<td>LV vent catheter 17Fr.</td>
			<td>Edwards</td>
			<td>E061</td>
		</tr>
		<tr>
			<td>Antegrade 9Fr. cardioplegia cannula</td>
			<td>Edwards</td>
			<td>AR012V</td>
		</tr>
		<tr>
			<td>Retrograde 14Fr. cardioplegia cannula&#160;</td>
			<td>Edwards</td>
			<td>NPC014&#160;</td>
		</tr>
		<tr>
			<td>Electrocautery</td>
			<td>Covidien</td>
			<td>Force FX</td>
		</tr>
		<tr>
			<td>Name</td>
			<td>Company</td>
			<td>Catalog number</td>
		</tr>
		<tr>
			<td>Sutures:</td>
			<td></td>
			<td></td>
		</tr>
		<tr>
			<td>Polypropylene 4/0</td>
			<td>Ethicon</td>
			<td>8871H</td>
		</tr>
		<tr>
			<td>Polypropylene 5/0</td>
			<td>Ethicon</td>
			<td>8870H</td>
		</tr>
		<tr>
			<td>Polypropylene 6/0</td>
			<td>Ethicon</td>
			<td>EH7400H</td>
		</tr>
		<tr>
			<td>Braided polyesther 2/0 ligature with polybutylate coating&#160;</td>
			<td>Ethicon</td>
			<td>X305H</td>
		</tr>
		<tr>
			<td>Intergard dacron graft 8 mm</td>
			<td>Maquet</td>
			<td>IGW0008-30</td>
		</tr>
		<tr>
			<td>Micro knife Sharpoint&#160;</td>
			<td>TYCO Healthcare PTY&#160;</td>
			<td>78-6900</td>
		</tr>
		<tr>
			<td>Name</td>
			<td>Company</td>
			<td>Catalog number</td>
		</tr>
		<tr>
			<td>Drugs:</td>
			<td></td>
			<td></td>
		</tr>
		<tr>
			<td>Midazolam</td>
			<td>Roche Pharma</td>
			<td>N05CD08</td>
		</tr>
		<tr>
			<td>Rocuronium</td>
			<td><a href="https://www.compendium.ch/comp/mnr/22695/de">MSD Merck Sharp &#38; Dohme&#160;</a></td>
			<td>M03AC09</td>
		</tr>
		<tr>
			<td>Propofol</td>
			<td>Fresenius Kabi</td>
			<td>N01AX10</td>
		</tr>
		<tr>
			<td>Fentanil</td>
			<td>Actavis</td>
			<td>N01AH01</td>
		</tr>
		<tr>
			<td>Name</td>
			<td>Company</td>
			<td>Catalog number</td>
		</tr>
		<tr>
			<td>Instruments:</td>
			<td></td>
			<td></td>
		</tr>
		<tr>
			<td>Cooley Derra anastomosis clamp</td>
			<td>Delacroix-Chevalier</td>
			<td>DC40810-16</td>
		</tr>
		<tr>
			<td>Cooley vascular clamp</td>
			<td>Delacroix-Chevalier</td>
			<td>DC40810-16</td>
		</tr>
		<tr>
			<td>Dissection forceps Carpentier</td>
			<td>Delacroix-Chevalier</td>
			<td>DC13110-28&#160;</td>
		</tr>
		<tr>
			<td>Scissors Metzenbaum</td>
			<td>Delacroix-Chevalier</td>
			<td>B351751</td>
		</tr>
		<tr>
			<td>Needle holder Ryder</td>
			<td>Delacroix-Chevalier</td>
			<td>DC51130-20&#160;</td>
		</tr>
		<tr>
			<td>Dissection forceps DeBakey</td>
			<td>Delacroix-Chevalier</td>
			<td>DC12000-21&#160;</td>
		</tr>
		<tr>
			<td>Micro needle holder Jacobson</td>
			<td>Delacroix-Chevalier</td>
			<td>DC50002-21&#160;</td>
		</tr>
		<tr>
			<td>Micro scisors Jacobson</td>
			<td>Delacroix-Chevalier</td>
			<td>DC20057-21&#160;</td>
		</tr>
		<tr>
			<td>Lung retractor</td>
			<td>Delacroix-Chevalier</td>
			<td>B803990</td>
		</tr>
		<tr>
			<td>Allis clamp</td>
			<td>Delacroix-Chevalier</td>
			<td>DC45907-25&#160;</td>
		</tr>
		<tr>
			<td>O&#8217;Shaugnessy Dissector</td>
			<td>Delacroix-Chevalier</td>
			<td>B60650</td>
		</tr>
		<tr>
			<td>Vessel loop</td>
			<td>Medline</td>
			<td>VLMINY</td>
		</tr>
		<tr>
			<td>18 blade knife</td>
			<td>Delacroix-Chevalier</td>
			<td>B130180</td>
		</tr>
		<tr>
			<td>Leriche haemostatic clamp</td>
			<td>Delacroix-Chevalier</td>
			<td>B86555</td>
		</tr>
	</tbody>
</table>

direct re-implantation of left coronary artery into the aorta in adults with anomalous origin of left coronary artery from the pulmonary artery (alcapa)

从肺动脉（ALCAPA）左冠状动脉起源异常是一种罕见的先天性异常是小儿心肌缺血和梗死的主要原因之一。如果不及时治疗，它会导致死亡率在生命的第一年90％。在谁存活到成年患者，冠状动脉偷窃现象，逆行左侧冠状动脉流量为慢性心内膜下缺血，这可能会导致左心功能不全，缺血性二尖瓣关闭不全，恶性室性心律失常和心源性猝死的基材。危及生命的表现，平均年龄为33岁，心脏性猝死31岁。因此，手术矫正高度一旦作出诊断建议，不论年龄。在成人型ALCAPA从肺动脉的右向窦起源的ALCAPA到主动脉的直接再注入是多种生理声音修复技术吨Ø重新建立双冠脉灌注系统和建议。这个协议描述成人型ALCAPA的直接再注入技术进入主动脉。

<html>介绍患者是一名48岁的女子与近期心绞痛加拿大心血管学会（CCS）毕业生III和偶尔的心悸发作呈现。她报告了三名波澜不惊怀孕。中度吸烟是主要的心血管危险因素。经胸超声心动图显示一个中度受损（45％）左室射血分数和无二尖瓣关闭不全。然后进行一个冠状动脉造影。它表明没有从主动脉引起的左冠状动脉主干的。右?...

Watch this Scientific Journal Video about Direct Re-implantation of Left Coronary Artery into the Aorta in Adults with Anomalous Origin of Left Coronary Artery from the Pulmonary Artery ALCAPA at JoVE

Direct Re-implantation of Left Coronary Artery into the Aorta in Adults with Anomalous Origin of Left Coronary Artery from the Pulmonary Artery ALCAPA

ALCAPA的手术矫正强烈建议，无论年龄或intercoronary抵押的程度。该协议提出了成年型ALCAPA的直接再植入到主动脉重新建立双冠状动脉灌注的技术。只要可行，直接再注入优选其它外科手术校正技术。

左冠状动脉直接再注入与从肺动脉左冠状动脉起源异常成人主动脉（ALCAPA）

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly which is one of leading causes of myocardial ...

direct-re-implantation-left-coronary-artery-into-aorta-adults-with

Research

JoVE Journal

Medicine

Direct Re-implantation of Left Coronary Artery into the Aorta in Adults with Anomalous Origin of Left Coronary Artery from the Pulmonary Artery (ALCAPA)

18.4K 次观看.  University of Zurich.  ALCAPA的手术矫正强烈建议，无论年龄或intercoronary抵押的程度。该协议提出了成年型ALCAPA的直接再植入到主动脉重新建立双冠状动脉灌注的技术。只要可行，直接再注入优选其它外科手术校正技术。 

视频: Direct Re-implantation of Left Coronary Artery into the Aorta in Adults with Anomalous Origin of Left Coronary Artery from the Pulmonary Artery ALCAPA

Use of a Hanging Weight System for Coronary Artery Occlusion in Mice

Murine studies of acute injury are an area of intense investigation, as knockout mice for different genes are becoming increasingly available 1-38. Cardioprotection by ischemic preconditioning (IP) remains an area of intense investigation. To further elucidate its molecular basis, the use of knockout mouse studies is particularly important 7, 14, 30, 39. Despite the fact that previous studies have already successfully performed cardiac ischemia and reperfusion in mice, this model is technically very challenging. Particularly, visual identification of the coronary artery, placement of the suture around the vessel and coronary occlusion by tying off the vessel with a supported knot is technically difficult. In addition, re-opening the knot for intermittent reperfusion of the coronary artery during IP without causing surgical trauma adds additional challenge. Moreover, if the knot is not tied down strong enough, inadvertent reperfusion due to imperfect occlusion of the coronary may affect the results. In fact, this can easily occur due to the movement of the beating heart.
Based on potential problems associated with using a knotted coronary occlusion system, we adopted a previously published model of chronic cardiomyopathy based on a hanging weight system for intermittent coronary artery occlusion during IP 39. In fact, coronary artery occlusion can thus be achieved without having to occlude the coronary by a knot. Moreover, reperfusion of the vessel can be easily achieved by supporting the hanging weights which are in a remote localization from cardiac tissues.
We tested this system systematically, including variation of ischemia and reperfusion times, preconditioning regiments, body temperature and genetic backgrounds39. In addition to infarct staining, we tested cardiac troponin I (cTnI)
as a marker of myocardial infarction in this model. In fact, plasma levels of cTnI correlated with infarct sizes (R2=0.8). Finally, we could show in several studies that this technique yields highly reproducible infarct sizes during murine IP and myocardial infarction6, 8, 30, 40, 41. Therefore, this technique may be helpful for researchers who pursue molecular mechanisms involved in cardioprotection by IP using a genetic approach in mice with targeted gene deletion. Further studies on cardiac IP using transgenic mice may consider this technique.

A murine model for myocardial ischemia and ischemic preconditioning is an important tool study cardioprotective mechanisms in vivo. Here, we report an easy applicable in situ model for cardiac IP using a hanging-weight system for coronary artery occlusion.

悬重系统的使用在小鼠冠状动脉闭塞

Murine studies of acute injury are an area of intense investigation, as knockout mice for different genes are becoming increasingly available 1-38. ...

科研

医学

Coronary Artery Ligation and Intramyocardial Injection in a Murine Model of Infarction

Mouse models are a valuable tool for studying acute injury and chronic remodeling of the myocardium in vivo. With the advent of genetic modifications to the whole organism or the myocardium and an array of biological and/or synthetic materials, there is great potential for any combination of these to assuage the extent of acute ischemic injury and impede the onset of heart failure pursuant to myocardial remodeling. 
Here we present the methods and materials used to reliably perform this microsurgery and the modifications involved for temporary (with reperfusion) or permanent coronary artery occlusion studies as well as intramyocardial injections. The effects on the heart that can be seen during the procedure and at the termination of the experiment in addition to histological evaluation will verify efficacy. 
Briefly, surgical preparation involves anesthetizing the mice, removing the fur on the chest, and then disinfecting the surgical area. Intratracheal intubation is achieved by transesophageal illumination using a fiber optic light. The tubing is then connected to a ventilator. An incision made on the chest exposes the pectoral muscles which will be cut to view the ribs. For ischemia/reperfusion studies, a 1 cm piece of PE tubing placed over the heart is used to tie the ligature to so that occlusion/reperfusion can be customized. For intramyocardial injections, a Hamilton syringe with sterile 30gauge beveled needle is used. When the myocardial manipulations are complete, the rib cage, the pectoral muscles, and the skin are closed sequentially. Line block analgesia is effected by 0.25% marcaine in sterile saline which is applied to muscle layer prior to closure of the skin. The mice are given a subcutaneous injection of saline and placed in a warming chamber until they are sternally recumbent. They are then returned to the vivarium and housed under standard conditions until the time of tissue collection. At the time of sacrifice, the mice are anesthetized, the heart is arrested in diastole with KCl or BDM, rinsed with saline, and immersed in fixative. Subsequently, routine procedures for processing, embedding, sectioning, and histological staining are performed. 
Nonsurgical intubation of a mouse and the microsurgical manipulations described make this a technically challenging model to learn and achieve reproducibility. These procedures, combined with the difficulty in performing consistent manipulations of the ligature for timed occlusion(s) and reperfusion or intramyocardial injections, can also affect the survival rate so optimization and consistency are critical.

Numerous genetic manipulations and/or intramyocardial injections of genes, proteins, cells, and/or biomaterials are superimposed upon the dimension of time in studies of acute ischemia/ reperfusion injury and chronic remodeling in mice. This video illustrates the microsurgical procedures for ischemia/reperfusion, permanent coronary artery ligation, and intramyocardial injection studies.

结扎冠状动脉内注射在小鼠模型梗死

Mouse models are a valuable tool for studying acute injury and chronic remodeling of the myocardium in vivo.  With the advent of genetic modifications to ...

Modified Technique for Coronary Artery Ligation in Mice

Myocardial infarction (MI) is one of the most important causes of mortality in humans1-3. In order to improve morbidity and mortality in patients with MI we need better knowledge about pathophysiology of myocardial ischemia. This knowledge may be valuable to define new therapeutic targets for innovative cardiovascular therapies4. Experimental MI model in mice is an increasingly popular small-animal model in preclinical research in which MI is induced by means of permanent or temporary ligation of left coronary artery (LCA)5. In this video, we describe the step-by-step method of how to induce experimental MI in mice.
The animal is first anesthetized with 2% isoflurane. The unconscious mouse is then intubated and connected to a ventilator for artificial ventilation. The left chest is shaved and 1.5 cm incision along mid-axillary line is made in the skin. The left pectoralis major muscle is bluntly dissociated until the ribs are exposed. The muscle layers are pulled aside and fixed with an eyelid-retractor. After these preparations, left thoracotomy is performed between the third and fourth ribs in order to visualize the anterior surface of the heart and left lung. The proximal segment of LCA artery is then ligated with a 7-0 ethilon suture which typically induces an infarct size ~40% of left ventricle. At the end, the chest is closed and the animals receive postoperative analgesia (Temgesic, 0.3 mg/50 ml, ip). The animals are kept in a warm cage until spontaneous recovery.

The surgical procedure used to induce experimental myocardial infarction in mice begins with left thoracotomy between the third and the fourth ribs in order to visualize the anterior surface of the heart and left lung. The left coronary artery is ligated, the chest is closed and the mouse is allowed to recover spontaneously.

改性技术在小鼠冠状动脉结扎

Myocardial infarction (MI) is one of the most important causes of mortality in humans1-3. In order to improve morbidity and mortality in patients with MI ...

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 ...

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure

Heart failure is a syndrome in which the heart fails to pump blood at a rate commensurate with cellular oxygen requirements at rest or during stress. It is characterized by fluid retention, shortness of breath, and fatigue, in particular on exertion. Heart failure is a growing public health problem, the leading cause of hospitalization, and a major cause of mortality. Ischemic heart disease is the main cause of heart failure.
Ventricular remodelling refers to changes in structure, size, and shape of the left ventricle. This architectural remodelling of the left ventricle is induced by injury (e.g., myocardial infarction), by pressure overload (e.g., systemic arterial hypertension or aortic stenosis), or by volume overload. Since ventricular remodelling affects wall stress, it has a profound impact on cardiac function and on the development of heart failure. A model of permanent ligation of the left anterior descending coronary artery in mice is used to investigate ventricular remodelling and cardiac function post-myocardial infarction. This model is fundamentally different in terms of objectives and pathophysiological relevance compared to the model of transient ligation of the left anterior descending coronary artery. In this latter model of ischemia/reperfusion injury, the initial extent of the infarct may be modulated by factors that affect myocardial salvage following reperfusion. In contrast, the infarct area at 24 hr after permanent ligation of the left anterior descending coronary artery is fixed. Cardiac function in this model will be affected by 1) the process of infarct expansion, infarct healing, and scar formation; and 2) the concomitant development of left ventricular dilatation, cardiac hypertrophy, and ventricular remodelling.
Besides the model of permanent ligation of the left anterior descending coronary artery, the technique of invasive hemodynamic measurements in mice is presented in detail.

Heart failure is the leading cause of hospitalization and a major cause of mortality. A model of permanent ligation of the left anterior descending coronary artery in mice is applied to investigate ventricular remodelling and cardiac dysfunction post-myocardial infarction. The technique of invasive hemodynamic measurements in mice is presented.

左冠状动脉前降支的小鼠结扎:对心肌梗死后重塑和心衰模型

Heart failure is a syndrome in which the heart fails to pump blood at a rate commensurate with cellular oxygen requirements at rest or during stress. It ...

Increasing Pulmonary Artery Pulsatile Flow Improves Hypoxic Pulmonary Hypertension in Piglets

Pulmonary arterial hypertension (PAH) is a disease affecting distal pulmonary arteries (PA). These arteries are deformed, leading to right ventricular failure. Current treatments are limited. Physiologically, pulsatile blood flow is detrimental to the vasculature. In response to sustained pulsatile stress, vessels release nitric oxide (NO) to induce vasodilation for self-protection. Based on this observation, this study developed a protocol to assess whether an artificial pulmonary pulsatile blood flow could induce an NO-dependent decrease in pulmonary artery pressure. One group of piglets was exposed to chronic hypoxia for 3 weeks and compared to a control group of piglets. Once a week, the piglets underwent echocardiography to assess PAH severity. At the end of hypoxia exposure, the piglets were subjected to a pulsatile protocol using a pulsatile catheter. After being anesthetized and prepared for surgery, the jugular vein of the piglet was isolated and the catheter was introduced through the right atrium, the right ventricle and the pulmonary artery, under radioscopic control. Pulmonary artery pressure (PAP) was measured before (T0), immediately after (T1) and 30 min after (T2) the pulsatile protocol. It was demonstrated that this pulsatile protocol is a safe and efficient method of inducing a significant reduction in mean PAP via an NO-dependent mechanism. These data open up new avenues for the clinical management of PAH.

Pulmonary hypertension is associated with a significant reduction in pulmonary artery pulsatility, contractility and elasticity, contributing to an increase in pulmonary artery pressure and pulmonary resistance. Using a hypoxic piglet model, this study demonstrated that improving pulmonary artery plasticity using a newly developed pulsatile catheter improves hypoxic pulmonary hypertension.

增加肺动脉脉动流改善缺氧性肺动脉高压的仔猪

Pulmonary arterial hypertension (PAH) is a disease affecting distal pulmonary arteries (PA). These arteries are deformed, leading to right ventricular ...

Ultrasound Based Assessment of Coronary Artery Flow and Coronary Flow Reserve Using the Pressure Overload Model in Mice

Transthoracic Doppler echocardiography (TTDE) is a clinically useful, noninvasive tool for studying coronary artery flow velocity and coronary flow reserve (CFR) in humans. Reduced CFR is accompanied by marked intramyocardial and pericoronary fibrosis and is used as an indication of the severity of dysfunction. This study explores, step-by-step, the real-time changes measured in the coronary flow velocity, CFR and systolic to diastolic peak velocity (S/D) ratio in the setting of an aortic banding model in mice. By using a Doppler transthoracic imaging technique that yields reproducible and reliable data, the method assesses changes in flow in the septal coronary artery (SCA), for a period of over two weeks in mice, that previously either underwent aortic banding or thoracotomy. 
During imaging, hyperemia in all mice was induced by isoflurane, an anesthetic that increased coronary flow velocity when compared with resting flow. All images were acquired by a single imager. Two ratios, (1) CFR, the ratio between hyperemic and baseline flow velocities, and (2) systolic (S) to diastolic (D) flow were determined, using a proprietary software and by two independent observers. Importantly, the observed changes in coronary flow preceded LV dysfunction as evidenced by normal LV mass and fractional shortening (FS). 
The method was benchmarked against the current gold standard of coronary assessment, histopathology. The latter technique showed clear pathologic changes in the coronary artery in the form of peri-coronary fibrosis that correlated to the flow changes as assessed by echocardiography. 
The study underscores the value of using a non-invasive technique to monitor coronary circulation in mouse hearts. The method minimizes redundant use of research animals and demonstrates that advanced ultrasound-based indices, such as CFR and S/D ratios, can serve as viable diagnostic tools in a variety of investigational protocols including drug studies and the study of genetically modified strains.

Coronary flow reserve (CFR) is useful for assessment of myocardial oxygen demand and evaluation of cardiovascular risk. This study establishes a step-by-step transthoracic Doppler echocardiographic (TTDE) method for longitudinal monitoring of the changes in CFR, as measured from coronary artery in mice, under the experimental pressure overload of aortic banding.

冠脉流量和冠状动脉血流储备用小鼠压力超负荷基于模型的超声评估

Transthoracic Doppler echocardiography (TTDE) is a clinically useful, noninvasive tool for studying coronary artery flow velocity and coronary flow ...

Murine Echocardiography of Left Atrium, Aorta, and Pulmonary Artery

The present methodology teaches the investigator how to measure and use the LAV as a surrogate of chronic elevations in Left Ventricular diastolic pressure through echocardiography, as well as to obtain measurements of the Aorta and PA diameter in mice.
Mice older than 10 d of age can be analyzed using the present technique. The technique is composed of 3 main steps: set-up, image acquisition, and image analysis. The set-up step consists of getting the mouse anesthetized with 1% isoflurane, shaving it, and taping it in a supine position to a heated EKG board where the image acquisition will take place. The image acquisition step consists of learning to identify the cardiac structures and obtaining all the required images with its correspondent probe and axis in order to be able to calculate volumes and diameters. The image analysis step consists of measuring the previously acquired images with the aid of computer software.
Advantages of the proposed technique include a fast (15 min) procedure that would allow the researcher to evaluate interventions in a non-invasive, non-terminal approach and therefore follow the same mouse over time; each mouse can be used as its own control. This fact plus having the same operator perform all the acquisition and analysis for the entire experiment minimizes the limitation of operator-dependency. The present methodology is useful for mouse researchers in cardiovascular and pulmonary medicine.

The following protocol describes the methodology for the acquisition and analysis of echocardiographic images used to obtain the Left Atrial Volume (LAV), Aorta (Ao) diameter, and Pulmonary Artery (PA) diameter in mice. This technique is a non-invasive, non-terminal procedure that allows assessment of the cardiopulmonary function.

左心房，主动脉和肺动脉的超声心动图小鼠

The present methodology teaches the investigator how to measure and use the LAV as a surrogate of chronic elevations in Left Ventricular diastolic ...

Murine Left Anterior Descending (LAD) Coronary Artery Ligation: An Improved and Simplified Model for Myocardial Infarction

Ischemic heart disease (IHD), or acute coronary syndrome (ACS), is one of the leading causes of death in the United States. IHD is characterized by reduced blood supply to the heart, resulting in the loss of oxygen to and the ensuing necrosis of the heart muscle. The MI model has gained popularity for its use as a short-term ischemia-reperfusion model and a long-term permanent ligation model. Below, we describe a reliable method for the permanent ligation of the LAD. With mouse genetic engineering technology becoming more advanced, and with an increasing availability of quality murine surgical instruments, the mouse has become a popular model for MI surgeries. Our surgical model incorporates the use of an easily reversible anesthetic for the rapid recovery of the mouse; a minimally invasive endotracheal intubation without involving a tracheotomy; and a thoracentesis through the original thoracotomy site without creating an additional incision in the chest, as is done in some other methods, to effectively remove excess blood and air from the chest cavity. This method is comparatively less invasive than other methods, which dramatically reduces surgical and post-surgical complications and mortality and improves reproducibility.

Murine Left Anterior Descending LAD Coronary Artery Ligation: An Improved and Simplified Model for Myocardial Infarction

We provide a reliable method for left anterior descending artery (LAD) ligation in a mouse model. This method is comparatively less invasive than other methods, involving endotracheal intubation, a left-sided thoracotomy approach, and thoracentesis. This method can be used as a model for both acute and chronic myocardial infarction (MI).

鼠左前降支（LAD）冠状动脉结扎:改进和简化模型的心肌梗死

Ischemic heart disease (IHD), or acute coronary syndrome (ACS), is one of the leading causes of death in the United States. IHD is characterized by ...

Identifying Coronary Artery Calcification on Non-gated Computed Tomography Scans

Coronary artery calcification (CAC) provides an objective measure of coronary artery disease and can readily be identified on non-gated computed tomography (CT) scans with a high correlation with gated cardiac CT scans. This standardized protocol takes a step-wise approach to not only optimizing an image for the identification of calcification but also to distinguishing CAC from other common causes of calcification in the cardiac silhouette. Recognition of CAC on non-gated CT scans helps to identify a very powerful prognostic factor that can influence therapeutic interventions or downstream diagnostic testing without requiring a gated cardiac scan. These non-gated CT scans are often acquired as part of the routine care of the patient, and this data is readily available without another dose of&#160;ionizing radiation. This protocol allows for the precise and accurate extraction of this data for the purposes of retrospective data analysis in clinical research studies, but also in the clinical evaluation and management of patients.

Here, we present a protocol to reliably and systematically identify coronary artery calcification (CAC) on non-gated computed tomography (CT) scans of the chest or abdomen. CAC provides an objective measure of coronary artery disease for both research and clinical purposes.