Name: permanent ligation of the left anterior descending coronary artery in mice: a model of post-myocardial infarction remodelling and heart failure
Uploaded: 2014-12-02T13:00:00.000+00:00
Duration: 9 min 37 s
Description: Watch this Scientific Journal Video about Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure at JoVE.com

This work was supported by Onderzoekstoelagen grant OT/13/090 of the KU Leuven and by grant G0A3114N of the FWO-Vlaanderen.

注：この項で説明するすべての実験手順は、動物実験ルーヴェン·カトリック大学の研究諮問委員会によって承認された（プロジェクト：2013分の154-B·デ·沖積層）。 左前下冠動脈の動脈の1常設ライゲーション<ol><li> / kgのペントバルビタールナトリウム70mgの40〜10mg / kgの腹腔内投与によりマウスを麻酔。それはもはやしっかりとつま先のピンチを反応するときに、マウスが麻酔のその適切な面に到達しないことを確認してください。常に適切な麻酔の前に、任意の外科的処置または介入にこの方法を確認する。麻酔下ながら、角膜の乾燥を防ぐために、眼軟膏、潤滑使用してください。手順（ブプレノルフィン0.05 mg / kgをSQ）の開始前に術前鎮痛2-4時間を提供します。 <ol><li>生存手術中に一貫性のある無菌技術を適用します。最大限可能な範囲で微生物詐欺に抑制する手順を実装tamination重大な感染や化膿が発生しないようにします。これらの手順は、このサイトの手術部位と消毒の上、滅菌器具及び無菌材料の使用、手術領域の消毒、および毛皮/髪の除去が含まれています。 </li></ol></li><li>自己準備平滑化20ゲージ針でマウスを挿管。 <ol><li>頭の過伸展と仰臥位でマウスを置きます。 <ol><li>首領域に光の焦点を合わせる。鈍いピンセットと舌を持ち上げます。喉頭の入口を明瞭に見ることができる。 </li><li>直視下気管内に喉頭を鈍化針を渡します。人工呼吸器にマウスを接続することにより、正しい挿管を評価する（μlのストローク量：3×体重（g）+ 155、周波数：毎分120ストローク）。 </li></ol></li><li>あるいは、第慎重に気管を露出することにより、気管内挿管の可視化を強化する。 <ol><li> 5ミリメートル半ば首の切開を作成し、撤回ちょうど気管上記筋肉組織。 </li><li>気管の直接可視化のための外科的実体顕微鏡を使用して挿管を実行します。舌を持ち上げ、気管内に自己準備平滑化20ゲージの針を入力してください。人工呼吸器にマウスを接続することにより、正しい挿管の確認（μlのストローク量：3×体重（g）+ 155、周波数：毎分120ストローク）。 </li></ol></li></ol></li><li>仰臥位でマウスを保持し、テープでマウスを修正。低体温症を防ぐために加熱パッド上に手術を行う。 <ol><li>剃るとベタジンで皮膚を消毒する。左後肢が手術中に左心室に、より良いビューを得るために、右後肢を横切るように注意してください。 </li></ol></li><li>胸骨までの小さな横方向の皮膚切開を作成し、下にある皮膚や筋肉を分離する。 </li><li> Mを脇に引き出します。胸マイナーであり、m。 5-0絹縫合糸で大胸筋 。 </li><li>私を作る鈍いピンセットを挿入することによって第3肋間でncision。 </li><li>胸骨に到達するまで、外側から内側の側方から肋間筋の下にピンセットを移動します。皮膚に内側からピンセットを押して胸壁を穿刺。慎重にちょうど小さなハサミとピンセットの上肋間筋を切断して開胸を完了します。肺のパンクチャリングを防ぐために、このテクニックを使用してください。 </li><li>肺を保護するために空洞に0.9％のNaCl中に浸漬したスポンジを入れてください。心臓の左側の露出を得るために、肋間空間に創傷スプレッダ（胸部リトラクタ）を導入する。今のところ、左心房、左心室、および左冠動脈前下行枝は実体顕微鏡下に表示されます。 </li><li>左心房の先端で約1ミリメートルシングル6-0プロレン合字と左冠動脈前下行枝の結紮を行います。これは最初の対角枝から遠位にある。 注：または、7-0（00.05ミリメートルの直径）または8-0のスレッド（0.04 mmの直径）を使用することができる。針は、C-1 13ミリメートル3/8円形テーパーポイントの針である。左冠動脈前下行枝の成功ライゲーションは、影響を受けた領土で淡い登場する心筋で、その結果、即時の変色を誘導する。 </li><li>傷スプレッダー（胸のリトラクター）を取り外します。 <ol><li>肋間スペースを中心に3 6-0のTi-Cronの縫合糸を配置します。縫合糸を締める前に、胸腔からスポンジを除去し、人工呼吸器の流出を遮断することによって、肺を再膨張する。そうすることによって、肺は壁側胸膜との再接続。 </li><li>その後、タイトな縫合糸を引っ張り、胸を下に押して、再膨張を繰り返します。生理食塩水を少量使用して胸部の成功した閉鎖を確認して（胸に圧力を適用する際に気泡が見られないことがあります）。 </li><li>肺の正常な展開を確認す​​るために、肋間筋に目を通す。 、両方の胸の筋肉を再配置として気胸の予防のための余分な障壁。 </li></ol></li><li> 5-0シルク縫合糸で皮膚を閉じます。 </li><li>人工呼吸器からマウスを外し、加熱パッド上で回復を可能に。それは胸骨横臥位を維持するのに十分な意識を取り戻したまでは無人の動物を放置しないでください。完全に回復するまで、他の動物の会社に手術を受けた動物を返さないでください。 </li><li>一貫して術後鎮痛（手術後少なくとも48時間ブプレノルフィン0.05 mg / kgをSQ BID）を提供する。 </li></ol>マウスの生体内侵襲血行動態測定2. <ol><li>手順の前に、信号ドリフトを最小限に抑えるために、少なくとも30分間37℃で滅菌水中1.0フレンチのMillar圧力カテーテルを沈める。電子的に2000ヘルツを0 mmHgでおよび100mmHgの圧力センサと記録データを較正する。 </li><li> 1.4グラム/ kgのウレタンの腹腔内投与により麻酔を行います。それを確認してくださいそれはもはやしっかりとつま先のピンチを反応するときに、マウスは、麻酔のその適切な面に到達しない。 </li><li>仰臥位で麻酔をかけたマウスを置きます。テープで手足を固定します。加熱パッドと体温を維持し、直腸プローブで監視。首領域を剃ると甲状腺が露出するように首領域における正中切開を作る。 </li><li>曲がった針で首を固定します。 </li><li>唾液腺を脇に引いて、右総頸動脈を公開します。 、白い糸に似ている迷走神経は、動脈に沿って存在する。慎重に湾曲した鉗子を用いて迷走神経から頸動脈を分離する。 </li><li>他の組織からそれを分離するために右総頸動脈の下に湾曲した鉗子を渡します。動脈周囲の結合組織を除去します。 </li><li>右総頸動脈の下2 6-0シルクワイヤーを渡します。近い頭に向かって配置され、トップワイヤー、上にタイトな結び目を作り、コッヘル（遠位閉塞性ライゲーション）で固定します。 proxiを渡すMALワイヤは二回から左から右へと2 kochers（近位非閉塞性ワイヤー）で固定します。 </li><li>無菌の0.9％NaClをドロップすることで、湿った頸動脈にしてください。綿棒で余分な液体をオフに乾燥させます。 </li><li>遠位連結および近位非閉塞性ワイヤとの間26ゲージ針で右総頸動脈の切開を行います。 </li><li>動脈に圧力センサを導入する。全く血液の損失がないことを確認します。ゆっくりと前進1.0フレンチのMillar圧力カテーテルをプッシュし、カテーテルが鎖骨の下にワイヤーを通して慎重に渡すことができるような方法で、近位非閉塞性ワイヤーを調整します。 <ol><li>近位非閉塞性ワイヤーの調整中に血液の損失を最小限に抑えます。それは非常に壊れやすいですので、進めながらあまりにも多くの圧力センサを圧縮しないでください。近ワイヤーが動脈を閉塞してはならないので、血管は血液で満たされたままにしてください。 </li></ol></li><li>圧力信号の記録を開始。動脈圧の信号fluctuat70 mmHgで100の収縮期血圧 - - 120 mmHgで60の拡張期血圧の間に健全なマウスにおけるES。 </li><li>無名動脈を介して左心室に大動脈を経由してカテーテルを向ける。 120 mmHgで - 心室の圧力が0ミリメートルHgのと100の間で変動する。カテーテルが左心室の内部で安定化させる。実験の要件に応じて60分まで30分間の信号を記録します。 </li><li>実験終了後、30分間、1％Alconoxカテーテルを浸す。 Milli-Q水でカテーテルを洗ってください。フォームブロックにカテーテルを保管してください。 </li><li>さらなる分析のために記録ソフトからデータを取得します。 <ol><li>データ分析のために、圧力信号が安定している時間間隔を考える。興味のある記録されたデータの少なくとも10の連続した​​心臓サイクルを選択してください。 </li><li>心拍数、最大収縮期左心室圧、最小の拡張期左ventrを分析するLabChartソフトウェアバージョン8.0または類似を使用icular圧力、等容性左心室収縮（のdP / dtの最大 ）、等容性左心室弛緩（のdP / dtの分 ）、拡張終期左心室圧のピークレートのピークレート、及び等容性左心室の時定数圧力秋（タウ）7。 注：拡張末期圧は直ちに等容性収縮によって誘発される圧力サージの前の時点での圧力に対応する。タウの計算は、単一指数減衰曲線に左心室圧を適合に基づいており、P（t）として表さこの式において、P 0電子-t /τの + bを=、P（t）は、時間における左心室圧であるDP / DTの最大の負の値の後トンに達しました。パラメータbは、簡略化されたアプローチではゼロであると仮定することができる理論的な漸近線に対応する。強化された等容性弛緩は、タウの小さい方の値になる。 </li></ol></li></OL&gt;

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H. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Expansion+of+transmural+myocardial+infarction:+a+pathophysiologic+factor+in+cardiac+rupture.">Expansion of transmural myocardial infarction: a pathophysiologic factor in cardiac rupture.</a> Circulation. 60, 1532-1538 (1979).</li><li>Jugdutt, B. I., Michorowski, B. L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Role+of+infarct+expansion+in+rupture+of+the+ventricular+septum+after+acute+myocardial+infarction:+a+two-dimensional+echocardiographic+study.">Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: a two-dimensional echocardiographic study.</a> Clin Cardiol. 10, 641-652 (1987).</li><li>Pacher, P., Nagayama, T., Mukhopadhyay, P., Batkai, S., Kass, D. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Measurement+of+cardiac+function+using+pressure-volume+conductance+catheter+technique+in+mice+and+rats.">Measurement of cardiac function using pressure-volume conductance catheter technique in mice and rats.</a> Nat Protoc. 3, 1422-1434 (2008).</li><li>Vanden Bergh, A., Flameng, W., Herijgers, P. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Parameters+of+ventricular+contractility+in+mice:+influence+of+load+and+sensitivity+to+changes+in+inotropic+state.">Parameters of ventricular contractility in mice: influence of load and sensitivity to changes in inotropic state.</a> Pflugers Arch. 455, 987-994 (2008).</li></ol>

None of the authors reports competing financial interests.

慢性心筋の構造および機能の変化、左心室機能不全の発症、および心不全への進行は、いくつかのマウスモデル12で調査することができる。心臓リモデリングおよび機能不全は、心筋障害、または圧力大動脈狭窄を横断する第二過負荷、または拡張型心筋12の遺伝モデルで研究することができることによって誘導することができる。明らかに、マウスモデルの最も顕著な利点?...

Heart failure is a syndrome in which the heart fails to pump blood at a rate commensurate with the 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 failure1.
Ventricular remodelling refers to changes in structure, size, and shape of the left ventricle. In other words, ventricular remodelling concerns an alteration of the left ventricular architecture. 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 (e.g., mitral insufficiency). Since ventricular remodelling affects wall stress, it has a profound impact on cardiac function and on the development of heart failure.
Loss of myocardial tissue following acute myocardial infarction results in a decreased systolic ejection and an increased left ventricular end-diastolic volume and pressure. The Frank-Starling mechanism, implying that an increased end-diastolic volume results in an increased pressure developed during systole, may help to restore cardiac output. However, the concomitant increased wall stress may induce regional hypertrophy in the non-infarcted segment, whereas in the infarcted area expansion and thinning may occur. Experimental animal studies show that the infarcted ventricle hypertrophies and that the degree of hypertrophy is dependent on the infarct size2. 
The loss of myocardial tissue following acute myocardial infarction results in a sudden increase in loading conditions. Post-infarct remodelling occurs in the setting of volume overload, since the stretched and dilated infarcted tissue increases the left ventricular volume. An increased ventricular volume not only implies increased preload (passive ventricular wall stress at the end of diastole) but also increased afterload (total myocardial wall stress during systolic ejection). Afterload is increased since the systolic radius is increased. Therefore, ventricular remodelling post-myocardial infarction is characterized by mixed features of volume overload and pressure overload.
The myocardium consists of 3 integrated components: cardiomyocytes, extracellular matrix, and the capillary microcirculation. All 3&#160;components are involved in the remodelling process. Matrix metalloproteinases produced by inflammatory cells induce degradation of intermyocyte collagen struts and cardiomyocyte slippage. This leads to infarct expansion characterized by the disproportionate thinning and dilatation of the infarct segment3. In later stages of remodelling, interstitial fibrosis is induced, which negatively affects the diastolic properties of the heart. 
The vascular and cardiomyocyte compartment in the myocardium should remain balanced in the process of ventricular remodelling to avoid tissue hypoxia4,5. Whether hypertrophy progresses to heart failure or not may be critically dependent on this balance between the vascular and cardiomyocyte compartment in the myocardium. 
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 reperfusion6. In contrast, the infarct area at 24 hours 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.

<table><tbody><tr><td>Buprenorphine (Buprenex)</td><td>Bedford Laboratories</td><td></td><td></td></tr><tr><td>Sodium Pentobarbital (Nembutal)</td><td>Ceva</td><td></td><td></td></tr><tr><td>Betadine</td><td>VWR internationals</td><td>200065-400</td><td></td></tr><tr><td>5 - 0 silk suture</td><td>Ethicon, Johnson &amp;amp; Johnson Medical</td><td>K890H</td><td></td></tr><tr><td>6 - 0 prolene suture&amp;nbsp;</td><td>Ethicon, Johnson &amp;amp; Johnson Medical</td><td>F1832</td><td></td></tr><tr><td>6 - 0 Ti- Cron suture</td><td>Ethicon, Johnson &amp;amp; Johnson Medical</td><td>F1823</td><td></td></tr><tr><td>Urethane&amp;nbsp;</td><td>Sigma</td><td>94300</td><td></td></tr><tr><td>Alconox</td><td>Alconox Inc.</td><td></td><td></td></tr><tr><td>Ventilator, MiniVent Model 845</td><td>Hugo Sachs</td><td>73-0043</td><td></td></tr><tr><td>Chest retractor or Thorax retractor</td><td>Kent Scientific corporation</td><td>INS600240</td><td>ALM Self-retaining, serrated, 7 cm long, 4 x 4 &quot;L&quot; shaped prongs, 3 mm x 3 mm</td></tr><tr><td>1.0 French Millar pressure catheter&amp;nbsp;</td><td>Millar Instruments&amp;nbsp;</td><td>SPR - 1000/NR</td><td></td></tr><tr><td>Powerlab</td><td>ADInstruments Pty Ltd.</td><td></td><td></td></tr><tr><td>LabChart&amp;reg; software</td><td>ADInstruments Pty Ltd.</td><td></td><td></td></tr><tr><td>Rectal probe</td><td>ADInstruments Pty Ltd.</td><td></td><td></td></tr></tbody></table>

permanent ligation of the left anterior descending coronary artery in mice: a model of post-myocardial infarction remodelling and heart failure

心不全は、心臓が、安静時またはストレス中の細胞酸素要求に見合った速度で血液を送り出すために失敗する症候群である。これは、労作時、特に、体液貯留、息切れ、疲労によって特徴付けられる。心不全は、成長している公衆衛生問題、入院の主要な原因であり、死亡率の主要な原因である。虚血性心疾患は、心不全の主な原因である。 心室リモデリングは、左心室の構造、大きさ、形状の変化を指す。左心室のこのアーキテクチャのリモデリング（ 例えば、全身性動脈高血圧症または大動脈弁狭窄症）、または容量過負荷による圧負荷により、傷害（ 例えば、心筋梗塞）によって誘導される。心室リモデリングは、壁応力に影響を与えるので、それは心機能及び心不全の発症に重大な影響を与える。左前descendinの永久結紮のモデルマウスにおけるグラム冠動脈心室リモデリングおよび心臓機能心筋梗塞後を調査するために使用される。このモデルは、左冠動脈前下行枝の過渡結紮のモデルに比べて目標や病態生理学的関連性の点で基本的に異なる。虚血/再灌流傷害のこの後者のモデルにおいて、梗塞の初期の程度は、再灌流後の心筋救済に影響を与える要因によって調節され得る。対照的に、左冠動脈前下行枝の永久結紮後24時間での梗塞領域は固定されている。このモデルにおける心機能は、1）梗塞拡大、梗塞の治癒、および瘢痕形成のプロセスによって影響される。 2）左心室拡張、心肥大、及び心室リモデリングの同時開発。 左冠動脈前下行枝の永久結紮モデル、侵襲的血行動態MEAの技術に加えてマウスにおけるsurements詳細に示されている。

心筋梗塞の程度は、エバンスブルー/塩化2,3,5-トリフェニルテトラゾリウム（TTC）の二重染色によって評価することができる。 TTCは、NADH 8の存在下で様々なデヒドロゲナーゼの活性による生体組織の深い赤1,3,5- triphenylformazanに変換され、酸化還元指示薬、ある。 図1は、24時間後に心臓の代表的な断面を示している左冠動脈前下行枝の結紮。ブルー染色領域が非虚血/正常?...

Watch this Scientific Journal Video about Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure at JoVE.com

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

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.

マウスの左前下冠動脈の動脈の常設ライゲーション：心筋梗塞後のリモデリングおよび心不全のモデル

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 ...

permanent-ligation-left-anterior-descending-coronary-artery-mice

Research

JoVE Journal

Medicine

27.7K ビュー.  Catholic University of Leuven. 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.

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

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.

心筋梗塞のマウスモデルにおける冠動脈結紮および心筋内注入

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 ...

医学

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.

マウスにおける冠動脈結紮のために修飾されたテクニック

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 ...

LAD-Ligation: A Murine Model of Myocardial Infarction

Research models of infarction and myocardial ischemia are essential to investigate the acute and chronic pathobiological and pathophysiological processes in myocardial ischemia and to develop and optimize future treatment.
Two different methods of creating myocardial ischemia are performed in laboratory rodents. The first method is to create cryo infarction, a fast but inaccurate technique, where a cryo-pen is applied on the surface of the heart (1-3). Using this method the scientist can not guarantee that the cryo-scar leads to ischemia, also a vast myocardial injury is created that shows pathophysiological side effects that are not related to myocardial infarction. The second method is the permanent ligation of the left anterior descending artery (LAD). Here the LAD is ligated with one single stitch, forming an ischemia that can be seen almost immediately. By closing the LAD, no further blood flow is permitted in that area, while the surrounding myocardial tissue is nearly not affected. This surgical procedure imitates the pathobiological and pathophysiological aspects occurring in infarction-related myocardial ischemia.
The method introduced in this video demonstrates the surgical procedure of a mouse infarction model by ligating the LAD. This model is convenient for pathobiological and pathophysiological as well as immunobiological studies on cardiac infarction. The shown technique provides high accuracy and correlates well with histological sections.

This video demonstrates how to use a fast and reliable model to study pathobiological and pathophysiological processes of myocardial ischemia.

LAD -ライゲーション：心筋梗塞のマウスモデル

Research models of infarction and myocardial ischemia are essential to investigate the acute and chronic pathobiological and pathophysiological processes ...

生物学

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

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

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

左前下の動脈の結紮を通して心筋虚血再灌流傷害のマウスモデル

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

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).

マウス左前方降順（LAD）冠動脈結紮：心筋梗塞のための改善と簡略化されたモデル

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 ...

Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery

Myocardial infarction (MI) and acute coronary diseases are among the most prominent causes of death in population with western lifestyle. The murine models of MI with permanent ligation of left-anterior descending (LAD) coronary artery closely mimics MI in humans. Murine models benefit from the extensive genetic engineering available nowadays. Here we propose a reproducible murine surgical model of myocardial infarction by permanent LAD coronary ligation. Our technique comprises anesthesia with ketamine/xylazine that can be rapidly reversed by administration of an antagonist, intubation without tracheotomy for mechanical-assisted ventilation, ventilation with application of extrinsic positive end-expiratory pressure (PEEP) to avoid alveolar collapse, a thoracotomy method limiting to the minimum surgical lesions made to skeletal muscles, and lung inflation without thoracentesis. This method is sparsely invasive, reproducible and reduces post-surgery mortality and complications.

Herein we describe a surgical procedure showing how to achieve permanent ligation of the left-anterior descending coronary artery in mice. This model is of high relevance to investigate the pathophysiology of myocardial infarction and the concomitant biological processes.

左前皮下冠動脈の永久的なライゲーションを用いたマウス心筋梗塞モデル

Myocardial infarction (MI) and acute coronary diseases are among the most prominent causes of death in population with western lifestyle. The murine ...

Induction of Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury in Mice

Acute myocardial infarction is a common cardiovascular disease with high mortality. Myocardial reperfusion injury can counteract the beneficial effects of heart reflow and induce secondary myocardial injury. A simple and reproducible model of myocardial infarction and myocardial ischemia-reperfusion injury is a good tool for researchers. Here, a customizable method to create a myocardial infarction (MI) model and MIRI by precision ligation of the left anterior descending coronary artery (LAD) through micromanipulation is described. Accurate and reproducible ligature positioning of the LAD helps obtain consistent results for heart injury. ST-segment changes can help to identify model accuracy. The serum level of cardiac troponin T (cTnT) is used to assess the myocardial injury, cardiac ultrasound is employed to evaluate the myocardial systolic function, and Evans-Blue/triphenyl tetrazolium chloride staining is used to measure infarct size. In general, this protocol reduces procedure duration, ensures controllable infarct size, and improves mouse survival.

Here we describe a simple and reproducible method that can induce myocardial infarction or myocardial ischemia-reperfusion injury in mice by precision ligation of the left anterior descending coronary artery through micromanipulation.

マウスにおける心筋梗塞および心筋虚血再灌流障害の誘発

Acute myocardial infarction is a common cardiovascular disease with high mortality. Myocardial reperfusion injury can counteract the beneficial effects of ...

Generation and Characterization of Right Ventricular Myocardial Infarction Induced by Permanent Ligation of the Right Coronary Artery in Mice

Right ventricular infarction (RVI) is a common presentation in clinical practice. Severe RVI can lead to fatal hemodynamic dysfunction and arrhythmia. In contrast to the extensively used mouse myocardial infarction (MI) model generated by left coronary artery ligation, the RVI mouse model is rarely employed due to the difficulty associated with model generation. Research on the mechanisms and treatment of RVI-induced RV remodeling and dysfunction requires animal models to mimic the pathophysiology of RVI in patients. This study introduces a feasible procedure for RVI model generation in C57BL/6J mice. Further, this model was characterized based on the following: infarct size evaluation at 24 h after MI, assessment of cardiac remodeling and function with echocardiography, RV hemodynamics assessment, and histology of the infarct zone at 4 weeks after RVI. In addition, a coronary vasculature cast was performed to observe the coronary arterial arrangement in RV. This mouse model of RVI would facilitate the research on mechanisms of right heart failure and seek new therapeutic targets of RV remodeling.

There are several differences between the right and left ventricles. However, the pathophysiology of right ventricular infarction (RVI) has not been clarified. In the present protocol, a reproducible method for RVI mouse model generation is introduced, which may provide a means to explain the mechanism of RVI.

マウスにおける右冠動脈の永久結紮による右心室心筋梗塞の生成と特徴付け

Right ventricular infarction (RVI) is a common presentation in clinical practice. Severe RVI can lead to fatal hemodynamic dysfunction and arrhythmia. In ...

Left Coronary Artery Ligation: A Surgical Murine Model of Myocardial Infarction

Ischemic heart disease and subsequent myocardial infarction (MI) is one of the leading causes of mortality in the United States and around the world. In order to explore the pathophysiological changes after myocardial infarction and design future treatments, research models of MI are required. Permanent ligation of the left coronary artery (LCA) in mice is a popular model to investigate cardiac function and ventricular remodeling post MI. Here we describe a less invasive, reliable, and reproducible surgical murine MI model by permanent ligation of the LCA. Our surgical model comprises of an easily reversible general anesthesia, endotracheal intubation that does not require a tracheotomy, and a thoracotomy. Electrocardiography and troponin measurement should be performed to ensure MI. Echocardiography at day 28 after MI will discern heart function and heart failure parameters. The degree of cardiac fibrosis can be evaluated by Masson's trichrome staining and cardiac MRI. This MI model is useful for studying the pathophysiological and immunological alterations after MI.

Presented here is a surgical procedure for permanent ligation of the left coronary artery in mice. This model can be used to investigate the pathophysiology and associated inflammatory response after myocardial infarction.

左冠動脈結紮術:心筋梗塞の外科用マウスモデル

Ischemic heart disease and subsequent myocardial infarction (MI) is one of the leading causes of mortality in the United States and around the world. In ...

An Experimental Model of Myocardial Infarction for Studying Cardiac Repair and Remodeling in Knockout Mice

Cardiovascular disease is the most prevalent cause of death in Western countries, with acute myocardial infarction (MI) being the most prevalent form. This paper describes a protocol for studying the role of galectin 3 (Gal-3) in the temporal evolution of cardiac healing and remodeling in an experimental animal model of MI. 
The procedures described include an experimental model of MI with a permanent coronary ligature in male C57BL/6J (control) and Gal-3 knockout (KO) mice, an echocardiography procedure to study cardiac remodeling and systolic function in vivo, a histological evaluation of interstitial myocardial fibrosis with picrosirius red-stained and rhodamine-conjugated lectin-stained sections for studying myocyte hypertrophy by the cross-sectional area (MCSA), and the quantification of infarct size and cardiac remodeling (scar thinning, septum thickness, and expansion index) by planimetry in slices stained with Masson's trichrome and triphenyl tetrazolium chloride. Gal-3 KO mice with MI showed disrupted cardiac remodeling and an increase in the scar thinning ratio and the expansion index. At the onset of MI, myocardial function and cardiac remodeling were also severely affected. At 4 weeks post MI, the natural evolution of fibrosis in infarcted Gal-3 KO mice was also affected. 
In summary, the experimental model of MI is a suitable model for studying the temporal evolution of cardiac repair and remodeling in mice with the genetic deletion of Gal-3 and other animal models. The lack of Gal-3 affects the dynamics of cardiac repair and disrupts the evolution of cardiac remodeling and function after MI.

Here, we describe an experimental model of myocardial infarction, an echocardiography procedure to study cardiac remodeling and function, and procedures for quantifying fibrosis and hypertrophy in picrosirius red-stained and rhodamine-stained sections, as well as the infarct size and expansion index in slices stained with Masson's trichrome.

Cardiovascular disease is the most prevalent cause of death in Western countries, with acute myocardial infarction (MI) being the most prevalent form. ...