Name: a model of cardiac remodeling through constriction of the abdominal aorta in rats
Uploaded: 2016-12-02T10:30:00.000+00:00
Duration: 7 min 31 s
Description: Watch this Scientific Journal Video about A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats at JoVE.com

The authors' work was supported by a grant from Ministry of Science and Technology (MOST 103-2320-B-002-068-MY2), the National Health Research Institute (NHRI-EX104-10418SC), and National Taiwan University (NTU 104R4000).

全ての動物実験は、実験動物の管理と使用に関する指針に従って行わ米国国立衛生研究所によって公開（NIH公開番号85-23、1996年改訂）しました。このプロトコルはにより、国立台湾大学の施設内動物管理使用委員会によって定められたガイドラインに基づいて承認されました。 1.動物の手術<ol><li>ホーニング石の上に針の先端を鈍化により、22 G注射針を準備します。ペンチを使用して、直角に針をひだのあります。 </li><li>手術前に、必要な手術器具や材料、ならびに回復ケージを準備します。使用前にすべての機器および外科用品をオートクレーブ。 </li><li> 200グラムの周りにラットを維持し、食物および水に自由にアクセス制御された温度（21±2℃）で12時間の明/暗サイクルの下でそれらを保ちます。各グループに少なくとも6匹のラットが含まれます。ペントバルビタールでラットを麻酔または別の適切な麻酔薬（0.5ミリリットル、腹腔内を75mg / kg）を。尾の反射をテストすることによって、麻酔の深さを確認してください。 注：テール反射の欠如は、適切な麻酔の指標です。 </li><li>体温を維持するために加熱パッドで手術台に仰臥位にラットを置きます。外科的な汚染を避けるために、動物のバリカンヘアリムーバーローションでラットの腹部を剃ります。手術前にベタジンまたは別のクレンジング試薬ときれい-坊主腹部をスクラブ。 注：これは、作業中は無菌領域を維持することが重要です。 </li><li>メスで、腹部の正中線に沿って2cmの切開を行います。通常の生理食塩水を使用して、手術中に湿った腹部臓器を維持します。後部腹膜領域にある下大静脈を露出させるためにコットンボールを使用して、側に慎重に消化器官を置き換えます。並置され、通常は上にある腹部大動脈を、識別下大静脈の左。 注：腹部大動脈は、心拍数に合わせて脈動する容器です。 </li><li>下の血管を明らかにピンセットで腹膜を貫通。静かに腎動脈に隣接する腹部大動脈を隔離し、右の起源と左腎動脈との間に腹部大動脈の下に8センチメートル長4-0絹縫合糸を渡します。 </li><li>縫合糸と緩い二重結び目を作ります。直径3mmのループを残して、ループ内の鈍化と曲がっ22 G針を配置します。大動脈と針の周りに結び目を締めて、直径0.7mmの収縮を達成するために、直ちに針を取り除きます。 </li><li> 6-0吸収性縫合糸材料と腹腔を閉じます。単純結節縫合で筋肉や皮膚切開を縫合。感染を防ぐために、ヨードチンキで手術部位を洗浄。 </li><li>それは十分な意識を取り戻すまで、自由な移動によって示されるように、慎重に動物を観察しますおよび食物摂取。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無人の動物を放置しないでください。術後の痛みを防ぐために、アセトアミノフェン（0.5ミリリットル中300ミリグラム/ kg、腹腔内）でラットを扱います。 注：制度的政策によって承認されたように、ユーザは、鎮痛薬を投与すべきです。 </li></ol> 2.組織および血液サンプル採取<ol><li> 10週間後の手術では、ラットを計量し、ペントバルビタール（0.5ミリリットル、腹腔内を75mg / kg）で、それを麻酔。手術前に、その尾の反射をテストすることによって、麻酔の深さを確認します。金属製のトレイにラットを置きます。 </li><li>メスを用いて首の正中線に沿って2cmの切開を行います。気管を露出するためにピンセットで慎重に筋肉を変位させます。気管に平行であり、心拍数と時間的に脈動頚動脈を識別するために慎重に観察します。 </li><li> EDTAでコーティングされた採血管に頸動脈から血液を採取します。すぐに遠心分離機2,000×gで15分間、血液および血漿を収集します。必要になるまで-80℃で血漿を保管してください。 </li><li>剣状突起の正中線の周りに、胸部に5cmの切開を行います。鋭いピンセットでダイアフラムを突き刺します。ハサミを使用して、心臓を露出するために、両側の半ば鎖骨ラインに沿って肋骨を切断して除去します。心臓と血管の境界線に沿って慎重に心を切り出します。組織をつかんずに静かに心を削除します。 </li><li>灌流針に大動脈トランクを結びつけることによって修正されたランゲンドルフ灌流装置に心をマウントします。クレブス緩衝液で心臓灌流（110 mMの塩化ナトリウム、2.6のKClを含有する1.2mMのKH 2 PO 4、1.2mMのMgSO 4を、25mMのNaHCO 3を、および11 mMグルコース[pHが7.4]）は、血液を洗い流します。心を計量し、心臓重量対体重比を算出します。氷上で4％パラホルムアルデヒドで心臓を修正しました。パラホルムアルデヒド蒸気はTOXであるため、マスクを着用することを忘れないでくださいIC。 </li></ol> 3.組織線維症の定量化<ol><li>組織切片デバイス上でパラホルムアルデヒド固定心臓組織を置き、2ミリメートルの厚さの切片を切りました。包埋カセットに組織切片を置きます。段階的なアルコール浴一連の組織を脱水（50％、75％、95％、1時間毎、100％）。 </li><li> 1時間ワックスに最終的に1時間キシレンで組織に浸潤し。包埋カセットに浸透組織を置き、パラフィンワックスに埋め込むことができます。ミクロトームまで室温でパラフィンブロック中に包埋組織を保管してください。 </li><li>厚さ4μmの切片に埋め込まれた組織をスライス。 45ºCの水浴中でセクションを配置します。角度で水浴中にスライドガラスを浸し、徐々にスライドへの部分的な付着を可能にするためにパラフィン切片のエッジに近づきます。 </li><li>組織切片の下で潜在的なエアポケットを除去するために、より良い取り付けを容易にするために、お風呂の中と外にスライドを移動します。ドライトン彼は1時間37ºCでスライドし、組織染色、室温で保管してください。 </li><li>タンクにスライドを置きます。 30分間キシレンでスライドを脱パラフィン化し、最後に蒸留水で（3分間それぞれ95％、75％、50％）を順次希釈アルコールでそれを再水和します。完全に1時間組織切片をカバーするために十分なピクロシリウス赤色の溶液を使用してください。 2変更のための0.5％酢酸溶液中でスライドを洗浄し、その後無水アルコールで2回のすすぎを行います。 </li><li>スライドを空気乾燥し、カバースリップで合成樹脂でスライドをマウントします。可視光フィールドでスライドを撮影。 注：写真の中の赤い部分は、200Xの倍率で顕微鏡下ピクロシリウス赤のプラスゾーンを示しています。線維症11の程度を示す総面積、オーバーピクロシリウス赤のプラスゾーンの割合を計算します。 </li></ol> 4.ブラッドトロポニン定量<ol><li>血漿トロポニンレベルを定量酵素結合免疫吸着アッセイ（ELISA）を使用。重複の各サンプルをアッセイ。負荷血漿50μlの、適切なウェルに抗体カクテル50μlの。プレートを密封し、400rpmでプレートシェーカー上で室温で1時間インキュベートします。 注：血漿中の心臓トロポニンは、心臓傷害のマーカーです。 </li><li>液体を吸引し、洗浄緩衝液250μlの3回各ウェルを洗浄します。最後の洗浄後、プレートを反転し、過剰な液体を除去するために清潔なペーパータオルに対してそれをブロット。 </li><li>各ウェルにテトラメチルベンジジン基質100μlを加え、400rpmでプレートシェーカー上で暗所で10分間インキュベートします。各ウェルに停止液100μLを加えます。混合するために1分間プレートシェーカー上でプレートを振ります。 450nmでの光学密度（OD）を記録します。 注：トロポニン濃度がOD値に比例します。 </li></ol>

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The authors have nothing to disclose.

Hypertensive heart disease, a major health problem that contributes greatly to morbidity and mortality, can lead to cardiac hypertrophy and heart failure5. The pathogenesis and progression of hypertensive heart disease in humans is complex, so an appropriate animal model is critical to investigate the underlying mechanisms and to test novel therapeutics that aim to improve cardiac structure and function5. The abdominal aortic constriction model, which simulates chronic heart disease, is an effective...

心不全は、複雑な臨床症候群、疲労、呼吸困難、運動不耐性を含むそれらの症状、および末梢組織における体液貯留です。これは、先進国1における死亡の主な原因です。別にサルコメアタンパク質またはイオンチャネル2における突然変異によって引き起こされる継承心筋から、心筋機能障害は、高血圧、心臓弁膜症、肥満、および糖尿病3を含む医学的状態、種々の方法により生じさせることができます。最終的には心不全3,4につながる循環要求を満たすために不十分な心臓のポンプ能力、に心筋の構造、電気伝導、およびエネルギー代謝のリードの変化。心不全のメカニズムを調査し、したがって、心臓血管研究の分野において重要です。心不全の進行につながる分子メカニズムを識別することは、最終的に新規治療標的または有用なバイオマーカーの発見を助けることができます<s&gt; 1アップ。ヒト5に心不全とキー臨床的特徴を共有する心不全の動物モデルを開発することが重要です。 心臓肥大及びリモデリングが心不全の発症において重要な役割を果たしています。高血圧性心疾患は、心臓肥大およびヒト患者1に見られる不適応リモデリングの主要な寄与因子です。これらの人間の条件を模倣するために、動物モデルは、多くの場合、外科的処置を介して確立されます。具体的には、横方向または腹部大動脈は、最終的に心臓内の圧負荷につながる左心室に対する抵抗力を高めるために狭窄することができます。この現象は通常、心臓血管系の機能的な要求を満たすために、心臓肥大、心筋細胞の生理学的補償をもたらします。しかし、機能的な需要は、心臓線維症およびcontracにつながる、通常の生理学的代償機構を無効にしますタイルの減損。横方向の大動脈狭窄（TAC）手術は、多くの場合、大動脈弓から開胸、機械換気、および胸腺の分離および脂肪組織を含む複雑な手順を伴います。これとは対照的に、腹部大動脈狭窄は、単純な実験手法6-8を必要とします 。腹部大動脈は、左右の腎動脈との間に、手術中の狭窄です。心肥大およびリモデリングは、数週間腹部大動脈狭窄手術6-8後に観察することができます。彼らは、横大動脈狭窄手術9,10によって生成されたものと同様の堅固な高血圧性心疾患を生じさせます。ここで、我々は、効率的な再現性の高い、かつ低侵襲性の方法を用いて、ラットで腹部大動脈狭窄を行うためのプロトコルを記述します。腎動脈に隣接し、腹部大動脈を4-0絹糸により形成さ0.72ミリメートルループによって絞られます。手術、心臓肥大およびremodelin後10週間gを観察することができます。腹部大動脈狭窄誘発性心肥大のラットモデルは、病気のメカニズムや病態生理学、ならびに潜在的な治療薬の開発を研究するためのプラットフォームを提供します。

<table><tbody><tr><td>22 G syringe needle&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>&amp;nbsp;&amp;nbsp; BD Biosciences&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>309572</td><td></td></tr><tr><td>EDTA Blood Collection Tubes</td><td>&amp;nbsp;&amp;nbsp; BD Biosciences&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>REF365974</td><td></td></tr><tr><td>4-0 silk suture&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>Sharpoint&amp;trade; Products&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>DC-2515N</td><td></td></tr><tr><td>6-0 silk suture&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>Sharpoint&amp;trade; Products&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>DC-2150N</td><td></td></tr><tr><td>Pentobarbital&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>Sigma Aldrich&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>1507002</td><td></td></tr><tr><td>Paraformaldehyde&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>Sigma Aldrich&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>441244</td><td></td></tr><tr><td>Acetaminophen</td><td>Sigma Aldrich&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>A7085</td><td></td></tr><tr><td>Picrosirius red solution&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>Abcam&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>ab150681</td><td></td></tr><tr><td>Cardiac troponin kit&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>&amp;nbsp;Abcam&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>ab200016</td><td></td></tr><tr><td>Imagequant</td><td>Molecular Dynamics</td><td></td><td></td></tr><tr><td>Langendorff&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>&amp;nbsp;ADInstruments&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;&amp;nbsp;</td><td>ML870B2</td><td></td></tr></tbody></table>

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.

10週間の腹部大動脈狭窄、手術後、得られた心臓の病状を分析しました。心臓の組織学は、体重に対する心臓重量の比を計算することによって、心臓におけるコラーゲンの量を検出することによって測定しました。心臓の損傷は、プラズマ心筋トロポニンの濃度を測定することにより確認しました。 図1Aに示...

Watch this Scientific Journal Video about A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats at JoVE.com

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

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.

ラットの腹部大動脈の収縮を通じて心臓リモデリングのモデル

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

a-model-cardiac-remodeling-through-constriction-abdominal-aorta

Research

JoVE Journal

Medicine

9.9K ビュー.  National Taiwan University. 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.

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

Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model

Ascending aortic constriction is the most common and successful surgical model for creating pressure overload induced cardiac hypertrophy and heart failure. Here, we describe a detailed surgical procedure for creating pressure overload and cardiac hypertrophy in rats by constriction of the ascending aorta using a small metallic clip. After anesthesia, the trachea is intubated by inserting a cannula through a half way incision made between two cartilage rings of trachea. Then a skin incision is made at the level of the second intercostal space on the left chest wall and muscle layers are cleared to locate the ascending portion of aorta. The ascending aorta is constricted to 50&#8211;60% of its original diameter by application of a small sized titanium clip. Following aortic constriction, the second and third ribs are approximated with prolene sutures. The tracheal cannula is removed once spontaneous breathing was re-established. The animal is allowed to recover on the heating pad by gradually lowering anesthesia. The intensity of pressure overload created by constriction of the ascending aorta is determined by recording the pressure gradient using trans-thoracic two dimensional Doppler-echocardiography. Overall this protocol is useful to study the remodeling events and contractile properties of the heart during the gradual onset and progression from compensated cardiac hypertrophy to heart failure stage.

We describe a stepwise procedure for creating pressure overload and left ventricular hypertrophy in Wistar rats by constriction of the ascending aorta using a small metallic clip. This model is extensively used for studying remodeling changes during cardiac hypertrophy and for identifying and evaluating strategies for regression of such changes.

圧負荷心肥大モデルの作成のためのラットの大動脈狭窄昇順

Ascending aortic constriction is the most common and successful surgical model for creating pressure overload induced cardiac hypertrophy and heart ...

医学

Assessment of Cardiac Morphological and Functional Changes in Mouse Model of Transverse Aortic Constriction by Echocardiographic Imaging

Transverse aortic constriction (TAC) in mice has been used as a valuable model to study mechanisms of cardiac hypertrophy and heart failure1. A reliable noninvasive method is essential to assess real-time cardiac morphological and functional changes in animal models of heart disease. Transthoracic echocardiography represents an important tool for noninvasive assessment of cardiac structure and function2. Here we used a high-resolution ultrasound imaging system to monitor myocardial remodeling and heart failure progression over time in a mouse model of TAC. B-mode, M-mode, and Doppler imaging were used to precisely assess cardiac hypertrophy, ventricular dilatation, and functional deterioration in mice following TAC. Color and pulse wave (PW) Doppler imaging was used to noninvasively measure pressure gradient across the aortic constriction created by TAC and to assess transmitral blood flow in mice. Thus transthoracic echocardiographic imaging provides comprehensive noninvasive measurements of cardiac dimensions and function in mouse models of heart disease.

The goal of this protocol is to noninvasively assess cardiac structural and functional changes in a mouse model of heart disease created by transverse aortic constriction, using B- and M-mode echocardiography and color/pulse wave Doppler imaging.

心臓形態学的および心エコーイメージングによって横大動脈狭窄のマウスモデルにおける機能の変更の評価

Transverse aortic constriction (TAC) in mice has been used as a valuable model to study mechanisms of cardiac hypertrophy and heart failure1. A reliable ...

Minimally Invasive Transverse Aortic Constriction in Mice

Minimally invasive transverse aortic constriction (MTAC) is a more desirable method for the constriction of the transverse aorta in mice than standard open-chest transverse aortic constriction (TAC). Although transverse aortic constriction is a highly functional method for the induction of high pressure in the left ventricle, it is a more difficult and lengthy procedure due to its use of artificial ventilation with tracheal intubation. TAC is oftentimes also less survivable, as the newer method, MTAC, neither requires the cutting of the ribs and intercostal muscles nor tracheal intubation with a ventilation setup. In MTAC, as opposed to a thoracotomy to access to the chest cavity, the aortic arch is reached through a midline incision in the anterior neck. The thyroid is pulled back to reveal the sternal notch. The sternum is subsequently cut down to the second rib level, and the aortic arch is reached simply by separating the connective tissues and thymus. From there, a suture can be wrapped around the arch and tied with a spacer, and then the sternal cut and skin can be closed. MTAC is a much faster and less invasive way to induce left ventricular hypertension and enables the possibility for high-throughput studies. The success of the constriction can be verified using high-frequency trans-thoracic echocardiography, particularly color Doppler and pulsed-wave Doppler, to determine the flow velocities of the aortic arch and left and right carotid arteries, the dimension of the blood vessels, and the left ventricular function and morphology. A successful constriction will also trigger significant histopathological changes, such as cardiac muscle cell hypertrophy with interstitial and perivascular fibrosis. Here, the procedure of MTAC is described, demonstrating how the resulting flow changes in the carotid arteries can be examined with echocardiography, gross morphology, and histopathological changes in the heart.

Minimally invasive transverse aortic constriction (MTAC) conserves the essentials of regular transverse aortic constriction (TAC) while eliminating the use of a ventilator with tracheal intubation. It proves to be a highly desirable method for high-throughput studies on left ventricular overload, particularly in translational studies.

マウスにおける低侵襲横大動脈狭窄

Minimally invasive transverse aortic constriction (MTAC) is a more desirable method for the constriction of the transverse aorta in mice than standard ...

A Closed-chest Model to Induce Transverse Aortic Constriction in Mice

Research on cardiac hypertrophy and heart failure is frequently based on pressure overload mouse models induced by TAC. The standard procedure is to perform a partial thoracotomy to visualize the transverse aortic arch. However, the surgical trauma caused by the thoracotomy in open-chest models changes the respiratory physiology as the ribs are dissected and left unattached after chest closure. To prevent this, we established a minimally invasive, closed chest approach via lateral thoracotomy. Herein we approach the aortic arch via the 2nd intercostal space without entering the chest cavities, leaving the mouse with a less traumatic injury to recover from. We perform this operation using standard laboratory settings for open chest TAC procedures with equal survival rates. Apart from maintaining physiological breathing patterns due to the closed chest approach, the mice seem to benefit by showing rapid recovery, as the less invasive technique appears to facilitate a fast healing process and to reduce immune response after trauma.

Here, we present a protocol of Transverse Aortic constriction (TAC) via a lateral thoracotomy. This technique is a minimally invasive, closed chest surgical procedure aiming to simulate pressure overload and heart failure in mice utilizing standard TAC laboratory settings.

マウスで横方向の大動脈狭窄を誘導するために閉じて胸モデル

Research on cardiac hypertrophy and heart failure is frequently based on pressure overload mouse models induced by TAC. The standard procedure is to ...

Studying Left Ventricular Reverse Remodeling by Aortic Debanding in Rodents

To better understand the left ventricular (LV) reverse remodeling (RR), we describe a rodent model wherein, after aortic banding-induced LV remodeling, mice undergo RR upon removal of the aortic constriction. In this paper, we describe a step-by-step procedure to perform a minimally invasive surgical aortic debanding in mice. Echocardiography was subsequently used to assess the degree of cardiac hypertrophy and dysfunction during LV remodeling and RR and to determine the best timing for aortic debanding. At the end of the protocol, terminal hemodynamic evaluation of the cardiac function was conducted, and samples were collected for histological studies. We showed that debanding is associated with surgical survival rates of 70-80%. Moreover, two weeks after debanding, the significant reduction of ventricular afterload triggers the regression of ventricular hypertrophy (~20%) and fibrosis (~26%), recovery of diastolic dysfunction as assessed by the normalization of left ventricular filling and end-diastolic pressures (E/e&#39;&#160;and LVEDP). Aortic debanding is a useful experimental model to study LV RR in rodents. The extent of myocardial recovery is variable between subjects, therefore, mimicking the diversity of RR that occurs in the clinical context, such as aortic valve replacement. We conclude that the aortic banding/debanding model represents a valuable tool to unravel novel insights into the mechanisms of RR, namely the regression of cardiac hypertrophy and the recovery of diastolic dysfunction.

Here we describe a step-by-step protocol of surgical aorta debanding in the well-established mice model of aortic-constriction. This procedure not only allows studying the mechanisms underlying the left ventricular reverse remodeling and regression of hypertrophy but also to test novel therapeutic options that might accelerate myocardial recovery.

げっ歯類における大動脈デベンディングによる左心室逆改造の研究

To better understand the left ventricular (LV) reverse remodeling (RR), we describe a rodent model wherein, after aortic banding-induced LV remodeling, ...

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure

In response to an injury, such as myocardial infarction, prolonged hypertension or a cardiotoxic agent, the heart initially adapts through the activation of signal transduction pathways, to counteract, in the short-term, for the cardiac myocyte loss and or the increase in wall stress. However, prolonged activation of these pathways becomes detrimental leading to the initiation and propagation of cardiac remodeling leading to changes in left ventricular geometry and increases in left ventricular volumes; a phenotype seen in patients with systolic heart failure (HF). Here, we describe the creation of a rat model of pressure overload induced moderate remodeling and early systolic dysfunction (MOD) by ascending aortic banding (AAB) via a vascular clip with an internal area of 2 mm2. The surgery is performed in 200 g Sprague-Dawley rats. The MOD HF phenotype develops at 8-12 weeks after AAB and is characterized noninvasively by means of echocardiography. Previous work suggests the activation of signal transduction pathways and altered gene expression and post-translational modification of proteins in the MOD HF phenotype that mimic those seen in human systolic HF; therefore, making the MOD HF phenotype a suitable model for translational research to identify and test potential therapeutic anti-remodeling targets in HF. The advantages of the MOD HF phenotype compared to the overt systolic HF phenotype is that it allows for the identification of molecular targets involved in the early remodeling process and the early application of therapeutic interventions. The limitation of the MOD HF phenotype is that it may not mimic the spectrum of diseases leading to systolic HF in human. Moreover, it is a challenging phenotype to create, as the AAB surgery is associated with high mortality and failure rates with only 20% of operated rats developing the desired HF phenotype.

We describe the creation of a rat model of pressure overload induced moderate remodeling and early systolic dysfunction where signal transduction pathways involved in the initiation of the remodeling process are activated. This animal model will aid in identifying molecular targets for applying early therapeutic anti-remodeling strategies for heart failure.

過圧過負荷のラットモデルは、過小収縮期心不全とは対照的に中程度のリモデリングと収縮期機能不全を誘発した

In response to an injury, such as myocardial infarction, prolonged hypertension or a cardiotoxic agent, the heart initially adapts through the activation ...

A Model of Reverse Vascular Remodeling in Pulmonary Hypertension Due to Left Heart Disease by Aortic Debanding in Rats

Pulmonary hypertension due to left heart disease (PH-LHD) is the most common form of PH, yet its pathophysiology is poorly characterized than pulmonary arterial hypertension (PAH). As a result, approved therapeutic interventions for the treatment or prevention of PH-LHD are missing. Medications used to treat PH in PAH patients are not recommended for treatment of PH-LHD, as reduced pulmonary vascular resistance (PVR) and increased pulmonary blood flow in the presence of increased left-sided filling pressures may cause left heart decompensation and pulmonary edema. New strategies need to be developed to reverse PH in LHD patients. In contrast to PAH, PH-LHD develops due to increased mechanical load caused by congestion of blood into the lung circulation during left heart failure. Clinically, mechanical unloading of the left ventricle (LV) by aortic valve replacement in aortic stenosis patients or by implantation of LV assist devices in end-stage heart failure patients normalizes not only pulmonary arterial and right ventricular (RV) pressures but also PVR, thus providing indirect evidence for reverse remodeling in the pulmonary vasculature. Using an established rat model of PH-LHD due to left heart failure triggered by pressure overload with subsequent development of PH, a model is developed to study the molecular and cellular mechanisms of this physiological reverse remodeling process. Specifically, an aortic debanding surgery was performed, which resulted in reverse remodeling of the LV myocardium and its unloading. In parallel, complete normalization of RV systolic pressure and significant but incomplete reversal of RV hypertrophy was detectable. This model may present a valuable tool to study the mechanisms of physiological reverse remodeling in the pulmonary circulation and the RV, aiming to develop therapeutic strategies for treating PH-LHD and other forms of PH.

The present protocol describes a surgical procedure to remove ascending-aortic banding in a rat model of pulmonary hypertension due to left heart disease. This technique studies endogenous mechanisms of reverse remodeling in the pulmonary circulation and the right heart, thus informing strategies to reverse pulmonary hypertension and/or right ventricular dysfunction.

ラットの大動脈剥離による左心疾患による肺高血圧症における逆血管リモデリングのモデル

Pulmonary hypertension due to left heart disease (PH-LHD) is the most common form of PH, yet its pathophysiology is poorly characterized than pulmonary ...

O-Ring Aortic Banding Versus Traditional Transverse Aortic Constriction for Modeling Pressure Overload-Induced Cardiac Hypertrophy

Aortic banding in mice is one of the most commonly used experimental models for cardiac pressure overload-induced cardiac hypertrophy and the induction of heart failure. The previously used technique is based on a threaded suture around the aortic arch tied over a blunted 27 G needle to create stenosis. This method depends on the surgeon manually tightening the thread and, thus, leads to high variance in the diameter size. A newly refined method described by Melleby et al. promises less variance and more reproducibility after surgery. The new technique, o-ring- aortic banding (ORAB), uses a non-slip rubber ring instead of a suture with a thread, resulting in reduced variation in pressure overload and reproducible phenotypes of cardiac hypertrophy. During surgery, the o-ring is placed between the brachiocephalic and left carotid arteries. Successful constriction is confirmed by echocardiography. After 1 day, correct placement of the ring results in an increased flow velocity in the transverse aorta over the o-ring-induced stenosis. After 2 weeks, impaired cardiac function is proven by decreased ejection fraction and increased wall thickness. Importantly, besides less variance in the diameter size, ORAB is associated with lower intra- and post-operative mortality rates compared with transverse aortic constriction (TAC). Thus, ORAB represents a superior method to the commonly used TAC surgery, resulting in more reproducible results and a possible reduction in the number of animals needed.

The present protocol describes a new technique of aortic banding in mice to induce pressure overload cardiac hypertrophy. For banding, a rubber ring with a fixed inner diameter is used. This new technique promises less variance and more reproducible data for future experiments.

圧力過負荷誘発心肥大をモデル化するためのOリング大動脈バンディングと従来の横大動脈狭窄の比較

Aortic banding in mice is one of the most commonly used experimental models for cardiac pressure overload-induced cardiac hypertrophy and the induction of ...

Modified Heterotopic Abdominal Heart Transplantation and a Novel Aortic Regurgitation Model in Rats

Over the past 50 years, many researchers have reported heterotopic abdominal heart transplantation in mice and rats, with some variations in the surgical technique. Modifying the transplantation procedure to strengthen the myocardial protection could prolong the ischemia time while preserving the donor&#39;s cardiac function. This technique&#39;s key points are as follows: transecting the donor&#39;s abdominal aorta before harvesting to unload the donor&#39;s heart; perfusing the donor&#39;s coronary arteries with a cold cardioplegic solution; and topical cooling of the donor&#39;s heart during the anastomosis procedure. Consequently, since this procedure prolongs the acceptable ischemia time, beginners can easily perform it and achieve a high success rate.
Moreover, a new aortic regurgitation (AR) model was established in this work using a technique different from the existing one,&#160;which is created by inserting a catheter from the right carotid artery and puncturing the native aortic valve under continuous echocardiographic guidance. A heterotopic abdominal heart transplantation was performed using the novel AR model. In the protocol, after the donor&#39;s heart is harvested, a stiff guidewire is inserted into the donor&#39;s brachiocephalic artery and advanced toward the aortic root. The aortic valve is punctured by pushing the guidewire further even after the resistance is felt, thus inducing AR. It is easier to damage the aortic valve using this method than with the procedure described in the conventional AR model. Additionally, this novel AR model does not contribute to the recipient&#39;s circulation; therefore, this method is expected to produce a more severe AR model than the conventional procedure.

This study demonstrates a reproducible heterotopic abdominal heart transplantation technique in rats that beginners can learn and perform. Additionally, a novel aortic regurgitation model in rats is generated by performing heterotopic abdominal heart transplantation and damaging the donor's aortic valve using a guidewire after harvesting.

ラットにおける修正異所性腹部心臓移植と新規大動脈閉鎖不全症モデル

Over the past 50 years, many researchers have reported heterotopic abdominal heart transplantation in mice and rats, with some variations in the surgical ...

<meta charset="utf8"></head><body>一貫した右心不全誘発のための肺動脈バンディングの最適化

Rat Model of Right-Sided Cardiac Remodeling and Arrhythmia Using Pulmonary Artery Banding

Clinical conditions, including chronic obstructive pulmonary disease or pulmonary arterial hypertension (PAH), can lead to chronic right ventricle pressure overload and progressive right heart failure (RHF). RHF can be identified by right-sided cardiac hypertrophy and dilation associated with abnormal myocardial function affecting the RV and the right atrium (RA). We recently demonstrated that severe RHF is accompanied by an increased risk of atrial inflammation, atrial fibrosis, and atrial fibrillation (AF), the most common type of cardiac arrhythmia (CA). Recent studies have shown that RV and RA inflammation plays an important role in the arrhythmogenesis of CA, including AF. However, the impact of inflammation in the development of CA and AF in RHF is poorly described.
Experimental models of RHF are required to better understand the association between right-sided myocardial inflammation and CA. The rat model of monocrotaline (MCT)-induced pulmonary hypertension (PH) is well-established to provoke RHF. However, MCT triggers severe pneumo-toxicity and pulmonary inflammation. Hence, MCT-induced RHF does not help to distinguish whether the subsequent myocardial inflammation originates from the RHF per se or circulating inflammatory signals secreted by the injured lung.
In this article, a mechanical method involving pulmonary artery trunk banding (PAB) was used to provoke right-sided cardiac arrhythmogenesis. The PAB consists of performing a permanent suture of the pulmonary artery trunk for 3 weeks. Such an approach generates increased right-sided pressure overload. At D21 post-PAB, the suture results in hypertrophied, dilated, and inflamed RV and RA. The PAB-induced RHF is also accompanied by vulnerability to ventricular and atrial arrhythmias, including AF.

<meta charset="utf8"></head><body>肺動脈バンディングを用いた右側心臓リモデリングと不整脈のラットモデル

Right heart failure (RHF) is characterized by right-sided cardiac dilation and hypertrophy, leading to ventricular and atrial malfunction. Cardiopulmonary conditions associated with RHF are accompanied by an increased risk for cardiac arrhythmias. This article describes a standardized model of pulmonary artery banding-induced RHF associated with enhanced ventricular and atrial arrhythmogenesis.