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).

모든 동물 실험은 미국 국립 보건 연구소에 의해 게시 된 실험 동물의 관리 및 사용에 대한 가이드 (NIH 간행물 없습니다. 85-23가 1996 년 개정)에 따라 실시 하였다. 이 프로토콜은에 의해 국립 대만 대학에서 기관 동물 케어 및 사용위원회에 의해 명시된 지침에 따라 승인을 받았다. 1. 동물 수술 <ol><li> 호닝 돌에 바늘의 끝을 둔화로 22 G 주사기 바늘을 준비합니다. 집게를 사용하여 직각으로 니들 plicate. </li><li> 수술 전에 필요한 수술기구 및 재료뿐만 아니라 회복 케이지를 준비한다. 사용하기 전에 모든 장비 및 수술 공급을 압력솥. </li><li> 200g의 주위에 쥐를 유지하고 음식과 물을 무료로 액세스 할 수있는 제어 온도 (21 ± 2 ° C)에서 12 시간 빛 / 어둠 사이클에서 보관하십시오. 각 그룹에서 최소 6 마리를 포함합니다. 펜토 바르 비탈로 쥐를 마취또는 다른 적절한 마취제 (0.5 ml의 IP를 75 ㎎ / ㎏). 꼬리 반사를 테스트하여 마취의 깊이를 확인합니다. 참고 : 꼬리 반사의 부재는 적절한 마취의 지표입니다. </li><li> 체온을 유지하기 위해 가열 패드와 수술 플랫폼 앙와위에서 쥐를 놓는다. 수술 오염을 방지하기 위해 동물 이발기 헤어 리무버 로션 래트의 복부를 면도. betadine 또는 수술 전에 다른 클렌징 시약으로 깔끔하게 면도 복부를 문질러. 참고 :이 절차를 통해 멸균 필드를 유지하는 것이 중요하다. </li><li> 메스와 복부의 정중선을 따라 2cm의 절개를합니다. 생리 식염수를 사용하여 수술 중 습기 복부 기관을 유지합니다. 후방 복막 영역에 놓여 하대 정맥을 노출 면봉을 사용하여 측면을주의 깊게 소화 기관을 대체. 온 일반적으로 병렬 및 거짓말 복부 대동맥을 확인대정맥의 왼쪽. 주 : 복부 대동맥은 심장 박동에 맞춰 맥동 용기이다. </li><li> 아래의 혈관을 밝히기 위해서 집게 한 쌍의 복막을 관통. 부드럽게 신장 동맥에 인접한 복부 대동맥을 분리하고, 오른쪽의 기원과 왼쪽 신장 동맥 사이의 복부 대동맥 아래 8 CM-긴 4-0 실크 봉합사를 전달합니다. </li><li> 봉합사와 느슨한 두 번 매듭을 확인; 3 mm 직경의 루프를두고 루프 내부의 무딘 구부러진 22 G 바늘을 배치합니다. 대동맥과 바늘 주위의 매듭을 체결 한 후 0.7 mm 직경의 수축을 달성하기 위해 즉시 바늘을 제거합니다. </li><li> 6-0 흡수성 봉합사 재료로 복강을 닫습니다. 간단한 중단 봉합과 근육이나 피부 절개를 봉합. 감염을 예방하기 위해, 요오드 팅크와 수술 부위 스크럽. </li><li> 충분한 의식을 회복 할 때까지 자유 이동에 의해 표시된 바와 같이,주의 동물을 관찰음식 섭취. 이 흉골 드러 누움을 유지하기 위해 충분한 의식을 회복 할 때까지 무인 동물을 두지 마십시오. 수술 후 통증을 방지하기 위해, 아세트 아미노펜 (0.5 ml를 300 ㎎ / ㎏, IP)와 쥐를 치료. 주 : 기관의 정책에 의해 승인 된 사용자 진통제를 관리해야합니다. </li></ol> 2. 조직과 혈액 샘플 컬렉션 <ol><li> 십주 수술 후에서, 쥐의 무게 (0.5 ml의 IP를 75 ㎎ / ㎏)을 펜토 바르 비탈로 마취. 수술 전에 꼬리 반사를 테스트하여 마취의 깊이를 확인합니다. 금속 트레이에 쥐를 놓습니다. </li><li> 메스를 사용하여 목의 정중선을 따라 2cm의 절개를합니다. 기관을 노출 집게로 조심스럽게 근육을 대체. 기관 평행 및 심박수에 맞춰 맥동 경동맥을 식별하기 위해주의 깊게 관찰한다. </li><li> EDTA로 코팅 된 혈액 수집 관에 경동맥에서 피를 수집합니다. 즉시 원심 분리기2,000 XG에 15 분 동안 혈액과 플라즈마를 수집합니다. 필요할 때까지 -80 ° C에서 혈장을 저장합니다. </li><li> xyphoid 과정의 중간 선 주위에, 흉부 영역에서 5cm의 절개를합니다. 날카로운 집게로 다이어프램을 관통. 가위를 사용하여 절단하고 심장을 노출 양쪽에 중반 쇄골 라인을 따라 흉곽을 제거합니다. 심장 및 혈관 국경을 따라 조심스럽게 마음을 절제. 조직을 잡아없이 부드럽게 마음을 제거합니다. </li><li> 관류 바늘에 대동맥 트렁크를 묶는하여 수정을 Langendorff 관류 장치에 마음을 탑재합니다. 크렙스 버퍼 심장 관류 (110 mM의 염화나트륨, 2.6 밀리미터의 KCl을 포함하는 1.2 밀리미터 KH 2 PO 4, 1.2 mM의 황산, 25 mM의 NaHCO3을, 11 mM의 포도당 [산도 7.4]) 혈액을 씻어. 심장의 무게를 측정하고 심장 무게 - 투 - 몸 무게 비율을 계산한다. 얼음에 4 % 파라 포름 알데히드와 심장을 수정합니다. 파라 포름 알데히드 증기 TOX이기 때문에, 마스크를 착용 기억IC. </li></ol> 3. 조직 섬유증 정량 <ol><li> 조직 절편 장치의 파라 포름 알데히드 고정 심장 조직을 놓고 2mm 두께 부분을 잘라. 매립 카세트에서 조직 섹션을 배치합니다. 등급 알코올 욕 (50 %, 75 %, 95 %, 1 시간마다, 100 %)의 일련의 조직을 탈수. </li><li> 1 시간 동안 왁스에 마지막 1 시간 동안 자일 렌과 조직을 침투합니다. 매립 카세트에 침투 조직을 놓고 파라핀 왁스 포함. microtoming 때까지 실온에서 파라핀 블록에 포함 된 조직을 저장합니다. </li><li> 4 μm의 두께 섹션으로 포함 된 조직을 조각입니다. 45 ºC 물을 욕조에 섹션을 놓습니다. 각도 수조에 유리 슬라이드를 담궈 서서히 슬라이드 부분 부착 있도록 파라핀 섹션 가장자리 접근. </li><li> 에 슬라이드를 이동하고 화장실에서 조직 섹션에서 잠재적 인 공기 주머니를 제거하고 더 나은 부착을 용이하게 할 수 있습니다. 드라이 t그 1 시간 동안 37 ºC에서 슬라이드 조직 학적 염색을 실온에서 보관. </li><li> 탱크에 슬라이드를 넣습니다. 30 분간 크실렌으로 슬라이드 Deparaffinize 최종적 증류수 (3 분마다 95 %, 75 %, 50 %)을 순차적으로 희석하여 알콜을 재수. 완전히 1 시간 동안 조직 섹션을 충당하기 위해 적절한 picrosirius 빨간 솔루션을 사용합니다. 두 변화 0.5 % 아세트산 용액에 슬라이드를 헹군 후 무수 알코올 두 헹굼을 수행한다. </li><li> 슬라이드를 공기 - 건조 및 커버 슬립과 합성 수지에서 슬라이드를 탑재합니다. 가시 광선 필드에 슬라이드를 사진. 참고 : 사진에서 빨간색 영역은 200X 배율의 현미경 아래 picrosirius 빨간색 긍정적 인 영역을 보여줍니다. 섬유증 (11)의 정도를 나타내는 총 면적 위에 picrosirius 적색 양 영역의 비율을 계산한다. </li></ol> 4. 혈액 트로포 닌 정량 <ol><li> 플라즈마 트로포 닌 농도를 정량화효소 결합 면역 분석법 (ELISA)을 사용. 중복 된 각 샘플을 분석. 로드 혈장 50 ㎕를 적절한 웰에 항체 칵테일 중 50 μL. 플레이트를 밀봉하고 400 rpm에서 플레이트 진탕 기에서 실온에서 1 시간 동안 배양한다. 참고 : 플라즈마의 심장 트로포 닌은 심장 부상 마커입니다. </li><li> 액체를 대기음 및 세척 버퍼의 250 μl를 3 회 각 웰을 씻는다. 마지막 세척 후, 플레이트를 반전 과도한 액체를 제거하기 위해 깨끗한 종이 타월에 대해 그것을시킨다. </li><li> 각 웰에 테트라 메틸 기판의 100 μl를 추가하고 400 rpm에서 접시 쉐이커에 어둠 속에서 10 분 동안 품어. 각 웰에 스톱 솔루션의 100 μl를 추가합니다. 1 분 혼합하는 접시 통에서 접시를 흔들어. 450 nm에서의 광학 밀도 (OD)를 기록한다. 주 : 트로포 닌 농도가 OD 값에 비례한다. </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 method for cardiovascular research. The abdominal aorta adjacent to the renal arteries is constricted to induce cardiac remodeling, which eventually leads to cardiac injury. The extent of cardiac remodeling is evaluated by calculating the ratio of heart weight to body weight, performing picrosirius staining for the measurement of collagen expression, and conducting an ELISA-based method for the detection of plasma cardiac troponin levels. The abdominal aortic constriction method allows more reproducible results simulating cardiac remodeling in rat models. 
Surgical models of heart disease are advantageous for closely mimicking the pathophysiology of hypertension and aortic stenosis1. Most of the currently-available surgical techniques to induce cardiac hypertrophy are conducted through transverse aortic constriction12,13, which is a common experimental procedure used to create a pressure overload. The sudden onset of hypertension that is achieved causes an approximately 50% increase in left ventricle mass within 2 weeks5, making the model an excellent choice to examine the molecular mechanisms leading to cardiac hypertrophy. However, transverse aortic constriction requires complex procedures and a high level of surgical skill. The stress associated with open-chest surgery and mechanical ventilation results in high surgical mortality. Moreover, the acute onset of severe hypertension, characteristic of this model, lacks direct clinical relevance5. In contrast, abdominal aortic constriction is less technically demanding. The onset and progression of cardiac hypertrophy is gradual, making this model clinically relevant to hypertensive cardiac diseases1,3. In addition, renal hypoperfusion by abdominal aortic constriction consequently activates the renin-angiotensin system, and therefore, the same surgical technique can be used as an animal model of kidney hypoperfusion injury15.
After surgery, cardiac pathology, including the appearance of fibrosis in the heart and changes in cardiac function, develops. In the early stages of hypertensive heart disease, myocardial contractility is enhanced by cardiac hypertrophy to compensate for the pressure overload10. In the later stages of hypertensive heart disease, cardiac function decompensates with fibrosis, which leads to heart failure10. We did not elaborate on the functional measurements of the heart, including pressure-volume loop analysis16 and echocardiography11. These approaches are invasive or non-invasive methods that are useful for understanding the changes in cardiac function. The time period after surgery can be varied to produce different degrees of cardiac remodeling. The longer the aorta is constricted, the greater the extent of cardiac dysfunction as a result of remodeling. The picrosirius red staining to measure fibrotic area and the ELISA measurements of plasma troponin levels are useful for the assessment of the degree of cardiac remodeling in order to set the endpoints after the surgery.
A key aspect of the surgery to induce cardiac hypertrophy is the clear identification and constriction of the abdominal aorta. Precision in the placement of the constriction site improves consistency of hypertrophy induction time, since variation in constriction placement may affect the length of time required for hypertrophy induction. The closer the stricture is to the heart, the shorter the induction time needed, although the harder it is to isolate the aorta. The abdominal aorta, between the origins of the right and left renal arteries, is a suitable site for performing constriction. The use of a rat model for the abdominal aortic constriction method has great advantages for the study of cardiac hypertrophy and heart failure. A limitation of this approach is that the surgical incision leads to tissue damage and to the secretion of inflammatory cytokines, which are different from the human cardiac hypertrophy and heart failure resulting from hypertension. Furthermore, the use of anesthetics and analgesics should be cautious, since some of these agents are reported to offer cardioprotective effects17. 
The method described here provides a simple and effective approach to produce cardiac remodeling and injury in rats. Our technique is easy to perform, and the results are robust and reproducible. Once our surgical approach is mastered, this procedure will prove to be a useful platform for the investigation of disease mechanisms and the development of therapeutics in cardiac hypertrophy and remodeling.

심장 장애는 말초 조직에서의 피로, 호흡 곤란을 포함하는의 증상이, 편협 운동 복잡한 임상 증후군, 및 체액 저류이다. 그것은 선진국 (1) 사망의 주요 원인이다. 이외에도 근절 단백질 또는 이온 채널이 돌연변이에 의한 유전 심근증, 심근 기능 부전, 고혈압, 판막 심장 질환, 비만, 당뇨병 및 3을 포함하는 의료 조건의 다양한 의해 야기 될 수있다. 부적절한 심장 펌핑 용량 심근 구조, 전기 전도 및 에너지 대사 리드의 변화는 궁극적으로 심장 마비 3,4 결과 순환 요구를 충족합니다. 심부전의 기초가되는 메카니즘을 연구 따라서 심혈관 연구 분야에서 매우 중요하다. 심부전의 진행으로 이어지는 분자 메커니즘을 식별하는 것은 궁극적으로 신규 한 치료 표적 또는 유용한 바이오 마커의 발견에 도움이 될 수있다 <s&gt; 1입니다. 인간 5에서 심장 마비로 키 임상 적 특징을 공유 심장 마비 동물 모델을 개발하는 것이 중요하다. 심장 비대 및 리모델링 심부전의 개발에 중요한 역할을한다. 고혈압 성 심장 질환, 심장 비대 및 인간 환자 1에서 보이는 부적응 리모델링의 주요 기여 요인이다. 이러한 인간의 조건을 모방하기 위해 동물 모델은 종종 수술을 통해 설정됩니다. 특히, 횡 방향 또는 복부 대동맥 궁극적 중심부의 압력 과부하를 초래 좌심실에 대한 저항을 증가 수축 될 수있다. 이 현상은 일반적으로 심장 비대에서, 심근 세포의 생리 보상 심장 혈관 시스템의 기능적 요구에 부응 할 결과. 그러나, 기능적인 수요가 심장 섬유증 및 contrac로 이어지는 정상 생리 보상 메커니즘을 대체타일 ​​손상. 가로 대동맥 수축 (TAC) 수술은 종종 대동맥 궁에서 개흉술, 기계 환기 및 흉선의 분리 및 지방 조직을 포함하는 복잡한 절차를 포함한다. 반면, 복부 대동맥 협착은 간단한 실험 방법 6-8이 필요합니다. 복부 대동맥은 좌우 신장 동맥 사이 수술 동안 수축된다. 심장 비대 및 리모델링은 복부 대동맥 수축 수술 6-8 후 몇 주를 관찰 할 수있다; 그들은 횡 대동맥 협착 수술 9,10 의해 생성 된 것과 유사한 강력한 고혈압 심장병을 생산한다. 여기서, 우리는 효율적인 높은 재현성하고 최소한의 침습적 인 방법을 이용하여 쥐의 복부 대동맥 수축을 수행하는 프로토콜을 기술한다. 신장 동맥에 인접한 복부 대동맥은 4-0 실크 스레드에 의해 형성된 0.72 mm 루프에 의해 수축된다. 텐 주 수술, 심장 비대 및 remodelin 후g가 관찰 될 수있다. 복부 대동맥 수축 유도 심비대의 래트 모델은 질병 및 병태 생리 메커니즘뿐만 아니라, 잠재적 인 치료제의 개발 연구를위한 기반을 제공한다.

<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.

10주 복부 대동맥 협착 수술 후, 생성 된 심장 병리를 분석 하였다. 심장 조직학은 체중 심장 중량의 비를 계산함으로써 상기 중심 콜라겐의 양을 검출함으로써 측정 하였다. 심장 손상 플라즈마 심장 트로포 닌 농도를 측정함으로써 확인 하였다. 도 1a에 도시 된 바와 같이 높은 심장 중량에 차체 중량의 비율 (도 1b), 심장 비대의 지표에 의해 입증 된 바와 같이, 심장의 크기는, 복부 대동맥 협착 수술 후 확대 하였다. picrosirius 레드 염색을 이용함으로써, 증가 된 콜라겐 함유량 (적색)로 염색 심근 섬유증 정상 영역 (황색도 2)와 구별 될 수있다. C에 비하여 심근 섬유증은 복부 대동맥 협착 수술 (도 2B) 후에 증가<html> ontrols (그림 2A). 결과는 플라즈마 트로포 닌 농도 (도 3)와 상관 관계. 증가 된 트로포 닌 농도는 압력 과부하시 심장 리모델링과 상해가 발생했음을 나타냅니다. 함께, 분명 심장 부상에서 복부 대동맥 수축 결과, 심장 비대, 조직 리모델링을 표시했다. <img alt="그림 1" src="/files/ftp_upload/54818/54818fig1.jpg" /> 그림 1 :. 압력 과부하시 심장 비대 (A) 대표 마음과 (B) 심장 무게 - 투 - 몸무게 비율은 십주 복부 대동맥 협착 수술 후 표시됩니다. 데이터는 수행 여섯 독립적 인 실험의 SEM ± 평균을 나타냅니다. 그룹 간의 차이는 학생의 t-시험으로 평가 하였다. * P &lt;컨트롤 대 0.05.<html> 8fig1large.jpg &quot;대상 =&quot;_ 빈 &quot;&gt;이 그림의 더 큰 버전을 보려면 여기를 클릭하십시오. <img alt="그림 2" src="/files/ftp_upload/54818/54818fig2.jpg" /> 그림 2 : 압력 과부하시 심장 섬유증. Picrosirius 빨간 염색이 증가 콜라겐 식을 밝혔다. (A) 대표 picrosirius 빨간색 염색 (스케일 바 = 200 μm의)과 십주 복부 대동맥 수축 수술 후 섬유 성 지역의 (B) 비율입니다. 데이터는 수행 여섯 독립적 인 실험의 SEM ± 평균을 나타냅니다. 그룹 간의 차이는 학생의 t-시험으로 평가 하였다. * P &lt;0.05 제어 대. <a href="https://ecsource-jove-com.bdigitaluss.remotexs.co/files/ftp_upload/54818/54818fig2large.jpg" target="_blank">이 그림의 더 큰 버전을 보려면 여기를 클릭하십시오.</a> S / ftp_upload / 54818 / 54818fig3.jpg &quot;/&gt; 그림 3 : 압력 과부하시 심장 손상. 혈장 트로포 닌 농도 10주 복부 대동맥 협착 수술 후 측정 하였다. 데이터는 수행 여섯 독립적 인 실험의 SEM ± 평균을 나타냅니다. 그룹 간의 차이는 학생의 t-시험으로 평가 하였다. * P &lt;0.05 제어 대. <a href="https://ecsource-jove-com.bdigitaluss.remotexs.co/files/ftp_upload/54818/54818fig3large.jpg" target="_blank">이 그림의 더 큰 버전을 보려면 여기를 클릭하십시오.</a>

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.

쥐의 복부 대동맥의 수축을 통해 심장 리모델링의 모델

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

Universidad San Sebastian

Research

JoVE Journal

Medicine

9.9K 조회수.  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.

비디오: 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.

압력 과부하 심장 비대 모델의 창조를위한 쥐의 대동맥 수축 오름차순

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

연구

의학

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.

심 초음파 이미징에 의해 가로 대동맥 수축의 마우스 모델에서 심장 형태 학적 평가 및 기능 변경

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

Creation of a Rodent Model of Abdominal Aortic Aneurysm by Blocking Adventitial Vasa Vasorum Perfusion

The adventitial vasa vasorum (VV) provides oxygen and nourishment to the aortic wall. Hypoxia in the aortic wall can cause enlarged abdominal aortic aneurysms (AAAs). This article introduces and describes a standard protocol used to induce AAAs through adventitial VV hypoperfusion created with a combination of polyurethane catheter insertion into the aortic lumen and suture ligation of the infrarenal abdominal aorta.
The protocol involves the use of male rats weighing 300-400 g, which are provided food and water ad libitum. After laparotomy with a ventral midline abdominal incision, exfoliation of the aorta is performed, which blocks blood flow from the perivascular tissue. Aortotomy involving a small incision adjacent to the renal artery branches is performed, and a polyurethane catheter is inserted using an 18-gauge indwelling needle. After repairing the incision, tight ligation of the aorta over the catheter blocks VV blood flow from the proximal direction through the aortic wall without disturbing the aortic blood flow. This technique can induce an AAA with progressive aortic dilatation.
The greatest benefit of this model is that VV hypoperfusion causes tissue hypoxia and the development of an infrarenal AAA, which has morphological and pathological characteristics similar to those of a human AAA.

Polyurethane catheter insertion into the aortic lumen and suture ligation of the aorta induce chronic hypoxia due to hypoperfusion of the adventitial vasa vasorum. This article describes a novel animal model of abdominal aortic aneurysm (AAA) with characteristics similar to those of AAA in humans.

Adventitial 바사 Vasorum 관류를 차단 하 여 복 부 대동맥 동맥 류의 설치류 모델의 생성

The adventitial vasa vasorum (VV) provides oxygen and nourishment to the aortic wall. Hypoxia in the aortic wall can cause enlarged abdominal aortic ...

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.

마우스에 가로 대동맥 수축 유도를 폐쇄 가슴 모델

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.

설치류에서 대동맥 탈밴드에 의해 왼쪽 심실 역 리모델링 공부

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.

압력 과부하의 쥐 모델은 오버트 수축기 심부전과 반대로 적당한 리모델링 및 수축기 기능 장애를 유도했습니다.

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.

쥐의 대동맥 해산에 의한 좌심 질환으로 인한 폐고혈압의 역혈관 리모델링 모델

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.

O-링 대동맥 밴딩 대 압력 과부하로 인한 심장 비대 모델링을 위한 기존의 횡대동맥 수축

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.

쥐의 수정된 이종 복부 심장 이식 및 새로운 대동맥 역류 모델

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>일관된 우측 심부전 유도를 위한 폐동맥 밴딩 최적화(Optimizing Pulmonary Artery Banding)

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>폐동맥 밴딩을 이용한 우측 심장 리모델링 및 부정맥의 쥐 모델

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.