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.

참고 :이 절에 설명 된 모든 실험 절차는 기관 동물 관리 및 Katholieke Universiteit Leuven의 연구 자문위원회에 의해 승인되었다 (프로젝트 : 2,013분의 154-B 드 기 스트). 왼쪽 앞쪽에 내림차순 관상 동맥 1. 영구 결찰 <ol><li> / kg의 펜 토바 비탈 나트륨 70 mg의 40 ㎎ / kg의 복강 내 투여에 의한 마우스를 마취. 더 이상 회사 발가락 핀치 반응 할 때 마우스가 마취의 적절한 비행기에 도달하지 확인합니다. 항상 적절한 마취 어떤 수술이나 간섭하기 전에이 방법을 확인합니다. 마취 동안 각막의 건조를 방지하기 위해 안과 연고를 윤활 사용합니다. 절차 (부 프레 노르 핀 0.05 ㎎ / kg SQ)이 시작되기 전에 수술 전 통증 2-4 시간을 제공합니다. <ol><li> 생존 수술 중 일치하는 무균 기술을 적용합니다. 최대로 가능한 범위 미생물 사기에 억제하는 절차를 구현오염물 중요한 감염이나 화농이 발생하지 않도록. 이러한 절차는이 사이트의 수술 부위 소독을 통해 멸균 악기와 멸균 자료의 사용, 외과 영역의 소독 및 모피 / 머리의 제거를 포함한다. </li></ol></li><li> 자기 제조 무디게 20 게이지 바늘을 가진 마우스를 삽관. <ol><li> 머리의 과신전으로 누운 위치에 마우스를 놓습니다. <ol><li> 목 부위에 빛을 초점을 맞 춥니 다. 무딘 pincet와 혀를 들어 올립니다. 후두의 입구는 명확하게 볼 수 있습니다. </li><li> 직접 비전 아래 기관에 후두를 통해 무딘 바늘을 전달합니다. 인공 호흡기에 마우스를 연결하여 올바른 삽관을 평가 (μL에 박출​​량 : 3 × 체중 (g) + (155), 주파수 : 분당 120 타). </li></ol></li><li> 또한, 먼저 신중하게기도를 노출하여 기관 내 삽관의 시각화를 향상시킬 수 있습니다. <ol><li> 5mm 중반 넥 절개를하고 철회다만기도 상기 근조직. </li><li> 기관의 직접 시각화를위한 수술 실체 현미경을 사용하여 삽관을 수행합니다. 혀를 들어 올려 기관에 자체 준비 무딘 20 게이지 바늘을 입력합니다. 인공 호흡기에 마우스를 연결하여 올바른 삽관을 확인 (μL에 박출​​량 : 3 × 체중 (g) + (155), 주파수 : 분당 120 타). </li></ol></li></ol></li><li> 앙와위에서 마우스를 유지하고 테이프로 마우스를 고정합니다. 저체온증을 방지하기 위해 가열 패드에 수술을 수행한다. <ol><li> 면도와 베타 딘으로 피부를 소독. 왼쪽 뒷다리가 수술 중 좌심실에 더 잘보기를 얻기 위해 오른쪽 뒷다리 교차주의한다. </li></ol></li><li> 흉골까지 작은 가로 피부 절개를하고 기본 피부와 근육을 분리합니다. </li><li> m를 옆으로 빼냅니다. pectoralis 미성년자와 m. 5-0 실크 봉합사와 주요 pectoralis. </li><li> 내가 확인무딘 pincet을 삽입하여 세 번째 늑간에서 ncision. </li><li> 흉골에 도달 할 때까지 내측하는 측면에서 늑간 근육 아래에 pincet 이동합니다. 피부 내부에서 pincet을 눌러 흉부 벽에 구멍을. 주의 깊게 단지 작은 가위로 pincet 위의 늑간 근육을 절단하여 개흉술을 완료합니다. 폐의 천공을 방지하기 위해이 기술을 사용합니다. </li><li> 폐를 보호하기 위해 공동에 0.9 % NaCl을 침지 스폰지를 넣어. 심장의 좌측의 노출을 얻을 늑간에 상처 스프레더 (가슴 권취)를 소개한다. 현재로서는, 좌심방, 좌심실, 관상 동맥 좌전 하행은 실체 현미경 아래에서 볼 수 있습니다. </li><li> 좌심방의 끝에서 1mm에 대한 하나의 6-0 prolene의 합자로 관상 동맥 좌전 하행의 결찰을 수행합니다. 이것은 제 분기에서 대각선 말단이다. 참고 : 또는 7-0 (00.05 mm 직경) 8-0 또는 스레드 (0.04 mm 직경)이 사용될 수있다. 바늘은 C-1 13mm 3/8 원 테이퍼 포인트 바늘입니다. 관상 동맥 좌전 하행의 성공적인 결찰은 영향을받는 지역에 옅은 나타나는 심근의 결과로, 즉시 변색을 유도한다. </li><li> 상처 스프레더 (가슴 트랙터)를 제거합니다. <ol><li> 늑간 공간 주위에 세 6-0 티 - Cron의 봉합을 놓습니다. 봉합을 체결하기 전에, 흉강에서 스폰지를 제거하고 인공 호흡기의 유출을 차단하여 폐를 다시 확장합니다. 이렇게함으로써, 폐 벽측 흉막과 다시. </li><li> 그 후, 단단히 봉합을 당겨 가슴을 눌러서 재 팽창을 반복합니다. (가슴에 압력을인가 할 때 기포가 보이지되어야 함)의 생리 식염수를 이용하여 소량의 흉부의 성공적인 폐쇄를 확인한다. </li><li> 폐의 정상적인 확장을 확인하는 늑간 근육을 통해 봐. 두 pectoralis 근육의 위치를​​ 조정 역할기흉의 예방을위한 여분의 장벽. </li></ol></li><li> 5-0 실크 봉합사로 피부를 닫습니다. </li><li> 인공 호흡기에서 마우스를 분리하고 가열 패드에 복구 할 수 있습니다. 이 흉골 드러 누움을 유지하기 위해 충분한 의식을 회복 할 때까지 무인 동물을 방치하지 마십시오. 완전히 회복 될 때까지 다른 동물의 회사에 수술을 한 동물을 반환하지 않습니다. </li><li> 지속적으로 수술 후 통증 (수술 후 최소 48 시간 동안 프레 노르 핀 0.05 ㎎ / kg SQ BID)를 제공합니다. </li></ol> 마우스 2. 생체 침략 혈역학 적 측정 <ol><li> 전 절차 신호 드리프트를 최소화하기 위해 적어도 30 분 동안 37 ℃에서 멸균 수 1.0 프랑스어 밀라 압력 카테터 잠수함. 전자적 2000 Hz에서 0 mmHg에서 100 mmHg의 압력에서 센서 및 기록 데이터를 보정. </li><li> 1.4 g / kg 우레탄의 복강 내 투여에 의해 마취를 수행합니다. 그 확인더 이상 회사 발가락 핀치 반응 할 때 마우스를 마취의 적절한 비행기에 도달하지 않습니다. </li><li> 앙와위에서 마취 마우스를 놓습니다. 테이프로 팔다리를 고정합니다. 가열 패드와 체온을 유지하고 직장 프로브를 모니터링 할 수 있습니다. 넥 영역을 면도 갑상선을 노출 넥 영역 정중선 절개. </li><li> 구부러진 바늘 목을 고정합니다. </li><li> 타액선을 옆으로 당겨 우측 총 경동맥을 노출. 흰색 스레드 유사한 미주 신경은, 동맥을 따라 놓여있다. 조심스럽게 곡선 집게를 사용하여 미주 신경에서 경동맥을 분리합니다. </li><li> 다른 조직에서 분리 오른쪽 경동맥에서 곡선 집게를 전달합니다. 동맥 주위의 결합 조직을 제거합니다. </li><li> 오른쪽 경동맥에서 두 6-0 실크 와이어를 전달합니다. 가까운 머리쪽으로 배치되는 상단 선에 꽉 매듭을 확인하고 KOCHER (원위부 폐색 결찰)로 고정한다. PROXI 전달말 와이어를 두 번 왼쪽에서 오른쪽으로 2 kochers (근위 비 폐쇄성 와이어) 고정하십시오. </li><li> 멸균 0.9 % NaCl을 놓아 습기 경동맥을 유지합니다. 면봉으로 물기를 닦아냅니다. </li><li> 원위부 결찰 및 근위부 비 폐쇄성 와이어 사이에 26 게이지 바늘로 오른쪽 경동맥의 절개를합니다. </li><li> 동맥에 압력 센서를 소개한다. 더 혈액 손실이 없는지 확인합니다. 부드럽게 전방 1.0 프랑스어 밀라 압력 카테터를 밀어 카테터 쇄골 아래 스루 와이어 신중하게 통과 할 수있는 방식으로 근위 비 폐쇄성 와이어를 조정한다. <ol><li> 근위 비 폐쇄성 와이어의 조정시 혈액 손실을 최소화합니다. 매우 깨지기 때문에 진행하는 동안 너무 많은 압력 센서를 압축하지 마십시오. 근위 와이어 동맥을 폐색되지해야하기 때문에, 혈관 혈액으로 가득 유지되어야합니다. </li></ol></li><li> 압력 신호를 기록하기 시작한다. 동맥압 신호 fluctuat70 mmHg에서 100의 수축기 압력 - - 120 mmHg로 (60)의 이완기 혈압 사이의 건강한 마우스에 말이지. </li><li> 무명 동맥을 통해 좌심실에 대동맥을 통해 카테터를 직접. 120 mmHg로 - 심실 압력 0 mmHg에서 100 사이의 변동. 카테터는 좌심실 내부 안정화 할 수 있습니다. 실험 조건에 따라 60 분, 30 분의 신호를 기록한다. </li><li> 실험 종료 후, 30 분 동안 1 % Alconox 사의 카테터 담근다. 밀리 Q 물 카테터를 씻으십시오. 발포체 블록에 저장 카테터. </li><li> 추가 분석을 위해 레코딩 소프트웨어에서 데이터를 검색합니다. <ol><li> 데이터 분석을 위해, 압력 신호가 안정 시간 간격을 고려한다. 관심있는 기록 된 데이터의 최소 10 연속 심장주기를 선택합니다. </li><li> 심박수, 최대 좌심실 수축기 압, 최소 이완기 왼쪽 ventr를 분석 LabChart 소프트웨어 버전 8.0을 사용하여 유사한icular 압력 isovolumetric 좌심실 수축 (DP / DT 최대), isovolumetric 좌심실 이완 (DP / DT 분), 이완 기말 좌심실 압력 피크 레이트의 최고 속도 및 isovolumetric 좌심실의 시정 압력 가을 (타우) 7. 참고 : 이완 기말 압력이 즉시 isovolumetric 수축에 의해 유도 된 압력 서지 전에 시간 시점에서의 압력에 해당합니다. 타우 계산은 단지 수 감쇠 곡선에 좌심실 압력 피팅에 기반 P (t)로 표현이 수식에서, P 0 즉 -t / 타우 + B에 = P (t)는 시간에 좌심실 압력은 DP / DT의 최대 음의 값을 후 t에 도달했습니다. 파라미터 B는 단순 접근법에서 0으로 가정 될 수있는 이론적 점근선에 대응한다. 향상된 isovolumetric 휴식은 타우의 작은 값을 초래한다. </li></ol></li></OL&gt;

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H., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Myocardial+ischemia+and+reperfusion:+a+murine+model.">Myocardial ischemia and reperfusion: a murine model.</a> Am J Physiol. 269, 2147-2154 (1995).</li><li>Salto-Tellez, M., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Myocardial+infarction+in+the+C57BL/6J+mouse:+a+quantifiable+and+highly+reproducible+experimental+model.">Myocardial infarction in the C57BL/6J mouse: a quantifiable and highly reproducible experimental model.</a> Cardiovasc Pathol. 13, 91-97 (2004).</li><li>Fernandez, B., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+coronary+arteries+of+the+C57BL/6+mouse+strains:+implications+for+comparison+with+mutant+models.">The coronary arteries of the C57BL/6 mouse strains: implications for comparison with mutant models.</a> J Anat. 212, 12-18 (2008).</li><li>Kumar, D., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Distinct+mouse+coronary+anatomy+and+myocardial+infarction+consequent+to+ligation.">Distinct mouse coronary anatomy and myocardial infarction consequent to ligation.</a> Coron Artery Dis. 16, 41-44 (2005).</li><li>Clauss, S. B., Walker, D. L., Kirby, M. L., Schimel, D., Lo, C. W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Patterning+of+coronary+arteries+in+wildtype+and+connexin43+knockout+mice.">Patterning of coronary arteries in wildtype and connexin43 knockout mice.</a> Dev Dyn. 235, 2786-2794 (2006).</li><li>Icardo, J. M., Colvee, E. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Origin+and+course+of+the+coronary+arteries+in+normal+mice+and+in+iv/iv+mice.">Origin and course of the coronary arteries in normal mice and in iv/iv mice.</a> J Anat. 199, 473-482 (2001).</li><li>Yoldas, A., Ozmen, E., Ozdemir, V. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Macroscopic+description+of+the+coronary+arteries+in+Swiss+albino+mice+(Mus+musculus).">Macroscopic description of the coronary arteries in Swiss albino mice (Mus musculus).</a> J S Afr Vet Assoc. 81, 247-252 (2010).</li><li>James, T. N., Burch, G. E. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Blood+supply+of+the+human+interventricular+septum.">Blood supply of the human interventricular septum.</a> Circulation. 17, 391-396 (1958).</li><li>Gao, X. M., Xu, Q., Kiriazis, H., Dart, A. M., Du, X. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Mouse+model+of+post-infarct+ventricular+rupture:+time+course,+strain-+and+gender-dependency,+tensile+strength,+and+histopathology.">Mouse model of post-infarct ventricular rupture: time course, strain- and gender-dependency, tensile strength, and histopathology.</a> Cardiovasc Res. 65, 469-477 (2005).</li><li>Muthuramu, I., Jacobs, F., Singh, N., Gordts, S. C., De Geest, B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Selective+homocysteine+lowering+gene+transfer+improves+infarct+healing,+attenuates+remodelling,+and+enhances+diastolic+function+after+myocardial+infarction+in+mice.">Selective homocysteine lowering gene transfer improves infarct healing, attenuates remodelling, and enhances diastolic function after myocardial infarction in mice.</a> PLoS One. 8, 63710 (2013).</li><li>Eaton, L. W., Weiss, J. L., Bulkley, B. H., Garrison, J. B., Weisfeldt, M. L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Regional+cardiac+dilatation+after+acute+myocardial+infarction:+recognition+by+two-dimensional+echocardiography.">Regional cardiac dilatation after acute myocardial infarction: recognition by two-dimensional echocardiography.</a> N Engl J Med. 300, 57-62 (1979).</li><li>Erlebacher, J. A., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Late+effects+of+acute+infarct+dilation+on+heart+size:+a+two+dimensional+echocardiographic+study.">Late effects of acute infarct dilation on heart size: a two dimensional echocardiographic study.</a> Am J Cardiol. 49, 1120-1126 (1982).</li><li>Schuster, E. H., Bulkley, B. 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.

심근 구조 및 기능의 변화는 만성 심부전에 좌심실 기능 장애의 개발, 진행은 여러 뮤린 모델 (12)에 조사 될 수있다. 심장 리모델링 및 기능 장애는 심근 손상에 의해 유발 또는 압력에 의해 대동맥 수축을 횡단하는 보조 과부하, 또는 팽창 심근 병증 (12)의 유전 적 모델에서 조사 할 수있다 할 수있다. 물론, 쥐 모델의 가장 뚜렷한 장점은 형질 전환 및 세포 형 특정 및 유도 유전자 ...

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

심장 마비는 심장이 휴식 또는 스트레스 동안 세포 산소 요구에 상응하는 속도로 혈액을 펌프에 실패하는 증후군이다. 그것은 노력에 특히 체액 저류, 호흡 곤란, 피로, 특징입니다. 심장 마비는 성장 공중 보건 문제, 입원의 주요 원인 및 사망의 주요 원인이다. 허혈성 심장 질환이 심장 기능 상실의 주요 원인이다. 심실 리모델링 좌심실의 구조, 크기 및 형태의 변화를 의미한다. 좌심실이 구조적 리모델링 (예, 전신 동맥 고혈압 또는 대동맥판 협착증), 또는 볼륨과 부하 압력 과부하에 의해 부상 (예를 들면, 심근 경색)에 의해 유도된다. 심실 벽 리모델링 응력에 영향을 받기 때문에, 이는 심장 기능에 심부전의 발전에 지대한 영향을 미친다. 왼쪽 전방 descendin의 영구 결찰 모델마우스에서 g 관상 동맥은 심실 리모델링과 심장 기능 심근 경색을 조사하는 데 사용됩니다. 이 모델은 관상 좌전 하행의 과도 결찰 모델의 비교 목적 및 병태 생리 학적 관련성의 관점에서 근본적으로 다르​​다. 허혈 / 재관류 손상의 후자의 모델에서 초기 경색의 정도는 재관류 심근 회수에 영향을 미치는 인자에 의해 조절 될 수있다. 대조적으로, 관상 좌전 하행 영구적 결찰 후 24 시간에서 경색 부분은 고정되어있다. 이 모델에서 심장 기능은 1) 경색 확장, 경색 치유 및 흉터 형성의 과정에 의해 영향을 받는다; 2) 좌심실 팽창, 심장 비대, 심실 리모델링의 수반 개발. 관상 동맥, 침습적 혈역학 MEA의 기술 좌전 하행의 영구 결찰의 모델 외에마우스의 숏 상세하게 제시된다.

심근 경색의 정도는 에반스 블루 / 2,3,5- 트리 페닐 클로라이드 (TTC)을 두 번 염색에 의해 평가 될 수있다. TTC는 NADH (8)의 존재의 다양한 탈수소 효소의 활성에 의한 조직 생활에 깊은 붉은 1,3,5- triphenylformazan로 변환됩니다 산화 환원 표시입니다. (1) 24 시간 이후에 심장의 대표 섹션을 보여줍니다 관상 동맥 좌전 하행의 결찰. 블루 염색 분야는 비 허혈성 / 일반 지역...

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.

마우스의 왼쪽 전방 내림차순 관상 동맥의 영구 결찰 : 심근 경색 리모델링과 심장 마비의 모델

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 ...

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Research

JoVE Journal

Medicine

27.7K 조회수.  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.

비디오: 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.

경색의 Murine 모델에서 관상 동맥 내고과 Intramyocardial 사출

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 ...

연구

의학

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.

마우스의 관상 동맥 결합에 대한 수정 기술

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.

내사 - 결합 : 심근 경색의 Murine 모델

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

생물학

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.

왼쪽 앞쪽에 내림차순 동맥의 결찰을 통해 심근 허혈 - 재관류 손상의 생쥐 모델

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).

쥐 왼쪽 앞쪽에 내림차순 (LAD) 관상 동맥 결찰 : 심근 경색에 대한 개선 및 단순화 된 모델

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.

왼쪽 전방 내림차순 관상 동맥의 영구 결찰을 사용하는 뮤린 심근 경색 모델

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.

마우스의 심근경색 및 심근 허혈-재관류 손상 유도

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.

마우스에서 우측 관상동맥의 영구적 결찰에 의해 유도되는 우심실 심근경색의 생성 및 특성화

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.

좌측 관상동맥 결찰술: 심근경색의 외과적 쥐 모델

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. ...