저자는 Stentgrafts의 선물 크리스틴 Guesdon (애보트)을 감사드립니다.

방법 프로토콜은 Bichat-Debré 윤리위원회 (N ° 2012-15/698-0074)에 의해 승인되었습니다. 엘라 관류 모델은 1990 년 1 Anidjar에 의해 설명되었다 : 복부 대동맥 동맥류는 8-9주, 250~300g 세, 남성의 Wistar 쥐 엘라 관류에 의해 유도된다. 두 ~ 4 주 후 재 개복술을 시행하고, 3 mm 직경은 관상 동맥 stentgraft이 동맥류를 제외하는 데 사용됩니다 덮여있다. 말초 aortotomy을 통해 삽입 이식은, 확대 시야에서 배포됩니다. 2 주 후, stentgraft의 개통은 희생하기 전에 왼쪽 경동맥에 의한 대동맥 조영술로 확인됩니다. 전체 스텐트 대동맥과 주변 조직은 다음 수확 및 분석을위한 조건입니다. 프로토콜 1. 1 단계 : 복부 대 동맥류 유도 (0 일) <ol><li> isoflurane을 가진 동물을 마취하고 perforM은 내부 복막 penthobarbital 주입. penthobarbitol 0.1 ml/100 g을 동물의 무게 saline/100 g 0.1 ㎖에 희석합니다. 마취 절차에 적합합니다. </li><li> 복부를 면도하고, 알코올로 피부를 청소합니다. </li><li> 블레이드 Xypho 음모의 피부 절개를합니다. 다음 복막 복부 근육 층은 내부 장기를 피하고, 가위로 이용하실 수 있습니다. 스프레더를 놓고 동물의 왼쪽에 젖은 압축에 내장을 래핑합니다. </li><li> 찢어 않고 직접 대동맥 위의 뒤쪽 복막을 엽니 다. 목표는 경제 해부 미래의 장 유착을 방지하기위한 것입니다. </li><li> 대동맥의 기원에서 왼쪽 신장 정맥에서 하나의 합자와 장골 분기에 대한 모든 담보를 결찰. 대동맥은 창자 또는 대정맥에 붙어있는 경우, 두 번째 개입시 출혈의 높은 위험이있다, 이것은 종종 쥐에 대한 치명적이다. </li><li> 배 대동맥 주위에 4-0 실크, LEF 아래에 15mm를 통과T 신장 정맥. 그것은 전적으로 대동맥, 약을 해부하는 것이 중요합니다. 왼쪽 신장 정맥 길버트 approximator 클램프의 삽입을 허용하는 장골 분기에 바로 인접 아래에 15mm. </li><li> 그냥 왼쪽 신장 정맥 아래의 근위부 대동맥을 체결 한 후, 및 원심 단지 장골 분기점 위에 외막을 제거하고 말초 클램프에 가능한 인접으로 작은 aortotomy을 수행합니다. 대동맥주의 깊게 식염수 각이 canula 및 declamping 때 혈전 색전을 방지하기 위해 세척 나머지 모든 피를 플러시해야합니다. </li><li> 대동맥 내부에 원활하게 열 테이퍼 폴리에틸렌 관 (PE 10) 소개 및 대동맥 주위의 4-0 실크 (단계 1.6)을 통과하여 튜브를 확보하고 압력 추방을 피하기 위해 묶어. </li><li> 대동맥의 10-13mm 길이 (근위 클램프에서 실크)에 엘라을 주입. </li><li> 엘라 용액의 주입 725 ㎕의 30 분의 속도 속도 상수에 d 개입니다. 그것은 신중 s의 중요urvey 주입 : 주입 동안 대동맥의 정상 직경의 140-150%으로 확대한다. </li><li> 주입의 끝에, 카테터를 제거 식염수 엘라를 세척, 실크를 잘라 10-0 Prolene으로 약 3 바늘 aortotomy를 닫습니다. 클램프를 제거 말초 후 근위부. 치료는 트랜스 대동맥 봉합을하지 않도록주의해야합니다. 약간의 연습과 aortotomy의 작은 길이를 고려하여, 대동맥 혈전증은 매우 드문 경우입니다. </li><li> 지속적인 흡수 봉합사 및 중단 비 흡수성 봉합사로 피부와 복벽을 닫습니다. 고통을 방지하기 위해 피하 Carprofen의 5 ㎎ / ㎏ 용량을 주입. 자신의 케이지에 쥐를 반환하고 표준 쥐 실험 차우와 물 광고 libidum을 제공합니다. </li></ol> 2. 2 단계 : 관상 동맥 PTFE (폴리 테트라 플루오로 에틸렌) 커버 Stentgraft와 복부 대 동맥류 제외 (주 15-30) <ol><li> 이전 작업으로, 물 1 L에 아스피린 1,000 밀리그램을 희석. 매일 워싱턴터의 섭취는 하루에 10-12 ml/100 g의 / 체중 추정되었다. </li><li> 앞에서 설명한대로 마취 한 후, 조심스럽게 복부 벽에 부착 잠재적 인 내부 장기를 피하고, 재 개복술을 수행합니다. 동맥류는 적어도 직시 하에서 측정 근위 대동맥 직경에 비해 대동맥의 50 %의 증가에 의해 정의되었다. 우리의 경험을 바탕으로, 성공률은 대동맥 파열로 주로 인해 조기 사망 (게시되지 않은 데이터)를 포함, 90 %이다 </li><li> 대동맥 분기에 또한 근위 목의 대동맥 해부. 이 말초 목 카테터를 삽입하는 말초 클램프 사이에 만족스러운 길이를 허용하고, 대동맥 봉합, 동맥류는 좌측 신장 정맥 아래 몇 mm를 발생합니다. Stentgraft 길이는 동맥류의 크기에 따라 달라집니다. 근위부와 원위부 모두 목은 최소한 2mm에 의해 커버되어야한다. </li><li> 근위 목에 두 배 반복 실크 래핑합니다. 동맥류와 b 위의 근위부 대동맥 클램프왼쪽 신장 동맥을 elow 및 원위부 대동맥 분기보다. </li><li> 다만 stentgraft을 도입 할 때 대동맥 벽을 찢어지지 않도록하려면 이전 aortotomy 위의 큰 aortotomy을 수행합니다. 혈전의 무결성을 유지하기 위해 대동맥을 씻어하지 마십시오. 근위 클램프를 향해 stentgraft을 누릅니다. 클램프는 제거하고 이식 진행을 허용하는 실크의 장력을 제어 할 수 있습니다. stentgraft의 근위 가장자리가 인접 목에 도달 할뿐만 아니라,이 근위 클램프 제거 후 대량 출혈을 방지 할 때까지 stentgraft 진행을 할 수 있도록 전달 카테터 주위의 긴장을 적응시킨다. 풍선 전달 카테터의 근위 끝은 신장 동맥, 그러나 신장 동맥 아래에 배치 할 수있다 stentgraft을 커버 할 수 있습니다. </li><li> 8 기압의 압력에서 공기 넣어 주사기를 사용하여 직접 시각적으로 제어 stentgraft를 배포합니다. 실크를 강화하는 동안 풍선을 수축하고 풍선 샤프트를 제거합니다. </li><li> 의 세척식염수 tentgraft. 단지 동맥류의 원위부 아래의 클램프 및 중단 10-0 Prolene으로 봉합과의 긴밀한 대동맥를 놓습니다. </li><li> 상처를 닫고, 피하 Carprofen를 주입하고 동물들이 케이지로 돌아가 보자. 표준 실험실 차우와 물 광고 libidum을 제공합니다. </li></ol> 3. 3 단계 : Stentgraft 명백 제어 (주 30) stentgraft 삽입 후 15 일, 이식 개통을 제어하는​​ 동맥을 수행 <ol><li> 마취 후, 팔꿈치 절개 가로 팔꿈치를 수행합니다. 왼쪽 경동맥은 턱밑과 설하 동맥 아래와 sternomastoid 근육 아래에 위치합니다. 2cm 길이 노출을 권장합니다. </li><li> 4-0 실크 원위부 동맥을 결찰. 클램핑 근위 후 retrogradely 18G 카테터를 삽입하고 경동맥 주위를 두 번 통과 묶어 4-0 실크로 고정합니다. 충분한 길이는 수를 삽입하고 카테터 수 확보앞 근위 클램프가 제거됩니다. 그것은 동맥의 2cm 노출 어려운 경우, 튜브, 식염수로 채워진 후 고정은 근위 클램프를 제거하는 동안 근위부 푸시 (push) 할 수 있습니다. </li><li> 직접 투시하에 도관을 통해 대비를 주입한다. 두 stentgraft의 부적절한 배치 결과 및 stentgraft 개통을 확인할 수있는 혈관 내 누출의 유무를 확인하는 stentgraft 혈관 컨트롤을 수행합니다. 담보 혈관의 높은 숫자도 혈전 stentgraft에 적절한 다리 관류 수 있기 때문에이 단계는 중요합니다. 우리는 이중 초음파 검사를 수행하려고하지 않았다 : 우리는 stentgraft 강철 구조 stentgraft 개통 및 혈관 내 누출의 정확한 평가를 방지하는 가정. </li><li> 권고 18에 따른 과다 출혈로 쥐를 희생하고, 동맥류, stentgraft, 혈전과 대동맥 벽 학적 또는 생화학 적 연구에 수확된다. </li></ol>

<ol>
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Proof of Concept in Rats.</a> PLoS One. 6, e18679 (2011).</li><li>Trollope, A., Moxon, J. V., Moran, C. S., Golledge, J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Animal+models+of+abdominal+aortic+aneurysm+and+their+role+in+furthering+management+of+human+disease.">Animal models of abdominal aortic aneurysm and their role in furthering management of human disease.</a> Cardiovasc Pathol. 20, 114-123 (2011).</li><li>Yamaguchi, T., 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=Factors+influencing+mortality+in+the+rat+elastase-induced-aneurysm+model.">Factors influencing mortality in the rat elastase-induced-aneurysm model.</a> J. Surg. Res. 94, 81-83 (2000).</li><li>von Bruhl, M. L., 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=Monocytes,+neutrophils,+and+platelets+cooperate+to+initiate+and+propagate+venous+thrombosis+in+mice+in+vivo.">Monocytes, neutrophils, and platelets cooperate to initiate and propagate venous thrombosis in mice in vivo.</a> J. Exp. Med. 209, 819-835 (2012).</li><li>Smith, P. D. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Neutrophil+activation+and+mediators+of+inflammation+in+chronic+venous+insufficiency.">Neutrophil activation and mediators of inflammation in chronic venous insufficiency.</a> J. Vasc. Res. 36, 24-36 (1999).</li><li>Zaragoza, C., 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=Animal+models+of+cardiovascular+diseases.">Animal models of cardiovascular diseases.</a> J. Biomed. Biotechnol. 2011, 497841 (2011).</li><li>Kuivaniemi, H., Elmore, J. R. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Opportunities+in+abdominal+aortic+aneurysm+research:+epidemiology,+genetics,+and+pathophysiology.">Opportunities in abdominal aortic aneurysm research: epidemiology, genetics, and pathophysiology.</a> Ann. Vasc. Surg. 26 (12), 862-870 (2012).</li><li>Schanzer, 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=Predictors+of+abdominal+aortic+aneurysm+sac+enlargement+after+endovascular+repair.">Predictors of abdominal aortic aneurysm sac enlargement after endovascular repair.</a> Circulation. 123, 2848-2855 (2011).</li></ol>

나는 공개 아무것도 없어.

AAA의 두 가지 모델은 이미 우리의 실험실에서 기술되었다 : 이종 이식 19 엘라 유도 모델 1 엘라 모델은 인간의 대동맥 동맥류에 가장 비슷합니다. 큰 원주 강내 혈전은 다음 혈관 동맥류 수리로 제외됩니다. 혈관 내 누출은 EVAR 14,15의 일반적인 합병증이다. 질문의 많은 미해결 남아 : AAA 파열 동맥류 낭 확대 16 않고 때로는 낮은 혈관 내 누출로...

혈관 기술은 거의 모든 복부 동맥류의 절반은 현재 EVAR 4에 의해 처리됩니다 1991 3 PARODI에 의해 처음 혈관 동맥류 수리 (EVAR) 이후 진행했다. 수술과는 달리, EVAR는 전신 혈류에서 제외, 혈전을 둡니다. 동맥류는 헤모글로빈 풍부한 멀티 레이어 혈전, 얇은 용지, 그리고 fibrosed과 염증 외막에 의해 특징입니다. 동맥류의 진행에 단백질 분해 5의 중요한 역할은 삼십년 전에 증명되었다 6, 7 : 동맥류 낭 혈전이 얇은 대동맥 벽, 엘라스틴의 용해, 미디어 평활근 세포의 낮은 밀도, 단백질의 높은 수준과 연관되어 염증 외막 반응 8,9. 이러한 변화는 단백질 분해 효소 활동이 혈전보다는 직접 대동맥 벽 내에서 발생하는 것이 좋습니다. 또한, 혈전의 내강 층 응집 적혈구 CE 풍부하다LLS는 헤모글로빈을 방출. 그들은 주로 섬유소 형성, 혈소판 활성화 및 트롬빈 형성을 유도에 참여하고 있습니다. 마지막으로, 혈전은 혈전 용해 및 모집 백혈구, 주로 호중구에 관여하는 T-PA 및 플라스 미노 겐 유지를 유도합니다. 이들은 혈액 스트림 (10)에 비해 혈전 더 12 배 중요하다. 자신의 존재가 매트릭스 metalloproteinase 유형 8 (MMP-1)의 높은 속도와 연결되어, MMP-9과 엘라 : 그들은 파열 9,11를 섬유의 매트릭스의 저하로 이어지는 세분화 된 세린 프로테아제와 프로 산화 에이전트를 해제하고, 궁극적으로 대동맥 벽 -13. 과목 동맥류 개입 파열을 방지하는 것을 목표로하고있다. EVAR는 동맥류 벽에 혈전이 모두 그대로 유지됩니다. 따라서, 대동맥 담보 (요추 동맥, 장간막 동맥 ...)에 의해 동맥류 혈류는 혈관 내 누출 이름 및 혈관 내 치료 14,15의 특정 합병증, 때로는 파열 이브 선도저압 혈관 내 누출 n으로. 또한, 특정 환자에서 동맥류 직경 16는 증가가 없습니다. 혈액 순환과 동맥류 벽 사이의 상호 작용은 언급 내부 내강 혈전 생물학적 활성을 유지합니다. 따라서, V 형 혈관 내 누출이 확인 된 혈관 내 누출없이 동맥류 낭의 확장으로 정의 동맥류의 혈전 내부의 효소 활성에 의해 설명 될 수있다. 도 방사선 영상 (18FDG-PET 검사, 혈소판 활성화 신티, 철 oxyde 대비 MRI17)이나 말초 혈액 샘플링 (MMP-9, 혈소판 유래 미세 입자, 플라스 / 안티 플라스 민 복합체)가 바로 인간의 대동맥 동맥류에 대한 혈관 미치는 영향을 탐구하는 데 사용 생화학 경로를 평가합니다. 우리의 지식, 모든 재생 및 싼 실험 동맥류 제외 동물 모델은 없습니다. 이 하나의 사전 및 사후 동맥류 제외 생물 조직 학적 수정이 탐험 할 수 있습니다.

<table border="1">
<tbody>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Animals </td>
 </tr>
 <tr>
 <td>Wistar rats</td>
 <td></td>
 <td></td>
 <td>aged from 8 to 9 weeks. Weight range from 350 to 400 g</td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Instruments</td>
 </tr>
 <tr>
 <td>Isoflurane anesthesic system</td>
 <td></td>
 <td></td>
 <td>4,5% at the beginning, then 2%</td>
 </tr>
 <tr>
 <td>Penthobarbital</td>
 <td>Ceva sante animale, Libourne, France</td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Dissection stereomicroscope</td>
 <td></td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Steriles gloves</td>
 <td></td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Microsurgical Steriles instruments</td>
 <td>Moria, Antony, France</td>
 <td></td>
 <td>Needle holder,	Forceps, Scissors,Gilbert approximator
o	3 Micro clamps</td>
 </tr>
 <tr>
 <td>N&deg;40 Silk string</td>
 <td></td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Prolen 9-0 and 10-0</td>
 <td>Ethicon, Johnson &amp; Johnson, Auneau, France</td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Heat-tapered polyethylene tubing</td>
 <td>PE 10</td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Syringe infusion pump</td>
 <td></td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Porcine pancreatic elastase</td>
 <td>Sigma, St. Louis, Mo., USA</td>
 <td></td>
 <td>550 &mu;l of salin is mixed with 175 &mu;l of elastase</td>
 </tr>
 <tr>
 <td>Indeflator</td>
 <td></td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>9 to 16 mm length, 3 mm diameter coronary PTFE covered stentgraft</td>
 <td>Abbott, Abbott Park, Illinois, USA</td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>C-Arm OEC 9800</td>
 <td>GE Medical Systems, Milwaukee, WI</td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td>Aspegic 1000 mg</td>
 <td>Aspirin, Sanofi-Aventis, Paris, France</td>
 <td></td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Reagent</td>
 </tr>
 <tr>
 <td>Aerane isoflurane 100ML</td>
 <td>Baxter</td>
 <td>Aerane</td>
 <td></td>
 </tr>
 <tr>
 <td>Penthobarbital</td>
 <td>Centravet</td>
 <td>053pen203</td>
 <td></td>
 </tr>
 <tr>
 <td>Silk Suture 4-0</td>
 <td>Fine Science</td>
 <td>18020-40</td>
 <td></td>
 </tr>
 <tr>
 <td>Microsurgical steriles instruments</td>
 <td>Moria</td>
 <td>9980-9983-9987-204/A-204/D-8148-4877A-4878A</td>
 <td></td>
 </tr>
 <tr>
 <td>Prolen 9-0 and 10-0</td>
 <td>Ethicon</td>
 <td>W2829 &ndash; NS2850</td>
 <td></td>
 </tr>
 <tr>
 <td>Heat tapered Polyethylene tubing : PE 10</td>
 <td>Bioseb</td>
 <td>MRE-010</td>
 <td></td>
 </tr>
 <tr>
 <td>Infusion pump</td>
 <td>World precision instrument</td>
 <td>AL-1000</td>
 <td></td>
 </tr>
 <tr>
 <td>Porcine pancreatic elastase</td>
 <td>Sigma</td>
 <td>E1250-100MG</td>
 <td></td>
 </tr>
 <tr>
 <td>Indeflator</td>
 <td>Longreal</td>
 <td>KY025 25 100</td>
 <td></td>
 </tr>
 <tr>
 <td>Aspegic 1000mg (Aspirin)</td>
 <td>Sanofi-Aventis</td>
 <td>3400931898191</td>
 <td></td>
 </tr>
 <tr>
 <td>C-Arm OEC 9800</td>
 <td>General electric.</td>
 <td>OEC 9800</td>
 <td></td>
 </tr>
 <tr>
 <td>Stentgraft : Jostent</td>
 <td>Abbott</td>
 <td>210CG1230 
 210CG1630</td>
 <td></td>
 </tr>
</tbody>
</table>

a new murine model of endovascular aortic aneurysm repair

혈관 동맥류 배제 동맥류 파열을 방지하기 위해 검증 된 기술입니다. 장기 결과 기술 제한 및 복부 대 동맥류 (AAA) 병태 생리의 새로운 측면을 강조 표시합니다. 치료 전후 AAA의 깊은 조사를 허용하는 저렴하고 재현성에는 복부 대동맥 동맥류 endograft 제외 모델은 없다. 우리는 이에 유도하는 방법을 설명하고 덮인 관상 동맥 stentgraft 쥐의 복부 대동맥 동맥류 제외 할 수 있습니다. 잘 알려진 엘라 유도 AAA 모델은 먼저 쥐 2에 설명 된 쥐, 1990 년 1보고되었다. 엘라스틴 저하는 인간의 AAA와 일치 복부 벽과 내부 내강 혈전의 염증성 침윤과 대동맥의 팽창에 이르게한다. 작은 커버 stentgraft와 혈관 배제 후 혈액 순환과 동맥류의 혈전 사이의 상호 작용을 제외하고, 수행됩니다. 적절한 배제 stentgraft 명백는혈관 조영술에 의해 안락사 전에 확인은 왼쪽 경동맥을 생각했다. 엘라 확산 부분적으로 제어는 각 동물에 대한 동맥류의 모양이 다른 수 있습니다. 그것은 쉽게 stentgraft 도입을위한 동맥류 아래 대동맥의 적절한 길이를 수 동맥류를 만들 어렵고, 적절한 원위부 목에 혈관 내 누출을 방지 할 수 있습니다. 실패의 많은 때때로 스티치 그것을 고통과 문제와 대동맥 파열로 이어질 stentgraft 도입 및 사후 영업 대동맥 혈전증 내피 세포 손상이 발생할 수 있습니다. stentgraft 주입하기 전에 쥐에게 아스피린을주는 것은 큰 출혈없이 실패율을 감소시킨다. 시간을 클램핑 호중구, 내피 세포 및 혈소판을 활성화하고, 생물학적 분석을 방해 할 수 있습니다.

<html> 동맥류는 후 수지 블록에 고정 될 때까지 생리 식염수 버퍼 인산염으로, 24 시간 동안 파라 포름 알데히드 4 % 용액에 고정되어 있습니다. 우리는 PTFE의 주위에 치유 증식 세포 (그림 2)를 보여주는 HPS (헤 마톡 실린 Phloxin 사프란) (그림 1) 염색을 사용합니다. 중간 엽 세포는 다음 α-액틴 염색 (그림 3)에 의해 특징입니다. <p class="jove_content" fo:keep-together.wit...

Watch this Scientific Journal Video about A New Murine Model of Endovascular Aortic Aneurysm Repair at JoVE.com

A New Murine Model of Endovascular Aortic Aneurysm Repair

동맥류 endograft 제외 후 조직 학적 및 생화학 적 수정은 아직 불분명하다. 우리는 쥐 동맥류에 endograft 이식의 새로운 모델을 설명합니다. 영속적 인 순환 혈액 스트림 인터페이스, 새로운 혈관 생체 적합 물질 평가와와없는 혈전 분석을 통해,이 모델은 더 나은 혈관 동맥류 제외 pathobiology을 이해하는 데 도움이 될 것입니다.

혈관 동맥류 수리의 새로운 쥐과 모델

Endovascular aneurysm exclusion is a validated technique to prevent aneurysm rupture. Long-term results highlight technique limitations and new aspects of ...

a-new-murine-model-of-endovascular-aortic-aneurysm-repair

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Medicine

14.3K 조회수.  Hôpital X. Bichat, AP-HP, Paris. 동맥류 endograft 제외 후 조직 학적 및 생화학 적 수정은 아직 불분명하다. 우리는 쥐 동맥류에 endograft 이식의 새로운 모델을 설명합니다. 영속적 인 순환 혈액 스트림 인터페이스, 새로운 혈관 생체 적합 물질 평가와와없는 혈전 분석을 통해,이 모델은 더 나은 혈관 동맥류 제외 pathobiology을 이해하는 데 도움이 될 것입니다.

비디오: A New Murine Model of Endovascular Aortic Aneurysm Repair

Reproducable Paraplegia by Thoracic Aortic Occlusion in a Murine Model of Spinal Cord Ischemia-reperfusion

Background 
Lower extremity paralysis continues to complicate aortic interventions. The lack of understanding of the underlying pathology has hindered advancements to decrease the occurrence this injury.&#160;The current model demonstrates reproducible lower&#160;extremity paralysis following thoracic aortic occlusion.
Methods 
Adult male C57BL6 mice were anesthetized with isoflurane. Through a cervicosternal incision the aorta was exposed. The descending thoracic aorta and left subclavian arteries were identified without entrance into pleural space. Skeletonization of these arteries was followed by immediate closure (Sham) or occlusion for 4 min (moderate ischemia) or 8 min (prolonged ischemia). The sternotomy and skin were closed and the mouse was transferred to warming bed for recovery.&#160; Following recovery, functional analysis was obtained at 12 hr intervals until 48 hr.
Results 
Mice that underwent sham surgery showed no observable hind&#160;limb deficit. Mice subjected to moderate ischemia for 4 min had minimal functional deficit at 12 hr followed by progression to complete paralysis at 48 hr. Mice subjected to prolonged ischemia had an immediate paralysis with no observable hind-limb movement at any point in the postoperative period. There was no observed intraoperative or post&#160;operative mortality.
Conclusion 
Reproducible lower extremity paralysis whether immediate or delayed can be achieved in a murine model. Additionally, by using a median sternotomy and careful dissection, high survival rates, and reproducibility can be achieved.

The lack of mechanistic understanding of spinal cord ischemia-reperfusion injury has hindered further adjuncts to prevent paraplegia following high risk aortic operations. Thus, the development of animal models is imperative. This manuscript demonstrates reproducible lower extremity paralysis following thoracic aortic occlusion in a murine model.

척수 허혈 - 재관류의 생쥐 모델에서 흉부 대동맥 폐색에 의해 재생산 할 하반신 마비

Background
Lower extremity paralysis continues to complicate aortic interventions. The lack of understanding of the underlying pathology has hindered ...

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의학

Open Tracheostomy Gastric Acid Aspiration Murine Model of Acute Lung Injury Results in Maximal Acute Nonlethal Lung Injury

Acid pneumonitis is a major cause of sterile acute lung injury (ALI) in humans. Acid pneumonitis spans the clinical spectrum from asymptomatic to acute respiratory distress syndrome (ARDS), characterized by neutrophilic alveolitis, and injury to both alveolar epithelium and vascular endothelium. Clinically, ARDS is defined by acute onset of hypoxemia, bilateral patchy pulmonary infiltrates and non-cardiogenic pulmonary edema. Human studies have provided us with valuable information about the physiological and inflammatory changes in the lung caused by ARDS, which has led to various hypotheses about the underling mechanisms. Unfortunately, difficulties determining the etiology of ARDS, as well as a wide range of pathophysiology have resulted in a lack of critical information that could be useful in developing therapeutic strategies.
Translational animal models are valuable when their pathogenesis and pathophysiology accurately reproduce a concept proven in both in vitro and clinical settings. Although large animal models (e.g., sheep) share characteristics of the anatomy of human trachea-bronchial tree, murine models provide a host of other advantages including: low cost; short reproductive cycle lending itself to greater data acquisition; a well understood immunologic system; and a well characterized genome leading to the availability of a variety of gene deletion and transgenic strains. A robust model of low pH induced ARDS requires a murine ALI that targets mainly the alveolar epithelium, secondarily the vascular endothelium, as well as the small airways leading to the alveoli. Furthermore, a reproducible injury with wide differences between different injurious and non-injurious insults is important.
The murine gastric acid aspiration model presented here using hydrochloric acid employs an open tracheostomy and recreates a pathogenic scenario that reproduces the low pH pneumonitis injury in humans. Additionally, this model can be used to examine interaction of a low pH insult with other pulmonary injurious entities (e.g., food particles, pathogenic bacteria).

This protocol induces acute lung injury in a mouse that has close fidelity to the pathogenesis of acid pneumonitis observed in humans. We generate a maximal acute nonlethal low pH lung injury and account for differences in rodent-human anatomic respiratory structure using an open tracheostomy coupled with circumferential pressure release.

급성 폐 손상의 열기 기관 절개 위산 흡인 쥐 모델은 최대한 급성 치명적 폐 손상의 결과

Acid pneumonitis is a major cause of sterile acute lung injury (ALI) in humans. Acid pneumonitis spans the clinical spectrum from asymptomatic to acute ...

Reproducible Arterial Denudation Injury by Infrarenal Abdominal Aortic Clamping in a Murine Model

Percutaneous vascular interventions uniformly result in arterial denudation injuries that subsequently lead to thrombosis and restenosis. These complications can be attributed to impairments in re-endothelialization within the wound margins. Yet, the cellular and molecular mechanisms of re-endothelialization remain to be defined. While several animal models to study re-endothelialization after arterial denudation are available, few are performed in the mouse because of surgical limitations. This undermines the opportunity to exploit transgenic mouse lines and investigate the contribution of specific genes to the process of re-endothelialization. Here, we present a step-by-step protocol for creating a highly reproducible murine model of arterial denudation injury in the infrarenal abdominal aorta using external vascular clamping. Immunocytochemical staining of injured aortas for fibrinogen and &#946;-catenin demonstrate the exposure of a pro-thrombotic surface and the border of intact endothelium, respectively. The method presented here has the advantages of speed, excellent overall survival rate, and relative technical ease, creating a uniquely practical tool for imposing arterial denudation injury in transgenic mouse models. Using this method, investigators may elucidate the mechanisms of re-endothelialization under normal or pathological conditions.

Understanding the cellular and molecular mechanisms of re-endothelialization following arterial denudation injury is of paramount importance in preventing thrombosis and restenosis of arteries. Here we describe a protocol for reproducible arterial denudation injury of the infrarenal abdominal aorta. The procedure was developed to investigate the underlying mechanisms that regulate endothelial regeneration using mouse models.

쥐 모델에서 Infrarenal 복부 대동맥 클램핑에 의해 재현 동맥 발가 벗김 부상

Percutaneous vascular interventions uniformly result in arterial denudation injuries that subsequently lead to thrombosis and restenosis. These ...

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 ...

Quantitative Micro-CT Analysis of Aortopathy in a Mouse Model of &#946;-aminopropionitrile-induced Aortic Aneurysm and Dissection

Aortic aneurysm and dissection is associated with significant morbidity and mortality in the population and can be highly lethal. While animal models of aortic disease exist, in vivo imaging of the vasculature has been limited. In recent years, micro-computerized tomography (micro-CT) has emerged as a preferred modality for imaging both large and small vessels both in vivo and ex vivo. In conjunction with a method of vascular casting, we have successfully used micro-CT to characterize the frequency and distribution of aortic pathology in &#946;-aminopropionitrile-treated C57/Bl6 mice. Technical limitations of this method include variations in the quality of the perfusion introduced by poor animal preparation, the application of proper methodologies for vessel size quantification, and the non-survivability of this procedure. This article details a methodology for the intravascular perfusion of a lead-based radiopaque silicone rubber for the quantitative characterization of aortopathy in a mouse model of aneurysm and dissection. In addition to visualizing aortic pathology, this method may be used for examining other vascular beds in vivo or vascular beds removed post-mortem.

Quantitative Micro-CT Analysis of Aortopathy in a Mouse Model of &amp;#946;-aminopropionitrile-induced Aortic Aneurysm and Dissection

This article describes a detailed methodology of using a radiopaque lead-based silicone rubber to perfuse the murine vasculature for aortic diameter quantification in a mouse model of aortic aneurysm and dissection.

Β-aminopropionitrile-유도 대동맥 동맥 및 해 부의 마우스 모델에서 Aortopathy의 양적 마이크로 CT 분석

Aortic aneurysm and dissection is associated with significant morbidity and mortality in the population and can be highly lethal. While animal models of ...

Murine Cervical Aortic Transplantation Model using a Modified Non-Suture Cuff Technique

With the introduction of powerful immunosuppressive protocols, distinct advances are possible in the prevention and therapy of acute rejection episodes. However, only minor improvement in the long-term results of transplanted solid organs could be observed over the past decades. In this context, chronic allograft vasculopathy (CAV) still represents the leading cause of late organ failure in cardiac, renal and pulmonary transplantation.
Thus far, the underlying pathogenesis of CAV development remains unclear, explaining why effective treatment strategies are presently missing and emphasizing a need for relevant experimental models in order to study the underlying pathophysiology leading to CAV formation. The following protocol describes a murine heterotopic cervical aortic transplantation model using a modified non-suture cuff technique. In this technique, a segment of the thoracic aorta is interpositioned in the right common carotid artery. With the use of the non-suture cuff technique, an easy to learn and reproducible model can be established, minimizing the possible heterogeneity of sutured vascular micro anastomoses.

Here, we present a protocol of heterotopic aortic transplantation in mice using the non-suture cuff technique in a cervical murine model. This model can be used to study the underlying pathology of chronic allograft vasculopathy (CAV) and can help evaluate new therapeutic agents in order to prevent its formation.

수정된 비봉합사 커프 기술을 사용한 뮤린 자궁 경부 대동맥 이식 모델

With the introduction of powerful immunosuppressive protocols, distinct advances are possible in the prevention and therapy of acute rejection episodes. ...

Murine Surgical Model of Topical Elastase Induced Descending Thoracic Aortic Aneurysm

According to the Center for Disease Control, aortic aneurysms (AAs) were considered a leading cause of death in all races and both sexes from 1999-2016. An aneurysm forms as a result of progressive weakening and eventual dilation of the aorta, which can rupture or tear once it reaches a critical diameter. Aneurysms of the descending aorta in the chest, called descending thoracic aortic aneurysms (dTAA), make up a large proportion of aneurysm cases in the United States. Uncontained dTAA rupture is almost universally lethal, and elective repair has a high rate of morbidity and mortality. The purpose of our model is to study dTAA specifically, to elucidate the pathophysiology of dTAA and to search for molecular targets to halt the growth or reduce the size of dTAA. By having a murine model to study thoracic pathology precisely, targeted therapies can be developed to specifically test dTAA. The method is based on the placement of porcine pancreatic elastase (PPE) directly on the outer murine aortic wall after surgical exposure. This creates a destructive and inflammatory reaction, which weakens the aortic wall and allows for aneurysm formation over weeks to months. Though murine models possess limitations, our dTAA model produces robust aneurysms of predictable size. Furthermore, this model can be used to test genetic and pharmaceutical targets which may arrest dTAA growth or prevent rupture. In human patients, interventions such as these could help avoid aneurysm rupture, and difficult surgical intervention.

We describe a surgical protocol to consistently induce robust descending thoracic aortic aneurysms in mice. The procedure involves left thoracotomy, thoracic aorta exposure, and placement of a sponge soaked in porcine pancreatic elastase on the aortic wall.

국소 엘라스타아제의 뮤린 외과 모델은 내림차순 흉부 대동맥류를 유도

According to the Center for Disease Control, aortic aneurysms (AAs) were considered a leading cause of death in all races and both sexes from 1999-2016. ...

Porcine Model of Infrarenal Abdominal Aortic Aneurysm

Large animal models to study abdominal aortic aneurysms are sparse. The purpose of this model is to create reproducible, clinically significant infrarenal abdominal aortic aneurysms (AAA) in swine. To achieve this, we use a combination of balloon angioplasty, elastase and collagenase, and a lysyl oxidase inhibitor, called &#946;-aminopropionitrile (BAPN), to create clinically significant infrarenal aortic aneurysms, analogous to human disease.
Noncastrated male swine are fed BAPN for 7 days prior to surgery to achieve a steady state in the blood. A midline laparotomy is performed and the infrarenal aorta is circumferentially dissected. An initial measurement is recorded prior to aneurysm induction with a combination of balloon angioplasty, elastase (500 units)/collagenase (8000 units) perfusion, and topical elastase application. Swine are fed BAPN daily until terminal procedure on either postoperative day 7, 14, or 28, at which time the aneurysm is measured, and tissue procured. BAPN + surgery pigs are compared to pigs that underwent surgery alone.
Swine treated with BAPN and surgery had a mean aortic dilation of 89.9% &#177; 47.4% at day 7, 105.4% &#177; 58.1% at day 14, and 113.5% &#177; 30.2% at day 28. Pigs treated with surgery alone had significantly smaller aneurysms compared to BAPN + surgery animals at day 28 (p &#60; 0.0003). The BAPN + surgery group had macroscopic and immunohistochemical evidence of end stage aneurysmal disease.
Clinically significant infrarenal AAA can be induced using balloon angioplasty, elastase/collagenase perfusion and topical application, supplemented with oral BAPN. This model creates large, clinically significant AAA with hallmarks of human disease. This has important implications for the elucidation of AAA pathogenesis and testing of novel therapies and devices for the treatment of AAA. Limitations of the model include variation in BAPN ingested by swine, quality of elastase perfusion, and cost of BAPN.&#160;

This novel model creates robust infrarenal abdominal aortic aneurysms in swine using a combination of balloon angioplasty, elastase/collagenase perfusion, topical elastase application, and oral compound &#946;-aminopropionitrile administration, which interferes with collagen cross-linking.

돼지 모델 의 관막 복 대동맥류

Large animal models to study abdominal aortic aneurysms are sparse. The purpose of this model is to create reproducible, clinically significant infrarenal ...

A Murine Model of Hemodialysis Access-Related Hand Dysfunction

Chronic kidney disease is a major public health problem, and the prevalence of end-stage renal disease (ESRD) requiring chronic renal replacement therapies such as hemodialysis continues to increase. Autogenous arteriovenous fistula (AVF) placement remains a primary vascular access option for ESRD patients. Unfortunately, approximately half of the hemodialysis patients experience dialysis access-related hand dysfunction (ARHD), ranging from subtle paresthesia to digital gangrene. Notably, the underlying biologic drivers responsible for ARHD are poorly understood, and no adequate animal model exists to elucidate the mechanisms and/or develop novel therapeutics for the prevention/treatment of ARHD. Herein, we describe a new mouse model in which an AVF is created between the left common iliac artery and vein, thereby facilitating the assessment of limb pathophysiology. The microsurgery includes vessel isolation, longitudinal venotomy, creation of arteriovenous anastomosis, and venous reconstruction. Sham surgeries include all the critical steps except for AVF creation. Iliac AVF placement results in clinically relevant alterations in central hemodynamics, peripheral ischemia, and impairments in hindlimb neuromotor performance. This novel preclinical AVF model provides a useful platform that recapitulates common neuromotor perturbations reported by hemodialysis patients, allowing researchers to investigate the mechanisms of ARHD pathophysiology and test potential therapeutics.

This protocol details the surgical steps of murine common iliac arteriovenous fistula creation. We developed this model to study hemodialysis access-related limb pathophysiology.

혈액 투석 접근 관련 손 기능 장애의 쥐 모델

Chronic kidney disease is a major public health problem, and the prevalence of end-stage renal disease (ESRD) requiring chronic renal replacement ...

Drug Treatment by Central Venous Catheter in a Mouse Model of Angiotensin II Induced Abdominal Aortic Aneurysm and Monitoring by 3D Ultrasound

Since pharmaceutical treatment options are lacking in the clinical management of abdominal aortic aneurysm (AAA), animal models, in particular mouse models, are applied to advance the understanding of the disease pathogenesis and to identify potential therapeutic targets. Testing novel drug candidates to block AAA growth in these models generally requires repeated drug administration during the time course of the experiment. Here, we describe a compiled protocol for AAA induction, insertion of an intravenous catheter to facilitate prolonged therapy, and serial AAA monitoring by 3D ultrasound. Aneurysms are induced in apolipoprotein E (ApoE) deficient mice by angiotensin II release over 28 days from osmotic mini-pumps implanted subcutaneously into the mouse back. Subsequently, the surgical procedure for external jugular vein catheterization is conducted to allow for daily intravenous drug treatment or repeated blood sampling via a subcutaneous vascular access button. Despite the two dorsal implants, the monitoring of AAA development is readily facilitated by sequential semi-automated 3D ultrasound analysis, which yields comprehensive information on the expansion of aortic diameter and volume and on aneurysm morphology, as illustrated by experimental examples.

This protocol describes the consecutive implantation of an osmotic pump to induce abdominal aortic aneurysm by angiotensin II release in apolipoprotein E (ApoE) deficient mice and of a vascular access port with a jugular vein catheter for repeated drug treatment. Monitoring of aneurysm development by 3D ultrasound is effectively conducted despite dorsal implants.

안지오텐신 II의 마우스 모델에서 중앙 정맥 카테터에 의한 약물 치료 유도 복부 대동맥류 및 3D 초음파에 의한 모니터링

Since pharmaceutical treatment options are lacking in the clinical management of abdominal aortic aneurysm (AAA), animal models, in particular mouse ...