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

ملاحظة: تمت الموافقة على جميع الإجراءات التجريبية الموضحة في هذا القسم من قبل رعاية الحيوان واللجنة الاستشارية للبحوث من جامعة لوفين الكاثوليكية المؤسسي (المشروع: 154/2013-B دي جيست). 1. ربط الدائم للالشريان الأيسر الأمامي تنازلي التاجي <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> تخدير الماوس عن طريق إدارة داخل الصفاق من 40 مغ / كغ إلى 70 ملغم / كغم من بنتوباربيتال الصوديوم. ضمان الماوس تصل الطائرة المناسبة لها التخدير عندما لم يعد يتفاعل قرصة اصبع القدم حازمة. تأكد دائما التخدير السليم بهذه الطريقة قبل أي إجراء أو التدخل الجراحي. استخدام زيوت التشحيم مرهم للعين لمنع جفاف القرنية في حين تحت التخدير. توفير تسكين قبل الجراحة 2-4 ساعة قبل بدء الإجراء (البوبرينورفين 0.05 ملغ / كغ SQ). <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> تطبيق تقنيات العقيم متناسقة أثناء الجراحة البقاء على قيد الحياة. تنفيذ الإجراءات التي تمنع إلى الحد الأقصى الممكن مدى يخدع الميكروبيtamination بحيث الإصابة كبير أو تقيح لا يحدث. وتشمل هذه الإجراءات استخدام الأدوات المعقمة ومواد معقمة تطهير المنطقة الجراحية، وإزالة الفراء / شعر على موقع الجراحية وتطهير هذا الموقع. </li></ol></li><li style=";text-align:right;direction:rtl"> أنبوبا الماوس مع اضعافها إبرة عيار 20-إعداد النفس. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> ضع الماوس في موقف ضعيف مع تمدد مفرط من الرأس. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> تركيز الضوء على منطقة الرقبة. رفع اللسان مع pincet اضعافها. مدخل الحنجرة يمكن رؤيتها بوضوح. </li><li style=";text-align:right;direction:rtl"> تمرير إبرة أضعفت من خلال الحنجرة إلى القصبة الهوائية تحت الرؤية المباشرة. تقييم التنبيب الصحيح من خلال ربط الماوس إلى التنفس الصناعي (حجم المخ في ميكرولتر: 3 × وزن الجسم (ز) + 155، تردد: 120 السكتات الدماغية في دقيقة). </li></ol></li><li style=";text-align:right;direction:rtl"> بدلا من ذلك، تعزيز التصور من التنبيب الرغامي من خلال تعريض أولا بعناية القصبة الهوائية. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> جعل 5 مم منتصف العنق شق وسحبالأنسجة العضلية فقط فوق القصبة الهوائية. </li><li style=";text-align:right;direction:rtl"> إجراء التنبيب باستخدام stereomicroscope الجراحي لرؤية مباشرة من القصبة الهوائية. رفع اللسان وأدخل قياس 20 إبرة اضعافها أعدت الذاتي في القصبة الهوائية. تأكيد التنبيب الصحيح من خلال ربط الماوس إلى التنفس الصناعي (حجم المخ في ميكرولتر: 3 × وزن الجسم (ز) + 155، تردد: 120 السكتات الدماغية في دقيقة). </li></ol></li></ol></li><li style=";text-align:right;direction:rtl"> الحفاظ على الماوس في موقف ضعيف وإصلاح الماوس مع الشريط. إجراء عمليات جراحية على وسادة التدفئة لمنع انخفاض حرارة الجسم. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> يحلق وتطهير الجلد مع بتدين. احرص على أن الطرف الخلفي الأيسر يعبر أطرافهم هند الصحيح من أجل الحصول على رؤية أفضل على البطين الأيسر أثناء الجراحة. </li></ol></li><li style=";text-align:right;direction:rtl"> إجراء شق صغير الجلدي عرضية تصل إلى القص والفصل بين الجلد والعضلات الأساسية. </li><li style=";text-align:right;direction:rtl"> سحب جانبا م. قاصر الصدرية وم. الصدرية الكبرى مع خياطة 5-0 الحرير. </li><li style=";text-align:right;direction:rtl"> تقديم طncision في الفضاء وربي الثالث عن طريق إدخال pincet اضعافها. </li><li style=";text-align:right;direction:rtl"> نقل pincet تحت العضلات الوربية من الأفقي إلى وسطي حتى يتم الوصول إلى القص. ثقب جدار الصدر عن طريق دفع pincet من الداخل إلى الجلد. استكمال بضع الصدر عن طريق قطع بعناية العضلات الوربية فقط فوق pincet مع مقص صغير. استخدام هذه التقنية لمنع فتعثر الرئتين. </li><li style=";text-align:right;direction:rtl"> وضع الاسفنجة غارقة في كلوريد الصوديوم 0.9٪ في تجويف لحماية الرئتين. إدخال رش الجرح (ضام الصدر) في الفضاء وربي الحصول على التعرض للجانب الأيسر من القلب. اعتبارا من الآن، الأذين الأيسر، البطين الأيسر، والأمامي الأيسر الشريان التاجي النازل مرئية تحت stereomicroscope. </li><li style=";text-align:right;direction:rtl"> إجراء عملية ربط للالأمامي الأيسر الشريان التاجي النازل مع واحد 6-0 البرولين ضمد حوالي 1 ملم تحت غيض من الأذين الأيسر. هذا هو القاصي من أول فرع قطري. ملاحظة: بدلا من ذلك، 7-0 (0ويمكن استخدام .05 مم) أو 8-0 الخيوط (0.04 مم). الإبرة هي عبارة عن دائرة تفتق نقطة الإبرة C-1 13 مم 3/8. ربط الناجح لالأمامي الأيسر الشريان التاجي النازل يدفع تلون فوري، مما أدى إلى عضلة القلب التي تظهر شاحبة في الأراضي المتضررة. </li><li style=";text-align:right;direction:rtl"> إزالة رش الجرح (ضام الصدر). <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> وضع ثلاثة 6-0 الغرز تي كرون حول الفضاء وربي. قبل تشديد خياطة الجروح، وإزالة الاسفنجة من تجويف الصدر وإعادة توسيع الرئتين عن طريق منع تدفق التنفس الصناعي. وبذلك، الرئتين إعادة الاتصال مع غشاء الجنب الجداري. </li><li style=";text-align:right;direction:rtl"> وفي وقت لاحق، وسحب خيوط ضيق وتكرار إعادة توسع عن طريق الضغط لأسفل على صدره. تأكيد الإغلاق الناجح للصدر باستخدام كمية صغيرة من المياه المالحة (يجب أن ينظر أي فقاعات الهواء عند الضغط على الصدر). </li><li style=";text-align:right;direction:rtl"> ننظر من خلال العضلات الوربية لتأكيد التوسع الطبيعي للرئتين. إعادة كلا العضلات الصدرية، بوصفه أحدحاجز إضافي للوقاية من استرواح الصدر. </li></ol></li><li style=";text-align:right;direction:rtl"> إغلاق الجلد مع 5-0 الحرير الغرز. </li><li style=";text-align:right;direction:rtl"> افصل الماوس من التنفس الصناعي والسماح باستعادة على لوحة التدفئة. لا تترك حيوان غير المراقب حتى استعاد وعيه أنه كاف للحفاظ على الاستلقاء القصية. لا يعودون الحيوان الذي خضع لعملية جراحية للشركة من الحيوانات الأخرى حتى تعافى تماما. </li><li style=";text-align:right;direction:rtl"> نقدم باستمرار تسكين بعد العملية الجراحية (البوبرينورفين 0.05 مغ / كغ SQ BID لمدة 48 ساعة على الأقل بعد الجراحة). </li></ol> 2. في الجسم الحي القياسات الغازية الدورة الدموية في الفئران <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> قبل الإجراء، غمر 1.0 الفرنسية ميلر قسطرة الضغط في الماء المعقم عند 37 درجة مئوية لمدة 30 دقيقة على الأقل لتقليل إشارة الانجراف. إلكترونيا معايرة استشعار الضغط في 0 ملم زئبق و 100 ملم زئبق وتسجيل البيانات في 2،000 هرتز. </li><li style=";text-align:right;direction:rtl"> أداء التخدير من قبل الإدارة داخل الصفاق من 1.4 جم / كجم من يوريتان. تأكد من أنالماوس تصل الطائرة المناسبة لها التخدير عندما لم يعد يتفاعل قرصة اصبع القدم حازمة. </li><li style=";text-align:right;direction:rtl"> ضع الماوس تخدير في موقف ضعيف. تأمين أطرافه مع الشريط. الحفاظ على درجة حرارة الجسم مع وسادة التدفئة ورصد مع التحقيق الذي تجريه المستقيم. حلق منطقة الرقبة وجعل شق خط الوسط في منطقة الرقبة لفضح الغدة الدرقية. </li><li style=";text-align:right;direction:rtl"> إصلاح الرقبة مع الإبر عازمة. </li><li style=";text-align:right;direction:rtl"> سحب جانبا الغدة اللعابية وفضح الصحيح الشريان السباتي المشترك. العصب المبهم، الذي يشبه الخيط الأبيض، وتقع على طول الشريان. فصل بعناية الشريان السباتي من العصب المبهم باستخدام ملقط منحنية. </li><li style=";text-align:right;direction:rtl"> تمرير ملقط المنحني تحت الصحيح الشريان السباتي المشترك لفصلها عن الأنسجة الأخرى. إزالة النسيج الضام حول الشريان. </li><li style=";text-align:right;direction:rtl"> تعدى اثنين من 6-0 أسلاك الحرير تحت الصحيح الشريان السباتي المشترك. جعل عقدة ضيقة على السلك العلوي، والتي وضعت نحو الرأس، على مقربة، وإصلاح مع كوشر (القاصي انسداد ربط). تمرير PROXIسلك سوء مرتين من اليسار إلى اليمين وإصلاح مع 2 kochers (الداني الأسلاك غير مسد). </li><li style=";text-align:right;direction:rtl"> إبقاء الشريان السباتي رطبة من خلال إسقاط معقم 0.9٪ كلوريد الصوديوم. تجف من السائل الزائد مع براعم القطن. </li><li style=";text-align:right;direction:rtl"> إجراء شق في الصحيح الشريان السباتي المشترك مع إبرة عيار 26 بين ربط القاصي وسلك غير مسد القريبة. </li><li style=";text-align:right;direction:rtl"> إدخال استشعار الضغط في الشريان. التحقق من عدم وجود فقدان الدم. دفع بلطف 1.0 الفرنسية ميلر الضغط القسطرة إلى الأمام وضبط سلك غير مسد الداني في مثل هذه الطريقة التي يمكن أن تمر القسطرة بعناية من خلال الأسلاك تحت الترقوة. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> تقليل فقدان الدم أثناء تعديل السلك غير مسد القريبة. لا ضغط استشعار الضغط أكثر من اللازم في حين تتقدم لأنها هشة للغاية. منذ يجب السلك الداني ليس انسداد الشريان والأوعية ينبغي أن تظل مليئة الدم. </li></ol></li><li style=";text-align:right;direction:rtl"> بدء تسجيل إشارة الضغط. والشرايين إشارة الضغط fluctuatوفاق في الماوس صحي بين الضغط الانبساطي من 60-70 ملم زئبق وضغط الانقباضي من 100-120 ملم زئبق. </li><li style=";text-align:right;direction:rtl"> توجيه القسطرة عبر الشريان اللامسماة وعبر الشريان الأبهر إلى البطين الأيسر. الضغط البطيني يتقلب بين 0 مم زئبق و100-120 ملم زئبق. السماح القسطرة لتحقيق الاستقرار داخل البطين الأيسر. تسجيل إشارة لمدة 30 دقيقة إلى 60 دقيقة تبعا لمتطلبات التجريبية. </li><li style=";text-align:right;direction:rtl"> بعد الانتهاء من التجربة، ونقع القسطرة في Alconox 1٪ لمدة 30 دقيقة. غسل القسطرة بالماء ملي-Q. تخزين القسطرة في كتلة الرغوة. </li><li style=";text-align:right;direction:rtl"> استرداد البيانات من برنامج تسجيل لمزيد من التحليل. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> لتحليل البيانات، والنظر في فترة زمنية حيث إشارة ضغط مستقرة. اختيار لا يقل عن 10 دورات القلب متتالية من البيانات المسجلة من الفائدة. </li><li style=";text-align:right;direction:rtl"> استخدام LabChart برنامج الإصدار 8.0 أو ما شابه ذلك لتحليل معدل ضربات القلب، ضغط الدم الانقباضي اليسار إلى أقصى حد الضغط البطيني، والحد الأدنى للventr الأيسر الانبساطيضغط icular، فإن معدل ذروة الإسوية الحجم تقلص البطين الأيسر (DP / دينارا كحد أقصى)، فإن معدل ذروة الإسوية الحجم استرخاء البطين الأيسر (DP / DT دقيقة)، والضغط البطين الأيسر نهاية الانبساط، وثابت الوقت من البطين الأيسر الإسوية الحجم سقوط الضغط (تاو) 7. ملاحظة: الضغط نهاية الانبساط يتوافق مع الضغط على نقطة في الوقت مباشرة قبل ارتفاع الضغط الناجم عن الانكماش الإسوية الحجم. ويستند حساب تاو على تركيب ضغط البطين الأيسر إلى منحنى الاضمحلال monoexponential، معبرا عنه P (ر) = P 0 البريد -t / تاو + ب، في هذه الصيغة، P (ر) هو ضغط البطين الأيسر في وقت ر بعد القيمة السلبية القصوى لموانئ دبي / دينارا تم التوصل إليها. المعلمة ب يتوافق مع الخط المقارب النظرية، والتي في نهج مبسطة يمكن افتراض أن يكون صفرا. النتائج تعزيز الاسترخاء الإسوية الحجم في قيمة أصغر من تاو. </li></ol></li></رأ&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.

تغييرات مزمنة في بنية عضلة القلب وظيفة، وتطوير اختلال البطين الأيسر، وتطور إلى فشل القلب يمكن التحقيق في عدة نماذج الفئران 12. إعادة عرض القلب واختلال وظيفي يمكن أن يتسبب عن إصابة عضلة القلب أو الضغط الزائد الثانوية لعرضية انقباض الشريان الأورطي، أو قد يتم التح...

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.

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			<td height="21" style="height:21px;">1.0 French Millar pressure catheter&#160;</td>
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			<td style="width:223px;">ADInstruments Pty Ltd.</td>
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permanent ligation of the left anterior descending coronary artery in mice: a model of post-myocardial infarction remodelling and heart failure

فشل القلب هو متلازمة الذي فشل القلب على ضخ الدم بمعدل يتناسب مع متطلبات الأكسجين الخلوية في الراحة أو أثناء الإجهاد. ويتميز هذا احتباس السوائل، وضيق في التنفس، والتعب، ولا سيما على الجهد المبذول. فشل القلب هو مشكلة متنامية للصحة العامة، والسبب الرئيسي في المستشفى، وسببا رئيسيا من أسباب الوفيات. مرض القلب الإقفاري هو السبب الرئيسي لفشل القلب. يشير إعادة هيكلة البطين للتغيرات في بنية وحجم وشكل البطين الأيسر. وبفعل هذا إعادة المعماري من البطين الأيسر بسبب الاصابة (على سبيل المثال، واحتشاء عضلة القلب)، عن طريق الضغط الزائد (على سبيل المثال، ارتفاع ضغط الدم الشرياني الجهازي أو تضيق الأبهر)، أو من حيث الحجم الزائد. منذ البطين إعادة عرض يؤثر الإجهاد جدار، ولها تأثير عميق على وظيفة القلب وعلى تطوير قصور القلب. نموذج للربط دائم في descendin الأمامي اليساريستخدم ز الشريان التاجي في الفئران لتحقيق إعادة عرض البطيني وظيفة القلب احتشاء عضلة القلب بعد. هذا النموذج يختلف اختلافا جذريا من حيث الأهداف والأهمية المرضية في جسم المريض مقارنة مع نموذج من ربط عابر الأمامي الأيسر النازل الشريان التاجي. في هذا النموذج الأخير من إصابة نقص التروية / ضخه، ومدى الأولي للاحتشاء يمكن عن طريق التضمين العوامل التي تؤثر على إنقاذ عضلة القلب بعد ضخه. في المقابل، يتم إصلاح منطقة احتشاء في 24 ساعة بعد ربط دائم في الأمامي الأيسر النازل الشريان التاجي. سوف تتأثر وظيفة القلب في هذا النموذج من قبل 1) عملية التوسع احتشاء، احتشاء الشفاء، وتشكيل ندبة. و2) تطوير ما يصاحب ذلك من توسع البطين الأيسر، وتضخم القلب، والبطين إعادة عرض. وإلى جانب نموذج ربط دائم في الأمامي الأيسر النازل الشريان التاجي، وتقنية الغازية الدورة الدموية الشرق الأوسط وأفريقيايتم تقديم surements في الفئران بالتفصيل.

مدى احتشاء عضلة القلب يمكن تقييمها من قبل ايفانز الأزرق / كلوريد 2،3،5-triphenyltetrazolium (TTC) تلطيخ مزدوجة. TTC هو مؤشر الأكسدة، والتي يتم تحويلها إلى عمق الحمراء 1،3،5-triphenylformazan في الأنسجة نتيجة لنشاط dehydrogenases مختلف في وجود NADH 8 الحية. الشكل 1 يوضح قسم التمثيل في الق?...

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.

ربط دائم في الشريان التاجي الأيسر الأمامي تنازلي في الفئران: نموذج ما بعد إعادة تشكيل عضلة القلب احتشاء وقصور القلب

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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27.6K Views.  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.

Video: 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.

الشريان التاجي ربط Intramyocardial وحقن الفئران في نموذج من احتشاء

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 Application Of Permanent Middle Cerebral Artery Ligation in the Mouse

Focal cerebral ischemia is among the most common type of stroke seen in patients. Due to the clinical significance there has been a prolonged effort to develop suitable animal models to study the events that unfold during ischemic insult. These techniques include transient or permanent, focal or global ischemia models using many different animal models, with the most common being rodents.
The permanent MCA ligation method which is also referred as pMCAo in the literature is used extensively as a focal ischemia model in rodents 1-6. This method was originally described for rats by Tamura et al. in 1981 7. In this protocol a craniotomy was used to access the MCA and the proximal regions were occluded by electrocoagulation. The infarcts involve mostly cortical and sometimes striatal regions depending on the location of the occlusion. This technique is now well established and used in many laboratories 8-13. Early use of this technique led to the definition and description of &#x201C;infarct core&#x201D; and &#x201C;penumbra&#x201D; 14-16, and it is often used to evaluate potential neuroprotective compounds 10, 12, 13, 17. Although the initial studies were performed in rats, permanent MCA ligation has been used successfully in mice with slight modifications 18-20 .
This model yields reproducible infarcts and increased post-survival rates. Approximately 80% of the ischemic strokes in humans happen in the MCA area 21 and thus this is a very relevant model for stroke studies. Currently, there is a paucity of effective treatments available to stroke patients, and thus there is a need for good models to test potential pharmacological compounds and evaluate physiological outcomes. This method can also be used for studying intracellular hypoxia response mechanisms in vivo. 
Here, we present the MCA ligation surgery in a C57/BL6 mouse. We describe the pre-surgical preparation, MCA ligation surgery and 2,3,5 Triphenyltetrazolium chloride (TTC) staining for quantification of infarct volumes.

Middle cerebral artery (MCA) ligation is a technique to study focal cerebral ischemia in animal models. In this method, the middle cerebral artery is exposed by craniotomy and ligated by cauterization. This method gives highly reproducible infarct volumes and increased post-operative survival rates compared to other methods available.

تطبيق الربط الدائم الشريان المخي الأوسط في الماوس

Focal cerebral ischemia is among the most common type of stroke seen in patients. Due to the clinical significance there has been a prolonged effort to ...

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.

تقنية لربط تعديل الشريان التاجي في الفئران

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 ...

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.

A الفئران نموذج من عضلة القلب إصابة نقص التروية، ضخه من خلال ربط الشريان الأمامي اليسار تنازليا

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).

الفئران اليسار الأمامي تنازلي (LAD) التاجي ربط الشريان: نموذج تحسين والمبسطة لاحتشاء عضلة القلب

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 ...

Direct Re-implantation of Left Coronary Artery into the Aorta in Adults with Anomalous Origin of Left Coronary Artery from the Pulmonary Artery (ALCAPA)

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly which is one of leading causes of myocardial ischemia and infarction in children. If left untreated, it results in a 90% mortality rate in the first year of life. In patients who survive to the adulthood, the coronary steal phenomenon and retrograde left-sided coronary flow provide a substrate for chronic subendocardial ischemia, which may lead to left ventricular dysfunction, ischemic mitral regurgitation, malignant ventricular arrhythmias, and sudden cardiac death. The average age of life-threatening presentation is 33 years and of sudden cardiac death 31 years. Therefore, surgical correction is highly recommended as soon as the diagnosis is made, regardless of age. In adult-type ALCAPA originating from the right-facing sinus of the pulmonary artery, direct re-implantation of the ALCAPA into the aorta is the more physiologically sound repair technique to re-establish the dual-coronary perfusion system and is recommended. This protocol describes the technique of direct re-implantation of adult-type ALCAPA into the aorta.

Direct Re-implantation of Left Coronary Artery into the Aorta in Adults with Anomalous Origin of Left Coronary Artery from the Pulmonary Artery ALCAPA

Surgical correction of ALCAPA is highly recommended, regardless of age or the degree of intercoronary collateralization. This protocol presents a technique for the direct re-implantation of adult-type ALCAPA into the aorta to re-establish the dual-coronary perfusion. Whenever feasible, direct re-implantation is preferred to other surgical correction techniques.

مباشر إعادة زرع الشريان التاجي الأيسر إلى الشريان الأبهر في البالغين الذين يعانون الشاذة منشأ الشريان التاجي الأيسر من الشريان الرئوي (ALCAPA)

Anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) is a rare congenital anomaly which is one of leading causes of myocardial ...

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.

نموذج احتشاء عضلة القلب Murine باستخدام الربط الدائم للشريان التاجي الأمامي الأيسر

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

Establishing a Swine Model of Post-myocardial Infarction Heart Failure for Stem Cell Treatment

Although advances have been achieved in the treatment of heart failure (HF) following myocardial infarction (MI), HF following MI remains one of the major causes of mortality and morbidity around the world. Cell-based therapies for cardiac repair and improvement of left ventricular function after MI have attracted considerable attention. Accordingly, the safety and efficacy of these cell transplantations should be tested in a preclinical large animal model of HF prior to clinical use. Pigs are widely used for cardiovascular disease research due to their similarity to humans in terms of heart size and coronary anatomy. Therefore, we sought to present an effective protocol for the establishment of a porcine chronic HF model using closed-chest coronary balloon occlusion of the left circumflex artery (LCX), followed by rapid ventricular pacing induced with pacemaker implantation. Eight weeks later, the stem cells were administered by intramyocardial injection in the peri-infarct area. Then the infarct size, cell survival, and left ventricular function (including echocardiography, hemodynamic parameters, and electrophysiology) were evaluated. This study helps establish a stable preclinical large animal HF model for stem cell treatment.

We sought to establish a swine model of heart failure induced by left circumflex artery blockage and rapid pacing to test the effect and safety of intramyocardial administration of stem cells for cell-based therapies.

إنشاء نموذج الخنازير من فشل القلب احتشاء ما بعد عضلة القلب لعلاج الخلايا الجذعية

Although advances have been achieved in the treatment of heart failure (HF) following myocardial infarction (MI), HF following MI remains one of the major ...

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in G&#246;ttingen Minipigs and Landrace Pigs

The development of heart failure is the most powerful predictor of long-term mortality in patients surviving acute myocardial infarction (MI). There is an unmet clinical need for prevention and therapy of post-myocardial infarction heart failure (post-MI HF). Clinically relevant pig models of post-MI HF are prerequisites for final proof-of-concept studies before entering into clinical trials in drug and medical device development.
Here we aimed to characterize a closed-chest porcine model of post-MI HF in adult G&#246;ttingen minipigs with long-term follow-up including serial cardiac magnetic resonance imaging (CMRI) and to compare it with the commonly used Landrace pig model.
MI was induced by intraluminal balloon occlusion of the left anterior descending coronary artery for 120 min in G&#246;ttingen minipigs and for 90 min in Landrace pigs, followed by reperfusion. CMRI was performed to assess cardiac morphology and function at baseline in both breeds and at 3 and 6 months in G&#246;ttingen minipigs and at 2 months in Landrace pigs, respectively.
Scar sizes were comparable in the two breeds, but MI resulted in a significant decrease of left ventricular ejection fraction (LVEF) only in G&#246;ttingen minipigs, while Landrace pigs did not show a reduction of LVEF. Right ventricular (RV) ejection fraction increased in both breeds despite the negligible RV scar sizes. In contrast to the significant increase of left ventricular end-diastolic (LVED) mass in Landrace pigs at 2 months, G&#246;ttingen minipigs showed a slight increase in LVED mass only at 6 months.
In summary, this is the first characterization of post-MI HF in G&#246;ttingen minipigs in comparison to Landrace pigs, showing that the G&#246;ttingen minipig model reflects post-MI HF parameters comparable to the human pathology. We conclude that the G&#246;ttingen minipig model is superior to the Landrace pig model to study the development of post-MI HF.

Post-Myocardial Infarction Heart Failure in Closed-chest Coronary Occlusion/Reperfusion Model in G&amp;#246;ttingen Minipigs and Landrace Pigs

The overall goal of the current study is to present the techniques of induction of myocardial infarction (MI) and post-myocardial infarction heart failure (post-MI HF) in closed-chest, adult G&#246;ttingen minipigs and the characterization of post-MI HF model in G&#246;ttingen minipigs as compared to Landrace pigs.

فشل القلب بعد احتشاء عضلة القلب في انسداد الشريان التاجي المغلق الصدر / نموذج إعادة التروية في الخنازير الصغيرة غوتنغن والخنازير لاندراس

The development of heart failure is the most powerful predictor of long-term mortality in patients surviving acute myocardial infarction (MI). There is an ...

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.

توليد وتوصيف احتشاء عضلة القلب البطيني الأيمن الناجم عن الربط الدائم للشريان التاجي الأيمن في الفئران

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