Name: murine isolated heart model of myocardial stunning associated with cardioplegic arrest
Uploaded: 2015-08-06T13:00:00.000+00:00
Duration: 8 min 30 s
Description: Watch this Scientific Journal Video about Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest at JoVE.com

<ol>
	<li>Kloner, R. a., Jennings, R. B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Consequences+of+Brief+Ischemia:+Stunning,+Preconditioning,+and+Their+Clinical+Implications:+Part+1.">Consequences of Brief Ischemia: Stunning, Preconditioning, and Their Clinical Implications: Part 1.</a> Circulation. 104 (24), 2981-2989 (2001).</li><li>Mentzer, R. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Myocardial+protection+in+heart+surgery.">Myocardial protection in heart surgery.</a> J Cardiovasc Pharmacol Ther. 16 (3-4), 290-297 (2011).</li><li>Chambers, D. J., Fallouh, H. B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Cardioplegia+and+cardiac+surgery:+pharmacological+arrest+and+cardioprotection+during+global+ischemia+and+reperfusion.">Cardioplegia and cardiac surgery: pharmacological arrest and cardioprotection during global ischemia and reperfusion.</a> Pharmacol Ther. 127 (1), 41-52 (2010).</li><li>Bolli, R., Marb&#225;n, E. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Molecular+and+cellular+mechanisms+of+myocardial+stunning.">Molecular and cellular mechanisms of myocardial stunning.</a> Physiol Rev. 79 (2), 609-634 (1999).</li><li>Kloner, R. a., Bolli, R., Marban, E., Reinlib, L., Braunwald, E. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Medical+and+Cellular+Implications+of+Stunning,+Hibernation,+and+Preconditioning+An+NHLBI+Workshop.">Medical and Cellular Implications of Stunning, Hibernation, and Preconditioning An NHLBI Workshop.</a> Circulation. 97 (18), 1848-1867 (1998).</li><li>Mersmann, J., Latsch, K., Habeck, K., Zacharowski, K. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Measure+for+measure-determination+of+infarct+size+in+murine+models+of+myocardial+ischemia+and+reperfusion:+a+systematic+review.">Measure for measure-determination of infarct size in murine models of myocardial ischemia and reperfusion: a systematic review.</a> Shock (Augusta, Ga). 35 (5), 449-455 (2011).</li><li>Bell, R. M., Mocanu, M. M., Yellon, D. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Retrograde+heart+perfusion:+the+Langendorff+technique+of+isolated+heart+perfusion).">Retrograde heart perfusion: the Langendorff technique of isolated heart perfusion).</a> J Mol Cell Cardiol. 50 (6), 940-950 (2011).</li><li>Skrzypiec-Spring, M., Grotthus, B., Szelag, A., Schulz, R. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Isolated+heart+perfusion+according+to+Langendorff---still+viable+in+the+new+millennium.">Isolated heart perfusion according to Langendorff---still viable in the new millennium.</a> J Pharmacol Toxicol Methods. 55 (2), 113-126 (2007).</li><li>Sutherland, F. J., Shattock, M. J., Baker, K. E., Hearse, D. 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+isolated+perfused+heart+characteristics+and+cautions.">Mouse isolated perfused heart characteristics and cautions.</a> Clin Exp Pharmacol Physiol. 30 (11), 867-878 (2003).</li><li>Miller, A., Wright, G. L. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Fabrication+of+Murine+Ventricular+Balloons+for+the+Langendorff+Heart+Preparation.">Fabrication of Murine Ventricular Balloons for the Langendorff Heart Preparation.</a> J Biotecnol Biomater. 1 (101), 1-4 (2011).</li><li>Curtis, M. J. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Characterisation,+utilisation+and+clinical+relevance+of+isolated+perfused+heart+models+of+ischaemia-induced+ventricular+fibrillation.">Characterisation, utilisation and clinical relevance of isolated perfused heart models of ischaemia-induced ventricular fibrillation.</a> Cardiovasc Res. 39 (1), 194-215 (1998).</li><li>Clements, R. T., Feng, J., Cordeiro, B., Bianchi, C., Sellke, F. W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=p38+MAPK-dependent+small+HSP27+and+&#945;B-crystallin+phosphorylation+in+regulation+of+myocardial+function+following+cardioplegic+arrest.">p38 MAPK-dependent small HSP27 and &#945;B-crystallin phosphorylation in regulation of myocardial function following cardioplegic arrest.</a> American journal of physiology. Heart and circulatory physiology. 300 (5), H1669-H1677 (2011).</li><li>Clements, R. T., Cordeiro, B., Feng, J., Bianchi, C., Sellke, F. W. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Rottlerin+increases+cardiac+contractile+performance+and+coronary+perfusion+through+BKCa+++channel+activation+after+cold+cardioplegic+arrest+in+isolated+hearts.">Rottlerin increases cardiac contractile performance and coronary perfusion through BKCa++ channel activation after cold cardioplegic arrest in isolated hearts.</a> Circulation. 124 (11 Suppl), S55-S61 (2011).</li></ol>

The authors have nothing to disclose.

تفاصيل بروتوكول السابقة أساليب لتقييم عضلة القلب مذهلة الثانوية لنقص التروية العالمية المرتبطة اعتقال شلل القلب. في أيدينا ينتج هذا البروتوكول تقريبي ~ تخفيض 40٪ في وظيفة القلب (LVDP، +/- موانئ دبي / دينارا) مع تغيرات طفيفة في معدل ضربات القلب في 30 دقيقة بعد ضخه نقطة في ال?...

عضلة القلب مذهلة يعرف بأنه انعكاس انخفاض النشاط مقلص على الرغم من استعادة تدفق الدم الكافي بعد فترة وجيزة من نقص التروية أو فترات طويلة من الشتائم الدماغية مع كارديوبروتيكتيون 1،2،3،4،5. يتم استخدام الطريقة المعروضة خصيصا لنموذج الشتائم الدماغية ذات الصلة سريريا والتي يمكن أن تؤدي إلى عاهات عكسها في وظيفة مقلص (أي إهانات الدماغية المرتبطة جراحة القلب باستخدام اعتقال شلل القلب، فترات قصيرة من نقص التروية، والذبحة الصدرية، وما إلى ذلك). وعلى النقيض من الدراسات نقص التروية الحاد (احتشاء عضلة القلب، نخر) تم تطوير هذا البروتوكول لتقييم الانتعاش وظيفية عضلة القلب وكارديوبروتيكتيون دون وقوع إصابات الأنسجة، وإعادة عرض، وموت الخلايا. الغالبية العظمى من ورقة تتناول معيار شلل القلب بروتوكول القبض مع عناصر مشابهة لجراحة القلب باستخدام حرارة الجسم ومتقطعة تسليم شلل القلب. بروت عضلة القلبection خلال معظم جراحات القلب يعتمد على شلل القلب وشرايين القلب. على الرغم من شلل القلب (CP) الحلول والاستراتيجيات تختلف على نطاق واسع (الدم، بلوراني والبرد، الخ دافئ) العناصر الأكثر شيوعا هي 1) فرط بوتاسيوم الدم و / أو غيرها من الاستراتيجيات للقبض على القلب في انبساط، مما يحد من استخدام الطاقة الناتجة من تقلص عضلة القلب، و2) انخفاض حرارة الجسم لإبطاء عملية التمثيل الغذائي وتساعد على الحفاظ على ATP واحتياطيات الطاقة الأخرى أثناء القبض عليه. حلول شلل القلب الحالية توفر الحماية للقلب ضد الشتائم الدماغية التي من شأنها أن يثبت خلاف ذلك قاتلة. ومع ذلك، استراتيجيات الوقاية من أمراض القلب خلال الشتائم الدماغية الجراحية ليست مثالية، وإصابة الدماغية الخفيفة الناتجة يمكن أن يؤدي إلى عكسها القلب ضعف مقلص على الرغم من تدفق الدم الكافي (عضلة القلب مذهلة)، الحماض، والضرر cardiomyocyte، وآثار الأوعية الدموية بما في ذلك انخفاض التروية التاجية وبالتشنج. هذا يختلف البروتوكولمن النماذج القياسية نقص تروية القلب معزولة تقييم احتشاء عضلة القلب ونقص التروية الحاد في أنه يقيم الشتائم الدماغية أكثر اعتدالا مما يمكن أن يؤدي إلى اختلال وظائف القلب بعد نقص التروية وجيزة أو الشتائم الدماغية المرتبطة اعتقال شلل القلب. (للمراجعة على تقنيات نضح Langendorff وI / دراسات R ترى 6-8). لمبادئ توجيهية عامة وتحليلا شاملا لالمعلمات التجريبية المرتبطة الماوس معزولة قلوب perfused لرؤية ساذرلاند ه ر ال. 2003 9 التقنية المقدمة هنا تفاصيل ما يلزم من معدات والكواشف، خطوات واستراتيجيات ونصائح للحث موثوق مذهلة في قلوب الماوس. تعديلات طفيفة ضرورية لتطبيق هذه التقنية على الفئران. لفترة وجيزة قلوب الماوس معزولة وLangendorff perfused للحوالي 30 دقيقة مع فيزيولوجي كريبس-هنسلايت العازلة (جسر الملك حسين)، تليها البارد السكتة القلبية محمية عن طريق تسليم hypotherm فرط بوتاسيوم الدمجيم حل شلل القلب. بعد الاعتقال، ويتم رصد الانتعاش وظيفية قلبية خلال إعادة التدفئة وضخه من القلب مع جسر الملك حسين. يمكن تقييم التغيرات في درجة استعادة وظيفة القلب مقلص لتقييم وكلاء الواقية للقلب واستراتيجيات كارديوبروتيكتيون مختلفة.

<table><tbody><tr><td>Cardioplegia Solution (St Thomas II)</td><td></td><td></td><td>Symbol / Concentrations (mM)</td></tr><tr><td>Sodium Chloride</td><td></td><td></td><td>NaCl; 110</td></tr><tr><td>Potassium chloride</td><td></td><td></td><td>KCl; 16</td></tr><tr><td>Calcium Chloride</td><td></td><td></td><td>CaCL2; 1.5</td></tr><tr><td>Magnesium Chloride</td><td></td><td></td><td>MgCL2; 16</td></tr><tr><td>Sodium Bicarbonate</td><td></td><td></td><td>NaHCO3; 10</td></tr><tr><td>Krebs-Heinslet Buffer</td><td></td><td></td><td></td></tr><tr><td>Sodium Chloride</td><td></td><td></td><td>NaCl; 118</td></tr><tr><td>Potassium Chloride</td><td></td><td></td><td>KCl; 4.8</td></tr><tr><td>Magnesium Sulfate</td><td></td><td></td><td>MgSO4; 1.7</td></tr><tr><td>Sodium Bicarbonate</td><td></td><td></td><td>NaHCO3; 24.9</td></tr><tr><td>Potassium Phosphate (monobasic)</td><td></td><td></td><td>KH2PO4; 1.2</td></tr><tr><td>Calcium Chloride</td><td></td><td></td><td>CaCL2; 1.4</td></tr><tr><td>Sodium Pyruvate</td><td></td><td></td><td>Na pyruvate; 2</td></tr><tr><td>Glucose</td><td></td><td></td><td>C6H12O6; 6</td></tr><tr><td>Balloon reagents</td><td></td><td></td><td></td></tr><tr><td>Corn Syrup</td><td></td><td></td><td></td></tr><tr><td>Spaghetti</td><td></td><td></td><td></td></tr><tr><td>Silicon Dispersion Gel</td><td></td><td></td><td></td></tr><tr><td>styrofoam block</td><td></td><td></td><td></td></tr><tr><td>lab oven/incubator ( 50C)</td><td></td><td></td><td></td></tr><tr><td>Langendorff Perfusion equipment</td><td></td><td></td><td></td></tr><tr><td>Isolated perfused heart sytem (IH-SR (Hugo-Sachs) or equivalent)</td><td></td><td></td><td></td></tr><tr><td>Data acquisition system (DSI, ADinstruments or equivalent)</td><td></td><td></td><td></td></tr><tr><td>Heated water circulator</td><td></td><td></td><td></td></tr><tr><td>Cooling water circulator</td><td></td><td></td><td></td></tr><tr><td>Perfusion pump capable of 2-30 ml/min</td><td></td><td></td><td></td></tr><tr><td>Inline perfusion filters - 1 um glass fiber</td><td></td><td></td><td></td></tr><tr><td>Pressure sensors and amplifiers for LVP and perfusion pressure</td><td></td><td></td><td></td></tr><tr><td>Small graduated cylinder (~10 mL)</td><td></td><td></td><td></td></tr><tr><td>Small temperature probe and thermometer (Werner or equivalent)</td><td></td><td></td><td></td></tr><tr><td>perfusion resevoir (1L)</td><td></td><td></td><td></td></tr><tr><td>cardioplegia resevoir (~200 mL)</td><td></td><td></td><td></td></tr><tr><td>gas bubbler</td><td></td><td></td><td></td></tr><tr><td>95/5 O2/CO2 mix</td><td></td><td></td><td></td></tr><tr><td>Surgical tools and reagents</td><td></td><td></td><td></td></tr><tr><td>Metzenbaum and Potz surgical scissors</td><td></td><td></td><td></td></tr><tr><td>two Dumont size 5 forceps</td><td></td><td></td><td></td></tr><tr><td>ketamine</td><td></td><td></td><td></td></tr><tr><td>xylazine</td><td></td><td></td><td></td></tr><tr><td>heparin</td><td></td><td></td><td></td></tr><tr><td>small clamp with soft sides to hold aorta (i.e. terminal clamp with taped ends)</td><td></td><td></td><td></td></tr><tr><td>Silk 2-0 and 4-0 sutures</td><td></td><td></td><td></td></tr></tbody></table>

murine isolated heart model of myocardial stunning associated with cardioplegic arrest

بروتوكول التالي من استخدام لتقييم وظيفة القلب ضعف أو مذهل يلي الشتائم الدماغية المعتدلة عضلة القلب. هذه التقنية مفيدة للنمذجة الإصابة الدماغية المرتبطة مع العديد من ظاهرة ذات الصلة سريريا بما في ذلك جراحة القلب بالاعتقال شلل القلب وشرايين القلب، بعيدا عن مضخة تحويل مسار الشريان التاجي، زرع، والذبحة الصدرية، نقص التروية وجيزة، وما إلى ذلك. يعرض بروتوكول طريقة عامة لنموذج تبريدي اعتقال شلل القلب فرط بوتاسيوم الدم وضخه في قلوب القوارض التركيز على قياس وظيفة مقلص عضلة القلب. باختصار، هو perfused لقلب الفأر في وضع langendorff، المجهزة مع بالون داخل البطينات، ويتم تسجيل المعلمات الأساسية وظيفية القلب. في أعقاب الاستقرار، والقلب هو بعد ذلك يخضع لاطلاع التسريب من الواقية للقلب حل شلل القلب تبريدي لبدء اعتقال الانبساطي. يتم تسليم شلل القلب بشكل متقطع أكثر من 2 ساعة. ثم يتم إشباعها القلب وWARMEويتم رصد د لدرجات حرارة سوي الحرارة واستعادة وظيفة عضلة القلب. استخدام هذه النتائج في بروتوكول موثوقة الاكتئاب وظيفة مقلص القلب خالية من الإجمالي تلف الأنسجة عضلة القلب في القوارض.

الشكل 1 يعرض نتائج نموذجية من التجربة الماوس واحد. LVP (خط أحمر)، DP / دينارا (الخط الأخضر)، ودرجة الحرارة (الخط البنفسجي) سجلت continusouly على ~ 3 ساعة. رسائل تشير إلى وجود - قياس خط الأساس، ب، ج، د، ه - تقديم حل شلل القلب، و - بدء ضخه، ز، ح، ط، ي - قياس تدفق cornary خلال ضخه. ملا?...

Watch this Scientific Journal Video about Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest at JoVE.com

Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest

The goal of this protocol to assess myocardial stunning following ischemic cardioplegic arrest in rodents.

عزل فأري موديل قلب عضلة القلب مذهل المصاحبة اعتقال شلل القلب

The following protocol is of use to evaluate impaired cardiac function or myocardial stunning following moderate ischemic insults. The technique is useful ...

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11.6K Views.  Brown University. The goal of this protocol to assess myocardial stunning following ischemic cardioplegic arrest in rodents.

Video: Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest

Normothermic Cardiac Arrest and Cardiopulmonary Resuscitation: A Mouse Model of Ischemia-Reperfusion Injury

Acute Kidney Injury (AKI) is a common, highly lethal, complication of critical illness which has a high mortality1-4 and which is most 
frequently caused by whole-body hypoperfusion.5,6 Successful reproduction of whole-body hypoperfusion in rodent models has been fraught with 
difficulty.7-9,9,10 Models which employ focal ischemia have repeatedly demonstrated results which do not translate to the clinical setting, and larger 
animal models which allow for whole body hypoperfusion lack access to the full toolset of genetic manipulation possible in the mouse.11,12 However, in recent 
years a mouse model of cardiac arrest and cardiopulmonary resuscitation has emerged which can be adapted to model AKI.13 This model reliably reproduces 
physiologic, functional, anatomic, and histologic outcomes seen in clinical AKI, is rapidly repeatable, and offers all of the significant advantages of a murine surgical 
model, including access to genetic manipulative techniques, low cost relative to large animals, and ease of use. Our group has developed extensive experience 
with use of this model to assess a number of organ-specific outcomes in AKI.14,15

A powerful model for perioperative and critical care related acute kidney injury is presented. Using whole body hypoperfusion induced by cardiac arrest it is possible to nearly replicate the histologic and functional changes of clinical AKI.

توقف القلب والإنعاش القلبي Normothermic : نموذج الفأر من نقص التروية ، إعادة إشباع الخلايا الإصابات

Acute Kidney Injury (AKI) is a common, highly lethal, complication of critical illness which has a high mortality1-4 and which is most 
frequently caused ...

A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

Surgical trauma by thoracotomy in open-chest models of coronary ligation induces an immune response which modifies different mechanisms involved in ischemia and reperfusion. Immune response includes cytokine expression and release or secretion of endogenous ligands of innate immune receptors. Activation of innate immunity can potentially modulate infarct size. We have modified an existing murine closed-chest model using hanging weights which could be useful for studying myocardial pre- and postconditioning and the role of innate immunity in myocardial ischemia and reperfusion. This model allows animals to recover from surgical trauma before onset of myocardial ischemia.
Volatile anesthetics have been intensely studied and their preconditioning effect for the ischemic heart is well known. However, this protective effect precludes its use in open chest models of coronary artery ligation. Thus, another advantage could be the use of the well controllable volatile anesthetics for instrumentation in a chronic closed-chest model, since their preconditioning effect lasts up to 72 hours. Chronic heart diseases with intermittent ischemia and multiple hit models are other possible applications of this model.
For the chronic closed-chest model, intubated and ventilated mice undergo a lateral blunt thoracotomy via the 4th intercostal space. Following identification of the left anterior descending a ligature is passed underneath the vessel and both suture ends are threaded through an occluder. Then, both suture ends are passed through the chest wall, knotted to form a loop and left in the subcutaneous tissue. After chest closure and recovery for 5 days, mice are anesthetized again, chest skin is reopened and hanging weights are hooked up to the loop under ECG control.
At the end of the ischemia/reperfusion protocol, hearts can be stained with TTC for infarct size assessment or undergo perfusion fixation to allow morphometric studies in addition to histology and immunohistochemistry.

Surgical trauma induces an inflammatory response. Cytokines and endogenous ligands are known to modulate myocardial infarct size following ischemia and reperfusion. We present a modified closed-chest model of murine ischemia and reperfusion using hanging weights to minimize effects of thoracotomy.

والفئران مغلقة الصدر نموذج نقص التروية القلبية وإعادة إشباع الخلايا

Surgical trauma by thoracotomy in open-chest models of coronary ligation induces an immune response which modifies different mechanisms involved in ...

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 ...

Confirmation of Myocardial Ischemia and Reperfusion Injury in Mice Using Surface Pad Electrocardiography

Many animal models have been established for the study of myocardial remodeling and heart failure due to its status as the number one cause of mortality worldwide. In humans, a pathologic occlusion forms in a coronary artery and reperfusion of that occluded artery is considered essential to maintain viability of the myocardium at risk. Although essential for myocardial recovery, reperfusion of the ischemic myocardium creates its own tissue injury. The physiologic response and healing of an ischemia/reperfusion injury is different from a chronic occlusion injury. Myocardial ischemia/reperfusion injury is gaining recognition as a clinically relevant model for myocardial infarction studies. For this reason, parallel animal models of ischemia/reperfusion are vital in advancing the knowledge base regarding myocardial injury. Typically, ischemia of the mouse heart after left anterior descending (LAD) coronary artery occlusion is confirmed by visible pallor of the myocardium below the occlusion (ligature). However, this offers only a subjective way of confirming correct or consistent ligature placement, as there are multiple major arteries that could cause pallor in different myocardial regions. A method of recording electrocardiographic changes to assess correct ligature placement and resultant ischemia as well as reperfusion, to supplement observed myocardial pallor, would help yield consistent infarct sizes in mouse models. In turn, this would help decrease the number of mice used. Additionally, electrocardiographic changes can continue to be recorded non-invasively in a time-dependent fashion after the surgery. This article will demonstrate a method of electrocardiographically confirming myocardial ischemia and reperfusion in real time.

During murine myocardial ischemia/reperfusion surgery, correct placement of the occluding ligature is typically confirmed by visible observation of myocardial pallor. Herein, a method of electrocardiographically confirming ischemia and reperfusion, to supplement observed myocardial pallor, is demonstrated in male C57Bl/6 mice.

تأكيدا لعضلة القلب نقص التروية وضخه إصابة في الفئران عن طريق الكهربائي الوسادة السطحية

Many animal models have been established for the study of myocardial remodeling and heart failure due to its status as the number one cause of mortality ...

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 ...

An Intact Pericardium Ischemic Rodent Model

This protocol has shown that the pericardium and its contents play an essential anti-fibrotic role in the ischemic rodent model (coronary ligation to induce myocardial injury). The majority of pre-clinical myocardial infarction models require the disruption of pericardial integrity with loss of the homeostatic cellular milieu. However, recently a methodology has been developed by us to induce myocardial infarction, which minimizes pericardial damage and retains the heart&#39;s resident immune cell population. An improved cardiac functional recovery in mice with an intact pericardial space following coronary ligation has been observed. This method provides an opportunity to study inflammatory responses in the pericardial space following myocardial infarction. Further development of the labeling techniques can be combined with this model to understand the fate and function of pericardial immune cells in regulating the inflammatory mechanisms that drive remodeling in the heart, including fibrosis.

This protocol outlines the steps for inducing myocardial infarction in mice while preserving the pericardium and its contents.

نموذج القوارض الإقفارية التامور سليمة

This protocol has shown that the pericardium and its contents play an essential anti-fibrotic role in the ischemic rodent model (coronary ligation to ...

نموذج فأر لدراسة فسيولوجيا الدماغ أثناء السكتة القلبية

Mouse Cardiac Arrest Model for Brain Imaging and Brain Physiology Monitoring During Ischemia and Resuscitation

Most cardiac arrest (CA) survivors experience varying degrees of neurologic deficits. To understand the mechanisms that underpin CA-induced brain injury and, subsequently, develop effective treatments, experimental CA research is essential. To this end, a few mouse CA models have been established. In most of these models, the mice are placed in the supine position in order to perform chest compression for cardiopulmonary resuscitation (CPR). However, this resuscitation procedure makes the real-time imaging/monitoring of brain physiology during CA and resuscitation challenging. To obtain such critical knowledge, the present protocol presents a mouse asphyxia CA model that does not require the chest compression CPR step. This model allows for the study of dynamic changes in blood flow, vascular structure, electrical potentials, and brain tissue oxygen from the pre-CA baseline to early post-CA reperfusion. Importantly, this model applies to aged mice. Thus, this mouse CA model is expected to be a critical tool for deciphering the impact of CA on brain physiology.

تسليط الضوء على المؤلف: نموذج فأر فريد للسكتة القلبية الناجمة عن الاختناق 

This protocol demonstrates a unique mouse model of asphyxia cardiac arrest that does not require chest compression for resuscitation. This model is useful for monitoring and imaging the dynamics of brain physiology during cardiac arrest and resuscitation.

نموذج السكتة القلبية للفأر لتصوير الدماغ ومراقبة فسيولوجيا الدماغ أثناء نقص التروية والإنعاش

Most cardiac arrest (CA) survivors experience varying degrees of neurologic deficits. To understand the mechanisms that underpin CA-induced brain injury ...

Neuroscience

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence suggests that thrombolytic therapy or primary percutaneous coronary intervention (PPCI) does not prevent reperfusion injury. There is still no ideal animal model for MIRI. This study aims to improve the MIRI model in rats to make surgery easier and more feasible. A unique method for establishing MIRI is developed by using a soft tube during a key step of the ischemic period. To explore this method, thirty rats were randomly divided into three groups: sham group (n = 10); experimental model group (n = 10); and existing model group (n = 10). Findings of triphenyltetrazolium chloride staining, electrocardiography, and percent survival are compared to determine the accuracies and survival rates of the operations. Based on the study results, it has been concluded that the improved surgery method is associated with a higher survival rate, elevated ST-T segment, and larger infarct size, which is expected to mimic the pathology of MIRI better.

Myocardial ischemia-reperfusion model of rat heart is improved by using a self-made retractor, polyvinyl chloride tube, and a unique knotting method. Electrocardiogram, triphenyltetrazolium chloride and histological staining, and percent survival analysis results showed that the improved model group has higher success and survival rates than the already existing model group.

تحسين نموذج القوارض من نقص تروية عضلة القلب وإصابة التروية

Myocardial ischemia and reperfusion injury (MIRI), induced by coronary heart disease (CHD), causes damage to the cardiomyocytes. Furthermore, evidence ...

عزل فأري موديل قلب عضلة القلب مذهل المصاحبة اعتقال شلل القلب

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توقف القلب والإنعاش القلبي Normothermic : نموذج الفأر من نقص التروية ، إعادة إشباع الخلايا الإصابات

والفئران مغلقة الصدر نموذج نقص التروية القلبية وإعادة إشباع الخلايا

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

تأكيدا لعضلة القلب نقص التروية وضخه إصابة في الفئران عن طريق الكهربائي الوسادة السطحية

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

نموذج القوارض الإقفارية التامور سليمة

نموذج السكتة القلبية للفأر لتصوير الدماغ ومراقبة فسيولوجيا الدماغ أثناء نقص التروية والإنعاش

نموذج السكتة القلبية للفأر لتصوير الدماغ ومراقبة فسيولوجيا الدماغ أثناء نقص التروية والإنعاش

نموذج السكتة القلبية للفأر لتصوير الدماغ ومراقبة فسيولوجيا الدماغ أثناء نقص التروية والإنعاش

تحسين نموذج القوارض من نقص تروية عضلة القلب وإصابة التروية