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	<li>Kirino, T., Sano, K. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Selective+vulnerability+in+the+gerbil+hippocampus+following+transient+ischemia.">Selective vulnerability in the gerbil hippocampus following transient ischemia.</a> Acta Neuropathologica. 62, 201-208 (1984).</li><li>Smith, M. L., Auer, R. N., Siesjo, B. K. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+density+and+distribution+of+ischemic+brain+injury+in+the+rat+following+2-10+min+of+forebrain+ischemia.">The density and distribution of ischemic brain injury in the rat following 2-10 min of forebrain ischemia.</a> Acta Neuropathologica. 64, 319-332 (1984).</li><li>Sanderson, T. H., Kumar, R., Sullivan, J. M., Krause, G. 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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=PKR-like+endoplasmic+reticulum+kinase+(PERK)+activation+following+brain+ischemia+is+independent+of+unfolded+nascent+proteins.">PKR-like endoplasmic reticulum kinase (PERK) activation following brain ischemia is independent of unfolded nascent proteins.</a> Neuroscience. 169, 1307-1314 (2010).</li><li>Hazelton, J. 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P. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Necrosis,+apoptosis+and+hybrid+death+in+the+cortex+and+thalamus+after+barrel+cortex+ischemia+in+rats.">Necrosis, apoptosis and hybrid death in the cortex and thalamus after barrel cortex ischemia in rats.</a> Brain Research. 1022, 54-61 (2004).</li><li>Zong, W. X., Thompson, C. B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Necrotic+death+as+a+cell+fate.">Necrotic death as a cell fate.</a> Genes &amp; Development. 20, 1-15 (2006).</li><li>Ito, U., Spatz, M., Walker, J. T., Klatzo, I. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Experimental+cerebral+ischemia+in+mongolian+gerbils.+I.+Light+microscopic+observations.">Experimental cerebral ischemia in mongolian gerbils. I. Light microscopic observations.</a> Acta Neuropathologica. 32, 209-223 (1975).</li><li>Saver, J. L., Albers, G. W., Dunn, B., Johnston, K. C., Fisher, M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Stroke+Therapy+Academic+Industry+Roundtable+(STAIR)+recommendations+for+extended+window+acute+stroke+therapy+trials.">Stroke Therapy Academic Industry Roundtable (STAIR) recommendations for extended window acute stroke therapy trials.</a> Stroke; a Journal of Cerebral Circulation. 40, 2594-2600 (2009).</li><li>Busto, R., Dietrich, W. D., Globus, M. Y., Ginsberg, M. D. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=The+importance+of+brain+temperature+in+cerebral+ischemic+injury.">The importance of brain temperature in cerebral ischemic injury.</a> Stroke; a Journal of Cerebral Circulation. 20, 1113-1114 (1989).</li><li>Voll, C. L., Auer, R. N. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Postischemic+seizures+and+necrotizing+ischemic+brain+damage:+neuroprotective+effect+of+postischemic+diazepam+and+insulin.">Postischemic seizures and necrotizing ischemic brain damage: neuroprotective effect of postischemic diazepam and insulin.</a> Neurology. 41, 423-428 (1991).</li><li>Yamaguchi, M., Calvert, J. W., Kusaka, G., Zhang, J. 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Yazarlar ç mali çatışmalar var.

Burada açıklanan modeli insanlarda bulunan benzer bir yaralanma sağlayan, kalp durması ve canlandırma bir sonucu olarak ortaya çıkabilir beyin İşemi üretir. Genel beyin iskemisinde üretmek için bu yöntem birden fazla protokol biridir. Biz, nispeten düşük ölüm oranı, hızlı iyileşme ve tekrarlanabilir sonuçlar için en önemli bu protokolü kullanır. Kardiyak arrest / resüsitasyon modeli ancak teknik olarak, belki sürekli yeniden en zor klinik olarak en uygun modeldir. Küresel beyin iskemi 4VO m...

Kalp durması ve inme bir sonucu olarak beyin hasarı ölüm ve uzun süreli sakatlık önde gelen nedenidir. Kardiyak arrest kurbanları için kardiyopulmoner resüsitasyon bu hastaların% 60 daha sonra hastanede ölen en az kapsamlı beyin hasarı sonucunda ABD&#39;de 7,8 yılda yaklaşık 70.000 hastalarda spontan dolaşımı sağlayacak başarılı ve ise sadece 3-10% yeniden hayata hastaların 9,10 eski yaşam devam edebilirsiniz. Açıkçası, küresel beyin iskemi sonrasında ve nörolojik travma en aza indirmek için tedavi yaklaşımları tasarımı beyin hasarına yol mekanizmalarını anlamak kritik önem taşımaktadır. Beyin iskemi birden çok yöntem kullanılarak modellenebilir. En sık olarak, beyin iskemisi, böylece bir odak iskemik inme 11,12 üreten, beyin, orta serebral arterin büyük bir damar oklüzyonu ile kemirgen üretilir. Klinik olarak önemli iken,fokal beyin iskemi kardiyak arrest / resüsitasyon tarafından üretilen beyin hasarı incelemek için doğru bir yöntem değildir. Bu klinik paradigma modellemek için bütün iskemik beyin kan akışının yeniden yerleştirilmesi, ardından yapılmalıdır. Yakından klinik taklit etmek için, araştırmacılar deneysel CPR ve defibrilasyon 13,14 ile resüsitasyon ardından kardiyak arrest neden. Bu model klinik, ancak öngörülemeyen resüsitasyon kez değişkenliği artırabilir ve yorumlamak için veri analizi zor hale getirebilir. Ayrıca, bu model daha bir hipotezi test etmek gerekli hayvan sayısının artırılması, yüksek ölüm oranı ile ilişkilidir. Daha, tekrarlanabilir tutarlı, ve hayatta hakaret küresel iskemi ve / veya reperfüzyon için serebral yanıt incelenmesi tercih edilebilir. Sistemik kan akışını korurken global iskemi beyinde uyarılabilir. Investigatio izin verirken Bu, ölüm azaltırN beyin 2&#39;de doku hasarının mekanizmaları. Küresel beyin iskemi üretmek için, kesme veya büyük ölçüde beyin, internal karotid arter ve vertebral arter tedarik dört damarlarındaki akışı sınırlamak için gereklidir. Bu gemiler bir anastomoz döngü oluşturur Willis, Çemberi adı verilen bir damar yapısı ile kan akımı ile beyin kaynağı. Bu mimari, beyin damar proksimal damar tıkanması durumunda perfüzyon korumak sağlar. Bu nedenle, tüm katkı damarları aracılığıyla beyin, kan akışının tam iskemi ikna etmek için gerçekleşmelidir. Karotis arter tıkanıklığı istenen bir süre için anevrizma klip bir minimal invaziv ventral boyun cut-down ve uygulamasını kullanarak gerçekleştirilebilir. Onlar omurga enine foramen içinde incased olarak vertebral arter yoluyla kan akımının kesilmesi, zor olabilir. Araştırmacılar karotis önce vertebral arterler 24-48 saat electrocauterizing bu ele sahiptıkanıklığı ve beyin iskemi (4VO modeli) 15. Bu yaklaşımın aksine, Smith ve ark. Azaltarak küresel beyin iskemi uyararak kan akımı 2 kayıp ya da büyük ölçüde azalır bir noktaya vertebral damar yoluyla perfüzyon azaltmak için 40 mmHg için sistemik kan basıncı (MAP) ortalama bir yöntem geliştirdi . Karotis tıkanıklığı ile birleştiğinde, bu yöntem yakın kardiyak arrest hayatta bu taklit beyin hasarı bir model ile sonuçlanan, ön beyin boyunca iskemi üretir. Bu yöntemin daha rafine, biz burada mevcut modeli 30 mmHg sıkı HARİTASI düzenleme ± 1mHg iskemi tüm 8 dakika boyunca gerektirir. Biz Smith ve arkadaşları tarafından tasarlanan özgün tekniğin düşük ölüm oranı koruyarak bu değişiklik bu model neden olduğu beyin hasarı tekrarlanabilirlik artırır bulundu. Hücre ölümü ve doku hasarının genel ölçüde hassas fenotipi nedenBurada sunulan model iskemik süresi 16 doğrudan bağlıdır. CA1 nöronlar reperfüzyon aşamasında 15,17 sırasında terapötik müdahale için geçici bir pencere olduğunu düşündüren, hücre ölümü gecikmiş, iskemi 8 dk sergilenirken ardından. Reperfüzyon başlangıcında, nöronlar hızlı fonksiyonu yeniden ve hemen bir hücre ölümü 18 saptanabilir. Ancak bu hakaret neden hücre ölümü şelaleden indüksiyon (apoptoz) bu reperfüzyon 3,19 4-6 saat arasında sitokrom-c, dahil olmak üzere mitokondri gelen apoptogenic proteinlerin açıklaması, sonuçlanan. Reperfüzyon saat 6 ila 24, CA1 hipokampus nöron hücre ölümü işledikleri ve apoptotik hücre ölümü programı 19 yürütülür. Iskemik hasar sorumlu hücre ölümü fenotipi yüksek tartışmalı olduğu not edilmelidir. Diğer diğer apopt rapor ise ilk çalışmalarda, nekroz birincil hücre ölümü fenotip 20,21 olduğunu ileri sürmüşlerdirtemel mekanizma 22,23 olarak osis. Toplamda, mevcut kanıtlar hücreleri klasik apoptoz gelen nekroz arasında değişen hücre ölümü fenotipleri bir spektrum ölmek öneririz. Hücre ölümü belirli modu her fenotip katkı derecesini diğer faktörler 24,25 arasında, hakaret şiddetine bağlı olarak, birçok faktöre bağlıdır. Reperfüzyon 24 saat olarak, ölen hücrelerin piknotik çekirdekleri, toplu hücresel içeriğinin açık kanıtlar ile yoğun sitozolde ve fonksiyonel mitokondriyal morfolojisi kaybı sahip. Ölü hücreleri daha fazla, bozuldu gibi makrofajlar ve / veya mikroglia gibi bağışıklık hücreleri tarafından yuttu ve CA1 hipokampal bölgeden temizlenir. Reperfüzyon 4-7 gün ile, ölü hücreleri kaldırılmış ve bütün bu kalıntılar inflamatuar hücreler ve glial hücreler 17,26 aktif hale gelir. Bu nedenle, reperfüzyon ile 7 gün CA1 hippokampal nöronal ölümde, basit, spesifik olmayan hücre lekeleri kullanılarak belirlenebilir optimal zamanı temsil ederkresil mor veya hemotoksilen-eozin cluding ve morfolojik dahil kriterlere göre sayılır. Bu geç reperfüzyon aralıkta kalan hücreleri böylece beyin hasarı bir dizin sağlayarak, hayatta kalan hücreler olarak sayılabilir. Bu modeli tedavi yöntemlerinin belirlenmesi için kullanılmak üzere ise, deneysel tasarım MERDİVEN kriterleri (İnme Tedavi Akademik Sanayi Yuvarlak Masa) 27 takip önerilmektedir. Tasarımı ve bir çalışma yaparken bu yönergeleri takip edilmelidir, ancak burada ele değildir.

<table border="1">
 <tbody>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Material Name</td>
 </tr>
 <tr>
 <td>5-0 VICRYL suture, reverse cutting </td>
 <td>Ethicon</td>
 <td>J391H</td>
 <td></td>
 </tr>
 <tr>
 <td>Scalpel, No.10</td>
 <td>Swann-Morton</td>
 <td>6601</td>
 <td></td>
 </tr>
 <tr>
 <td>Gauze Sponges</td>
 <td>Fisher</td>
 <td>22-362-178</td>
 <td></td>
 </tr>
 <tr>
 <td>18G x 1 &frac12; in needle</td>
 <td>BD</td>
 <td>305201</td>
 <td></td>
 </tr>
 <tr>
 <td>23G x 1 in needle</td>
 <td>BD</td>
 <td>305145</td>
 <td></td>
 </tr>
 <tr>
 <td>26 G x 3/8 in needle</td>
 <td>BD</td>
 <td>305110</td>
 <td></td>
 </tr>
 <tr>
 <td>18 G x 1 &frac14; catheter</td>
 <td>EXEL</td>
 <td>26735</td>
 <td></td>
 </tr>
 <tr>
 <td>1 ml syringe</td>
 <td>BD</td>
 <td>309659</td>
 <td></td>
 </tr>
 <tr>
 <td>10 ml syringe</td>
 <td>BD</td>
 <td>309604</td>
 <td></td>
 </tr>
 <tr>
 <td>60 ml syringe</td>
 <td>BD</td>
 <td>309653</td>
 <td></td>
 </tr>
 <tr>
 <td>Surgilube</td>
 <td>Henry Schein</td>
 <td>1152666</td>
 <td></td>
 </tr>
 <tr>
 <td>.9% Saline, plastic IV bag</td>
 <td>Henry Schein</td>
 <td>1537468</td>
 <td></td>
 </tr>
 <tr>
 <td>Suture 3-0 Silk</td>
 <td>Henry Schein</td>
 <td>1007842</td>
 <td></td>
 </tr>
 <tr>
 <td>Puralube Ophthalmic Ointment</td>
 <td>Henry Schein</td>
 <td>3390017</td>
 <td></td>
 </tr>
 <tr>
 <td>Betadine</td>
 <td>Henry Schein</td>
 <td>6903564</td>
 <td></td>
 </tr>
 <tr>
 <td>Sterile Towel Drape</td>
 <td>Moore Medical</td>
 <td>14170</td>
 <td></td>
 </tr>
 <tr>
 <td>Polyethylene Tubing, 50</td>
 <td>Intramedic</td>
 <td>427411</td>
 <td></td>
 </tr>
 <tr>
 <td>Stopcock, 3 way</td>
 <td>Smiths medical</td>
 <td>MX9311L</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Drug Name</td>
 </tr>
 <tr>
 <td>AERRANE (isoflurane)</td>
 <td>Henry Schein</td>
 <td>2091966</td>
 <td></td>
 </tr>
 <tr>
 <td>Mapap Liquid (Tylenol)</td>
 <td>Major Pharmaceuticals</td>
 <td>1556</td>
 <td></td>
 </tr>
 <tr>
 <td>Kedavet (ketamine)</td>
 <td>Ketathesia Butney</td>
 <td>NDC 50989-996-06</td>
 <td></td>
 </tr>
 <tr>
 <td>Butorphic (butorphanol)</td>
 <td>Lloyd Labs</td>
 <td>4881</td>
 <td></td>
 </tr>
 <tr>
 <td>Heparin</td>
 <td>APP Pharmaceuticals</td>
 <td>504011</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Chemical Name </td>
 </tr>
 <tr>
 <td>Paraformaldehyde prills</td>
 <td>Elecron Microscopy Sci.</td>
 <td>19202</td>
 <td></td>
 </tr>
 <tr>
 <td>2-methylbutane</td>
 <td>Sigma</td>
 <td>270342</td>
 <td></td>
 </tr>
 <tr>
 <td>Cresyl Violet Acetate</td>
 <td>Sigma</td>
 <td>C5042</td>
 <td></td>
 </tr>
 <tr>
 <td>Sucrose</td>
 <td>Sigma</td>
 <td>S9378</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Software</td>
 </tr>
 <tr>
 <td>ImageJ</td>
 <td>NIH</td>
 <td></td>
 <td></td>
 </tr>
 </tbody>
</table>

2-vessel occlusion/hypotension: a rat model of global brain ischemia

Resüsitasyon takip Kardiyak arrest genellikle iskemi ve beynin sonraki reperfüzyon kaynaklanan dramatik beyin hasarı ile sonuçlanır. Küresel beyin iskemi iskemi 1 son derece duyarlı olduğu gösterilmiştir belirli beyin bölgelerinin zarar üretir. Hipokampal nöronlar özellikle diğer hücre popülasyonlarının ve göre iskemik hakaret daha yüksek duyarlılığa sahip, hipokampus CA1 bölgesinde iskemi / reperfüzyon 2 özellikle savunmasızdır. Terapötik girişimlerin, ya da beyin hasarı dahil mekanizmalarının çalışması, tasarımı klinik durumu benzer ve tekrarlanabilir bir şekilde zarar üreten bir model gerektirir. Hipotansiyon ile iki taraflı karotis damar tıkanıklığı (2VOH) kardiyak arrest ve resüsitasyon sırasında oluşabilir serebral olaylar taklit, geri ön beyin iskemi üreten bir modeldir. Biz, Smith ve ark değiştirilmiş bir modeli açıklar. (1984) 2, Ilk olarak Sanderson ve ark. (2008) 3, seçici hassas beyin bölgelerinde 3-6 tekrarlanabilir yaralanma üreten mevcut haliyle sunulmaktadır. Bu modelin güvenilirliği uygulanan hipotansiyon, iskemi süresi, yakın sıcaklık kontrolü, belirli bir anestezi rejimi ve çalışkan ameliyat sonrası bakım sırasında sistemik kan basıncı hassas kontrolü ile belirlenir. Daha az hassas beyin bölgelerinde kurtulmuş ise 8 dakikalık bir iskemik hakaret, reperfüzyon 6 ile 24 saat boyunca ilerler CA1 hipokampal nöron hücre ölümü üretir. Bu aşamalı hücre ölümü kolayca CA1 nöronlarının yakın tam kaybı bu zamanda belirgin olduğu gibi, reperfüzyon ile 7-14 gün sonra ölçülür. Bu beyin hasarı modele ek olarak, basit ama kapsamlı, metodoloji kullanılarak CA1 zarar miktarının tayini için bir yöntem mevcut. Önemlisi, miktar bir, basit bir kamera monte mikroskop kullanılarak gerçekleştirilebilirda ücretsiz ImageJ (NIH) yazılım eklentisi, maliyet-engelleyici stereology yazılım programları için ihtiyaç ve hasar tespit için motorlu bir mikroskobik sahne kalmayabilir.

Genel bir beyin iskemi / reperfüzyon 2VOH modeli hipokampusun CA1 bölgesinde nöronal ölüme neden olur. Şekil 2, 14 gün sonra, reperfüzyon işleme genel bir beyin iskemisi 8 dak, tarafından üretilen hasarı temsil eder. Şekiller 2A ve 2B, plasebo arasındaki hipokampi karşılaştırarak kresil violet ile boyandı sonrası iskemik beyin,. Şekil 2A sağlam CA1 dahil olmak üzere, normal morfoloji sergileyen bir sahte operasyona sıçan bir hip...

Watch this Scientific Journal Video about 2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia at JoVE.com

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

Sistemik hipotansiyon ile birlikte iki taraflı karotis tıkanıklığı tekrarlanabilir şiddeti ile hipokampus hasar görebilir, sıçan küresel beyin iskemi üretir. Hayvanlar üzerinde beyin hasarı tahmin modelleri ile engelli, onlar expediently kurtarmak ve ölüm oranları nispeten düşüktür.

2-Gemi Tıkanıklığı / Hipotansiyon: Küresel Beyin İskemi Rat Modeli

Cardiac arrest followed by resuscitation often results in dramatic brain damage caused by ischemia and subsequent reperfusion of the brain. Global brain ...

2-vessel-occlusionhypotension-a-rat-model-of-global-brain-ischemia

Research

JoVE Journal

Medicine

19.8K Görüntüleme.  Wayne State University School of Medicine. Sistemik hipotansiyon ile birlikte iki taraflı karotis tıkanıklığı tekrarlanabilir şiddeti ile hipokampus hasar görebilir, sıçan küresel beyin iskemi üretir. Hayvanlar üzerinde beyin hasarı tahmin modelleri ile engelli, onlar expediently kurtarmak ve ölüm oranları nispeten düşüktür.

Video: 2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

MRI-guided Disruption of the Blood-brain Barrier using Transcranial Focused Ultrasound in a Rat Model

Focused ultrasound (FUS) disruption of the blood-brain barrier (BBB) is an increasingly investigated technique for circumventing the BBB1-5. The BBB is a significant obstacle to pharmaceutical treatments of brain disorders as it limits the passage of molecules from the vasculature into the brain tissue to molecules less than approximately 500 Da in size6. FUS induced BBB disruption (BBBD) is temporary and reversible4 and has an advantage over chemical means of inducing BBBD by being highly localized. FUS induced BBBD provides a means for investigating the effects of a wide range of therapeutic agents on the brain, which would not otherwise be deliverable to the tissue in sufficient concentration. While a wide range of ultrasound parameters have proven successful at disrupting the BBB2,5,7, there are several critical steps in the experimental procedure to ensure successful disruption with accurate targeting. This protocol outlines how to achieve MRI-guided FUS induced BBBD in a rat model, with a focus on the critical animal preparation and microbubble handling steps of the experiment.

Microbubble-mediated focused ultrasound disruption of the blood-brain barrier (BBB) is a promising technique for non-invasive targeted drug delivery in the brain1-3. This protocol outlines the experimental procedure for MRI-guided transcranial BBB disruption in a rat model.

Sıçan Modelinde Transkraniyal Odaklanmış Ultrason kullanarak Kan-beyin bariyeri MRG eşliğinde bozulması

Focused ultrasound (FUS) disruption of the blood-brain barrier (BBB) is an increasingly investigated technique for circumventing the BBB1-5. The BBB is a ...

Tıp

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.

Miyokard İskemi ve Reperfüzyon bir Mürin Kapalı göğüs Modeli

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

Rat Model of Blood-brain Barrier Disruption to Allow Targeted Neurovascular Therapeutics

Endothelial cells with tight junctions along with the basement membrane and astrocyte end feet surround cerebral blood vessels to form the blood-brain barrier1. The barrier selectively excludes molecules from crossing between the blood and the brain based upon their size and charge. This function can impede the delivery of therapeutics for neurological disorders. A number of chemotherapeutic drugs, for example, will not effectively cross the blood-brain barrier to reach tumor cells2. Thus, improving the delivery of drugs across the blood-brain barrier is an area of interest.
The most prevalent methods for enhancing the delivery of drugs to the brain are direct cerebral infusion and blood-brain barrier disruption3. Direct intracerebral infusion guarantees that therapies reach the brain; however, this method has a limited ability to disperse the drug4. Blood-brain barrier disruption (BBBD) allows drugs to flow directly from the circulatory system into the brain and thus more effectively reach dispersed tumor cells. Three methods of barrier disruption include osmotic barrier disruption, pharmacological barrier disruption, and focused ultrasound with microbubbles. Osmotic disruption, pioneered by Neuwelt, uses a hypertonic solution of 25% mannitol that dehydrates the cells of the blood-brain barrier causing them to shrink and disrupt their tight junctions. Barrier disruption can also be accomplished pharmacologically with vasoactive compounds such as histamine5 and bradykinin6. This method, however, is selective primarily for the brain-tumor barrier7. Additionally, RMP-7, an analog of the peptide bradykinin, was found to be inferior when compared head-to-head with osmotic BBBD with 25% mannitol8. Another method, focused ultrasound (FUS) in conjunction with microbubble ultrasound contrast agents, has also been shown to reversibly open the blood-brain barrier9. In comparison to FUS, though, 25% mannitol has a longer history of safety in human patients that makes it a proven tool for translational research10-12.
In order to accomplish BBBD, mannitol must be delivered at a high rate directly into the brain's arterial circulation. In humans, an endovascular catheter is guided to the brain where rapid, direct flow can be accomplished. This protocol models human BBBD as closely as possible. Following a cut-down to the bifurcation of the common carotid artery, a catheter is inserted retrograde into the ECA and used to deliver mannitol directly into the internal carotid artery (ICA) circulation. Propofol and N2O anesthesia are used for their ability to maximize the effectiveness of barrier disruption13. If executed properly, this procedure has the ability to safely, effectively, and reversibly open the blood-brain barrier and improve the delivery of drugs that do not ordinarily reach the brain 8,13,14.

Blood-brain barrier disruption aids the delivery of certain drugs to the brain. Mannitol delivered intra-arterially shrinks cells surrounding blood vessels in order to physically disrupt the barrier.

Kan-beyin bariyer bozulması arasında Rat Modeli Nörovasküler Therapeutics Hedefli izin ver için

Endothelial cells with tight junctions along with the basement membrane and astrocyte end feet surround cerebral blood vessels to form the blood-brain ...

In situ Transverse Rectus Abdominis Myocutaneous Flap: A Rat Model of Myocutaneous Ischemia Reperfusion Injury

Free tissue transfer is the gold standard of reconstructive surgery to repair complex defects not amenable to local options or those requiring composite tissue. Ischemia reperfusion injury (IRI) is a known cause of partial free flap failure and has no effective treatment. Establishing a laboratory model of this injury can prove costly both financially as larger mammals are conventionally used and in the expertise required by the technical difficulty of these procedures typically requires employing an experienced microsurgeon. This publication and video demonstrate the effective use of a model of IRI in rats which does not require microsurgical expertise. This procedure is an in situ model of a transverse abdominis myocutaneous (TRAM) flap where atraumatic clamps are utilized to reproduce the ischemia-reperfusion injury associated with this surgery. A laser Doppler Imaging (LDI) scanner is employed to assess flap perfusion and the image processing software, Image J to assess percentage area skin survival as a primary outcome measure of injury.

In situ Transverse Rectus Abdominis Myocutaneous Flap: A Rat Model of Myocutaneous Ischemia Reperfusion Injury

Free tissue transfer is widely employed in reconstructive surgery to restore form and function following oncological resection and trauma. Preconditioning this tissue prior to surgery may improve outcome. This article describes an in situ transverse rectus abdominis myocutaneous flap (TRAM) in rats as a means for testing preconditioning strategies.

Miyokutanöz İskemi Reperfüzyon Hasarı Rat Modeli: in situ Enine Rektus abdominis kas deri Flap

Free tissue transfer is the gold standard of reconstructive surgery to repair complex defects not amenable to local options or those requiring composite ...

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Ischemia-Reperfusion (IR) injury is known to contribute significantly to the morbidity and mortality associated with ischemic strokes. Ischemic cerebrovascular accidents account for 80% of all strokes. A common cause of IR injury is the rapid inflow of fluids following an acute/chronic occlusion of blood, nutrients, oxygen to the tissue triggering the formation of free radicals.
Ischemic stroke is followed by blood-brain barrier (BBB) dysfunction and vasogenic brain edema. Structurally, tight junctions (TJs) between the endothelial cells play an important role in maintaining the integrity of the blood-brain barrier (BBB). IR injury is an early secondary injury leading to a non-specific, inflammatory response. Oxidative and metabolic stress following inflammation triggers secondary brain damage including BBB permeability and disruption of tight junction (TJ) integrity.
Our protocol presents an in vitro example of oxygen-glucose deprivation and reoxygenation (OGD-R) on rat brain endothelial cell TJ integrity and stress fiber formation. Currently, several experimental in vivo models are used to study the effects of IR injury; however they have several limitations, such as the technical challenges in performing surgeries, gene dependent molecular influences and difficulty in studying mechanistic relationships. However, in vitro models may aid in overcoming many of those limitations. The presented protocol can be used to study the various molecular mechanisms and mechanistic relationships to provide potential therapeutic strategies. However, the results of in vitro studies may differ from standard in vivo studies and should be interpreted with caution.

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Ischemia-Reperfusion (IR) injury is associated with a high rate of morbidity and mortality. The goal of the in vitro model of oxygen-glucose deprivation and reoxygenation (OGD-R) described here is to assess the effects of ischemia reperfusion injury on a variety of cells, particularly in blood-brain barrier (BBB) endothelial cells.

Bir oksijen-Glukoz Yoksunluk ve reoksijenizasyonun<em&gt; In Vitro</em&gt; İskemi-Reperfüzyon Modeli incelenmesi Kan-Beyin Bariyeri Disfonksiyon için

Ischemia-Reperfusion (IR) injury is known to contribute significantly to the morbidity and mortality associated with ischemic strokes. Ischemic ...

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Stroke research has endured many setbacks in translating neuroprotective therapies into clinical practice. In contrast, the real-world therapy (tPA thrombolysis) rarely produces benefits in mechanical occlusion-based experimental models, which dominate preclinical stroke research. This split between the bench and bedside suggests the need to employ tPA-responsive models in preclinical stroke research. To this end, a simple and tPA-reactive thrombotic stroke model is invented and described here. This model consists of transient occlusion of the unilateral common carotid artery and delivery of 7.5% oxygen through a face mask in adult mice for 30 min, while maintaining the animal rectal temperature at 37.5 &#177; 0.5 &#176;C. Although reversible ligation of the unilateral carotid artery or hypoxia each suppressed cerebral blood flow only transiently, the combination of both insults caused lasting reperfusion deficits, fibrin and platelet deposition, and large infarct in the middle cerebral artery-supplied territory. Importantly, tail-vein injection of recombinant tPA at 0.5, 1, or 4 hr post-tHI (10 mg/kg) provided time-dependent reduction of the mortality rate and infarct size. This new stroke model is simple and can be standardized across laboratories to compare experimental results. Further, it induces thrombosis without craniectomy or introducing pre-formed emboli. Given these unique merits, the tHI model is a useful addition to the repertoire of preclinical stroke research.

Thromboembolic stroke models are vital tools for optimizing the recanalization therapy. Here we report a murine thrombotic stroke model based on transient cerebral hypoxic-ischemic (tHI) insult, which triggers thrombosis and infarction, and responds favorably to tissue plasminogen activator (tPA)-mediated fibrinolysis in a therapeutic window similar to those in stroke patients.

Geçici Serebral Hipoksi-iskemi Dayalı Bir Trombotik İnme Modeli

Stroke research has endured many setbacks in translating neuroprotective therapies into clinical practice. In contrast, the real-world therapy (tPA ...

Reproducible Motor Deficit Following Aortic Occlusion in a Rat Model Of Spinal Cord Ischemia

Spinal cord ischemia is a fatal complication following thoracoabdominal aortic aneurysm surgery. Researchers can investigate the strategies for preventing and treating this complication using experimental models of spinal cord ischemia. The model described here demonstrates varying degrees of paraplegia that relate to the length of occlusion following thoracic aortic occlusion in a rat spinal cord ischemia model.
A 2-Fr. balloon-tipped catheter was advanced through the femoral artery into the descending thoracic aorta until the catheter tip was placed at the left subclavian artery in anesthetized male Sprague-Dawley rats. Spinal cord ischemia was induced by inflating the catheter balloon. After a set period of occlusion (9, 10, or 11 min), the balloon was deflated. Neurologic assessment was performed using the motor deficit index at 24 h after surgery, and the spinal cord was harvested for histopathological examination.
Rats that underwent 9 min of aortic occlusion showed mild and reversible motor impairment in the hind limb. Rats subjected to 10 min of aortic occlusion presented with moderate but reversible motor impairment. Rats subjected to 11 min of aortic occlusion displayed complete and persistent paralysis. The motor neurons in the spinal cord sections were more preserved in rats subjected to shorter duration of aortic occlusion.
Researchers can achieve a reproducible hind limb motor deficit following thoracic aortic occlusion using this spinal cord ischemia model.

This study demonstrates the technique to make a minimally invasive and easily reproducible model of spinal cord ischemia in rats. Various degrees of hind limb motor deficit can be produced by controlling the aortic occlusion time.

Spinal Kord İskemisinin Sıçan Modelinde Aortik Oklüzyon Sonrası Tekrarlanabilir Motor Bozukluğu

Spinal cord ischemia is a fatal complication following thoracoabdominal aortic aneurysm surgery. Researchers can investigate the strategies for preventing ...

Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia

Critical limb ischemia (CLI) is a serious condition that entails a high risk of lower limb amputation. Despite revascularization being the gold-standard therapy, a considerable number of CLI patients are not suited for either surgical or endovascular revascularization. Angiogenic therapies are emerging as an option for these patients but are currently still under investigation. Before application in humans, those therapies must be tested in animal models and its mechanisms must be clearly understood. An animal model of hindlimb ischemia (HLI) has been developed by the ligation and excision of the distal external iliac and femoral arteries and veins in mice. A comprehensive panel of tests was assembled to assess the effects of ischemia and putative angiogenic therapies at functional, histologic and molecular levels. Laser Doppler was used for the flow measurement and functional assessment of perfusion. Tissue response was evaluated by the analysis of capillary density after staining with the anti-CD31 antibody on histological sections of gastrocnemius muscle and by measurement of collateral vessel density after diaphonization. Expression of angiogenic genes was quantified by RT-PCR targeting selected angiogenic factors exclusively in endothelial cells (ECs) after laser capture microdissection from mice gastrocnemius muscles. These methods were sensitive in identifying differences between ischemic and non-ischemic limbs and between treated and non-treated limbs. This protocol provides a reproducible model of CLI and a framework for testing angiogenic therapies.

Here, a critical hindlimb ischemia experimental model is presented followed by a battery of functional, histologic and molecular tests&#160;to assess the effectiveness of angiogenic therapies.&#8203;

Hindekstremite Iskemi bir Murine modelinde terapötik anjiyogenezi değerlendirilmesi

Critical limb ischemia (CLI) is a serious condition that entails a high risk of lower limb amputation. Despite revascularization being the gold-standard ...

A Pre-clinical Rat Model for the Study of Ischemia-reperfusion Injury in Reconstructive Microsurgery

Ischemia-reperfusion injury is the main cause of flap failure in reconstructive microsurgery. The rat is the preferred preclinical animal model in many areas of biomedical research due to its cost-effectiveness and its translation to humans. This protocol describes a method to create a preclinical free skin flap model in rats with ischemia-reperfusion injury. The described 3 cm x 6 cm rat free skin flap model is easily obtained after the placement of several vascular ligatures and the section of the vascular pedicle. Then, 8 h after the ischemic insult and completion of the microsurgical anastomosis, the free skin flap develops the tissue damage. These ischemia-reperfusion injury-related damages can be studied in this model, making it a suitable model for evaluating therapeutic agents to address this pathophysiological process. Furthermore, two main monitoring techniques are described in the protocol for the assessment of this animal model: transit-time ultrasound technology and laser speckle contrast analysis.

Here, we describe a pre-clinical animal model for studying the pathophysiology of ischemia-reperfusion injury in reconstructive microsurgery. This free skin flap model based on the superficial caudal epigastric vessels in the rat may also allow for the evaluation of different therapies and compounds to counteract ischemia-reperfusion injury-related damage.

Rekonstrüktif Mikrocerrahide İskemi-Reperfüzyon Hasarı Nın İnceleştirilmesinde Klinik Öncesi Sıçan Modeli

Ischemia-reperfusion injury is the main cause of flap failure in reconstructive microsurgery. The rat is the preferred preclinical animal model in many ...

Acupuncture in a Rat Model of Asthma

A high platform can fix rats without restriction and completely expose the acupoints on the back during acupuncture manipulation. This article describes methods for the fabrication of the high platform, establishes a rat model of asthma and measures changes in respiratory function using a noninvasive and real-time whole-body plethysmography (WBP) system.

Astımın Sıçan Modelinde Akupunktur

A high platform can fix rats without restriction and completely expose the acupoints on the back during acupuncture manipulation. This article describes ...