The authors would like to acknowledge Dr. Wanchun Tang MD, MCCM, FCCP, FAHA and Jena Cahoon of the Weil Institute of Critical Care Medicine in Rancho Mirage, CA. for their contributions to the resuscitation protocol outline and for having helped train the rodent surgeon (LL). The preparation of this article was in part supported by a gift in memory of US Navy Retired SKC Robert W. Ply by Ms. Monica Ply for research in heart disease and Parkinson&#8217;s disease and by a discretionary fund from the Department of Medicine at Rosalind Franklin University of Medicine and Science.

The authors have nothing to disclose.

Protokol Kritik Adımlar Protokol kritik adımlar vardır. Hakim olduğunda, hazırlık ve protokol olarak kısaca aşağıda açıklanmıştır ilerleyiniz. Cerrahi hazırlık tek veya birkaç girişimi (ler) sonra başarılı entübasyon ardından, az ya da hiç damar spazmı tetikleyen ve amaçlandığı gibi kateter ipuçları konumlandırma küçük kesiler yoluyla hızla ilerleyen kateter, süratli şekilde; Bu şekilde, bir referans değerler arasında temel ölçümler <stro...

Amerika Birleşik Devletleri&#39;nde 1 360,000 kişiye yakın ve daha dünyada 2 Birçok ani kardiyak arrest bir bölüm her yıl muzdarip. Sadece kardiyak aktivite yeniden tesis edilmesi ancak hayati organlara zarar veren, önlenebilir minimize veya iptal edilemez gerektiren hayatı geri girişimleri. Güncel kardiyopulmoner resüsitasyon teknikleri yaklaşık% 30 bir başlangıç ​​resüsitasyon oranı elde; Ancak, hastane taburcu hayatta kalma sadece% 5 1. Miyokard disfonksiyonu, nörolojik disfonksiyon, sistemik inflamasyon, araya giren hastalıklar, ya da dolaşım ilk karşılığında rağmen ölmektedir hastaların büyük bir kısmı için resüsitasyon sonrası hesabı meydana bunların bir kombinasyonu. Böylece, fizyopatolojisi ve yeni resüsitasyon yaklaşımları daha büyük bir anlayış acilen ilk resüsitasyon ve sağlam bir organ fonksiyonu ile daha sonraki hayatta kalma oranını arttırmak için gereklidir. Hayvan modukardiyak arrest ls kardiyak arrest ve resüsitasyon patofizyolojisi üzerine anlayışlar ve kavramsallaştırma ve insanlarda 3 test edilebilir önce yeni müdahaleleri test etmek için pratik bir araç sunarak yeni resüsitasyon tedavilerin geliştirilmesinde önemli bir rol oynamaktadır. kapalı göğüs kardiyopulmoner resüsitasyon sıçan modeli (CPR) burada açıklanan önemli bir rol oynamıştır. Geç Profesör Max Harry Weil MD, Ph.D. laboratuvarda 4 ve onun işbirlikçileri - anda araştırma görevlisi - modeli Irene von Planta tarafından 1988 yılında geliştirilen Sağlık Bilimleri Üniversitesi (2004 yılında Tıp ve Bilim, Rosalind Franklin Üniversitesi olarak değiştirildi) ve yaygın ağırlıklı Profesör Weil ve kursiyerlerin arkadaşlarının tarafından resüsitasyon alanında kullanılmaktadır. Model geleneksel CPR teknikleri ile teşebbüs resüsitasyon ile ani kalp durması bir bölüm taklit ve böylece askere içerireş zamanlı oksijen zenginleştirilmiş gaz ile pozitif basınçlı ventilasyon sunarken bir pnömatik tahrik piston cihazı ile sağ ventrikül endokarda ve kapalı göğüs CPR sağlanması için elektrik akımı vererek ventriküler fibrilasyon (VF) iyon. VF Fesih elektrik şoku transtorasik teslim gerçekleştirilir. sıçan modeli küçük hayvanlarda geliştirilen büyük hayvanlar (örneğin, domuz) ve modellerde geliştirilen modeller arasında bir denge (örneğin, fareler) sağlam erişimi olan bir iyi-standardize tekrarlanabilir ve verimli bir şekilde yeni araştırma kavramları keşif izin ilgili ölçümlerin envanter. Model, ancak daha büyük bir translasyon etkisi, daha pahalı olan büyük hayvan modellerinde çalışmalar yapmadan önce karıştırıcıların etkilerini yeni kavramlar araştırmak ve incelemek için araştırmaya erken aşamalarında özellikle yararlıdır. Tüm hakemli makaleler gibi raporlama için bir Medline aramailk 1988 4 yılında yayımlandığı tarihten itibaren kardiyak arrest mekanizması ve kapalı göğüs resüsitasyon çeşit olarak VF sahip imilar sıçan modeli modeli kullanılarak 69 ek orijinal çalışmalar toplam görüldü. Araştırma alanları resüsitasyon 5-17 patofizyolojik yönlerini içermektedir, sonuçları 18-30 etkileyen faktörler, vazopressör ajanlar 31-43, tampon maddeleri inceleyerek farmakolojik müdahalelerin rolü 44, inotropik ajanlar 45, miyokard veya serebral koruma 46-70 yönelik ajanlar, ve aynı zamanda mezenkimal kök hücrelerin 71-73 etkileri. Bu makalede açıklanan model ve protokol şu anda Resüsitasyon Enstitüsü&#39;nde kullanılmaktadır. Ancak, bireysel araştırmacılar ve çalışmaların hedefleri mevcut yetenekleri dayalı modeli &quot;özelleştirmek&quot; birden fazla fırsatlar vardır.

<table><tbody><tr><td>Sodium pentobarbital</td><td>Sigma Aldrich</td><td>P3761</td><td>http://www.sigmaaldrich.com/catalog/product/sigma/p3761?lang=en&amp;amp;region=US</td></tr><tr><td>Rectal thermistor</td><td>BIOPAC Systems, INC</td><td>TSD202A</td><td>http://www.biopac.com/fast-response-thermistor</td></tr><tr><td>Needle electrode biopolar concentric 25 mm TP</td><td>BIOPAC Systems, INC</td><td>EL451</td><td>http://www.biopac.com/needle-electrode-concentric-25mm</td></tr><tr><td>PE25 polyethylene tubing&amp;nbsp;</td><td>Solomon Scientific</td><td>BPE-T25</td><td>http://www.solsci.com/products/polyethylene-pe-tubing</td></tr><tr><td>26GA female luer stub adapter</td><td>Access Technologies</td><td>LSA-26</td><td>http://www.norfolkaccess.com/needles.html</td></tr><tr><td>Stopcocks with luer connections; 3-way; male lock, non-sterile</td><td>Cole-Parmer</td><td>UX-30600-02</td><td>http://www.coleparmer.com/Product/Large_bore_3_way&lt;br/&gt; _male_lock_stopcocks&lt;br/&gt; _10_pack_Non_sterile/EW-30600-23</td></tr><tr><td>TruWave disposable pressure transducer</td><td>Edwards Lifesciences</td><td>PX600I&amp;nbsp;</td><td>http://www.edwards.com/products/pressuremonitoring/Pages/truwavemodels.aspx?truwave=1</td></tr><tr><td>Type-T thermocouple</td><td>Physitemp Instruments</td><td>IT-18</td><td>http://www.physitemp.com/products/probesandwire/flexprobes.html</td></tr><tr><td>Central venous pediatric catheter&amp;nbsp;</td><td>Cook Medical&amp;nbsp;</td><td>C-PUM-301J</td><td>https://www.cookmedical.com/product/-/catalog/display?ds=cc_pum1lp_webds</td></tr><tr><td>Abbocath-T subclavian I.V. catheter (14 g x 5 1/2&quot;)</td><td>Hospira</td><td>453527</td><td>http://www.hospira.com/products_and_services/iv_sets/045350427</td></tr><tr><td>Novametrix Medical Systems, Infrared CO2 monitor</td><td>Soma Technology, Inc.</td><td>7100 CO2SMO&amp;nbsp;</td><td>http://www.somatechnology.com/MedicalProducts/novametrix_respironics_co2smo_&lt;br/&gt; 7100.asp</td></tr><tr><td>Harvard Model 683 small animal ventilator</td><td>Harvard Apparatus</td><td>555282</td><td>http://www.harvardapparatus.com/webapp/wcs/stores/servlet/haisku2_10001_11051_44453_-1_&lt;br/&gt; HAI_ProductDetail_N_37322_37323</td></tr><tr><td>Double-flexible tipped wire guides</td><td>Cook Medical&amp;nbsp;</td><td>C-DOC-15-40-0-2</td><td>https://www.cookmedical.com/product/-/catalog/display?ds=cc_doc_webds</td></tr><tr><td>High accuracy AC LVDT displacement sensor</td><td>Omega Engineering</td><td>LD320-25</td><td>http://www.omega.com/pptst/LD320.html</td></tr><tr><td>HeartStart XL defibrillator/monitor</td><td>Phillips Medical Systems</td><td>M4735A</td><td>http://www.healthcare.philips.com/main/products/resuscitation/products/xl/</td></tr><tr><td>Graefe micro dissection forceps 4 inches</td><td>Roboz&amp;nbsp;</td><td>RS-5135</td><td>http://shopping.roboz.com/Surgical-Instrument-Online-Shopping?search=RS-5135</td></tr><tr><td>Graefe micro dissection forceps 4 inches with teeth</td><td>Roboz&amp;nbsp;</td><td>RS-5157</td><td>http://shopping.roboz.com/Surgical-Instrument-Online-Shopping?search=RS-5157</td></tr><tr><td>Extra fine micro dissection scissors 4 inches</td><td>Roboz&amp;nbsp;</td><td>RS-5882</td><td>http://shopping.roboz.com/micro-scissors-micro-forceps-groups/micro-dissecting-scissors/Micro-Dissecting-Scissors-4-Straight-Sharp-Sharp</td></tr><tr><td>Heiss tissue retractor</td><td>Fine Science Tools&amp;nbsp;</td><td>17011-10</td><td>http://www.finescience.com/Special-Pages/Products.aspx?ProductId=321&amp;amp;CategoryId=134&amp;amp;&lt;br/&gt; lang=en-US</td></tr><tr><td>Crile curve tip hemostats</td><td>Fine Science Tools&amp;nbsp;</td><td>13005-14</td><td>http://www.finescience.com/Special-Pages/Products.aspx?ProductId=372</td></tr><tr><td>Visistat skin stapler&amp;nbsp;</td><td>Teleflex Incorporated</td><td>528135</td><td>http://www.teleflexsurgicalcatalog.com/weck/products/9936</td></tr><tr><td>Braided silk suture, 3-0</td><td>Harvard Apparatus</td><td>517706</td><td>http://www.harvardapparatus.com/webapp/wcs/stores/servlet/haisku2_10001_11051_43051_-1_&lt;br/&gt; HAI_ProductDetail_N_37916_37936</td></tr><tr><td>Betadine solution</td><td>Butler Schein</td><td>3660</td><td>https://www.henryscheinvet.com/</td></tr><tr><td>Sterile saline, 250 ml bags</td><td>Fisher</td><td>50-700-069</td><td>http://www.fishersci.com/ecomm/servlet/itemdetail?catnum=50700069&amp;amp;storeId=10652</td></tr><tr><td>Heparin sodium injection, USP</td><td>Fresenius Kabi</td><td>504201</td><td>http://fkusa-products-catalog.com/files/assets/basic-html/page25.html</td></tr><tr><td>Loxicom (meloxicam)</td><td>Butler Schein</td><td>045-321</td><td>https://www.henryscheinvet.com/</td></tr><tr><td>Thermodilution cardiac output computer for small animals</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Resuscitation Institute using National Instruments hardware and LabVIEW software</td></tr><tr><td>Analog-to-digital data acquisition and analysis system</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Resuscitation Institute using National Instruments hardware and LabVIEW software</td></tr><tr><td>Pneumatically-driven and electronically controlled piston device for chest compression in small animals</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Weil Institute of Critical Care Medicine</td></tr><tr><td>60 Hz alternating current generator</td><td>N/A</td><td>N/A</td><td>Custom-developed at the Weil Institute of Critical Care Medicine</td></tr></tbody></table>

a rat model of ventricular fibrillation and resuscitation by conventional closed-chest technique

A rat model of electrically-induced ventricular fibrillation followed by cardiac resuscitation using a closed chest technique that incorporates the basic components of cardiopulmonary resuscitation in humans is herein described. The model was developed in 1988 and has been used in approximately 70 peer-reviewed publications examining a myriad of resuscitation aspects including its physiology and pathophysiology, determinants of resuscitability, pharmacologic interventions, and even the effects of cell therapies. The model featured in this presentation includes: (1) vascular catheterization to measure aortic and right atrial pressures, to measure cardiac output by thermodilution, and to electrically induce ventricular fibrillation; and (2) tracheal intubation for positive pressure ventilation with oxygen enriched gas and assessment of the end-tidal CO2. A typical sequence of intervention entails: (1) electrical induction of ventricular fibrillation, (2) chest compression using a mechanical piston device concomitantly with positive pressure ventilation delivering oxygen-enriched gas, (3) electrical shocks to terminate ventricular fibrillation and reestablish cardiac activity, (4) assessment of post-resuscitation hemodynamic and metabolic function, and (5) assessment of survival and recovery of organ function. A robust inventory of measurements is available that includes &#8211; but is not limited to &#8211; hemodynamic, metabolic, and tissue measurements. The model has been highly effective in developing new resuscitation concepts and examining novel therapeutic interventions before their testing in larger and translationally more relevant animal models of cardiac arrest and resuscitation.

Burada anlatılan sıçan modeli son zamanlarda göğüs sıkıştırma ve post-resüsitasyon sırasında 61 miyokard ve hemodinamik fonksiyonu üzerindeki sarkolemmal sodyum-hidrojen değiştirici izoformu 1 (NHE-1) iki inhibitörlerinin etkilerini karşılaştırmak için kullanıldı. Daha önce NHE-1 inhibitörleri sodyum kaynaklı sitozolik ve mitokondriyal kalsiyum aşırı sınırlayarak miyokard reperfüzyon hasarı zayıflatır, ve böylece göğüs sıkıştırma sırasında sol ventrikül genişley...

Watch this Scientific Journal Video about A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique at JoVE.com

A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique

This article describes a rat model of electrically-induced ventricular fibrillation and resuscitation by chest compression, ventilation, and delivery of electrical shocks that simulates an episode of sudden cardiac arrest and conventional cardiopulmonary resuscitation. The model enables gathering insights on the pathophysiology of cardiac arrest and exploration of new resuscitation strategies.

Konvansiyonel Kapalı göğüs Tekniği ile Rat Ventriküler Fibrilasyon Modeli ve Resüsitasyon

A rat model of electrically-induced ventricular fibrillation followed by cardiac resuscitation using a closed chest technique that incorporates the basic ...

a-rat-model-ventricular-fibrillation-resuscitation-conventional

Universidad de Cartagena UDEC

Research

JoVE Journal

Medicine

15.8K Görüntüleme.  Rosalind Franklin University of Medicine and Science. This article describes a rat model of electrically-induced ventricular fibrillation and resuscitation by chest compression, ventilation, and delivery of electrical shocks that simulates an episode of sudden cardiac arrest and conventional cardiopulmonary resuscitation. The model enables gathering insights on the pathophysiology of cardiac arrest and exploration of new resuscitation strategies.

Video: A Rat Model of Ventricular Fibrillation and Resuscitation by Conventional Closed-chest Technique

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.

Normotermik Kardiyak Arrest ve Kardiyopulmoner Resusitasyon: İskemi-Reperfüzyon Hasarı Fare Modeli

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 ...

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 ...

Testing the Efficacy of Pharmacological Agents in a Pericardial Target Delivery Model in the Swine

To date, many pharmacological agents used to treat or prevent arrhythmias in open-heart cases create undesired systemic side effects. For example, antiarrhythmic drugs administered intravenously can produce drops in systemic pressure in the already compromised cardiac patient. While performing open-heart procedures, surgeons will often either create a small port or form a pericardial cradle to create suitable fields for operation. This access yields opportunities for target pharmacological delivery (antiarrhythmic or ischemic preconditioning agents) directly to the myocardial tissue without undesired side effects.
We have developed a swine model for testing pharmacological agents for target delivery within the pericardial fluid. While fully anesthetized, each animal was instrumented with a Swan-Ganz catheter as well as left and right ventricle pressure catheters, and pacing leads were placed in the right atrial appendage and the right ventricle. A medial sternotomy was then performed and a pericardial access cradle was created; a plunge pacing lead was placed in the left atrial appendage and a bipolar pacing lead was placed in the left ventricle. Utilizing a programmer and a cardiac mapping system, the refractory period of the atrioventricular node (AVN), atria and ventricles was determined. In addition, atrial fibrillation (AF) induction was produced utilizing a Grass stimulator and time in AF was observed. These measurements were performed prior to treatment, as well as 30 min&#160;and 60 min&#160;after pericardial treatment. Additional time points were added for selected studies. The heart was then cardiopleged and reanimated in a four chamber working mode. Pressure measurements and function were recorded for 1 hr after reanimation. This treatment strategy model allowed us to observe the effects of pharmacological agents that may decrease the incidence of cardiac arrhythmias and/or ischemic damage, during and after open-heart surgery.

We have developed a swine model for the target delivery of pharmacological agents within the pericardial space/fluid. Using this approach, the relative benefits of administered agents on induced atrial fibrillation, relative refractory periods and/or ischemic protection can be investigated.

Domuzda bir perikard Hedef Teslim Modelinde Farmakolojik Ajanlar Etkilerinin Test

To date, many pharmacological agents used to treat or prevent arrhythmias in open-heart cases create undesired systemic side effects. For example, ...

Pre-clinical Model of Cardiac Donation after Circulatory Death

Cardiac transplantation demand is on the rise; nevertheless, organ availability is limited due to a paucity of suitable donors. Organ donation after circulatory death (DCD) is a solution to address this limited availability, but due to a period of prolonged warm ischemia and the risk of tissue injury, its routine use in cardiac transplantation is seldom seen. In this manuscript we provide a detailed protocol closely mimicking current clinical practices in the context of DCD with continuous monitoring of heart function, allowing for the evaluation of novel cardioprotective strategies and interventions to decrease ischemia-reperfusion injury.
In this model, the DCD protocol is initiated in anesthetized Lewis rats by stopping ventilation to induce circulatory death. When systolic blood pressure drops below 30 mmHg, the warm ischemic time is initiated. After a pre-set warm ischemic period, hearts are flushed with a normothermic cardioplegic solution, procured, and mounted onto a Langendorff ex vivo heart perfusion system. Following 10 min of initial reperfusion and stabilization, cardiac reconditioning is continuously evaluated for 60 min using intraventricular pressure monitoring. A heart injury is assessed by measuring cardiac troponin T and the infarct size is quantified by histological staining. The warm ischemic time can be modulated and tailored to develop the desired amount of structural and functional damage. This simple protocol allows for the evaluation of different cardioprotective conditioning strategies introduced at the moment of cardioplegia, initial reperfusion and/or during ex vivo perfusion. Findings obtained from this protocol can be reproduced in large models, facilitating clinical translation.

This protocol shows a simple and flexible approach for the evaluation of new conditioning agents or strategies to increase the feasibility of cardiac donation after circulatory death.

Dolaşım ölümünden sonra kardiyak bağış öncesi klinik model

Cardiac transplantation demand is on the rise; nevertheless, organ availability is limited due to a paucity of suitable donors. Organ donation after ...

Standardized Model of Ventricular Fibrillation and Advanced Cardiac Life Support in Swine

Cardiopulmonary resuscitation after cardiac arrest, independent of its origin, is a regularly encountered medical emergency in hospitals as well as preclinical settings. Prospective randomized trials in human subjects are difficult to design and ethically ambiguous, which results in a lack of evidence-based therapies. The model presented in this report represents one of the most common causes of cardiac arrests, ventricular fibrillation, in a standardized setting in a large animal model. This allows for reproducible observations and various therapeutic interventions under clinically accurate conditions, hence facilitating the generation of better evidence and eventually the potential for improved medical treatment.

Cardiopulmonary resuscitation and defibrillation are the only effective therapeutic options during cardiac arrest caused by ventricular fibrillation. This model presents a standardized regimen to induce, assess, and treat this physiological state in a porcine model, thus providing a clinical approach with various opportunities for data collection and analysis.

Domuzda Standart Ventriküler Fibrilasyon Ve İleri Kardiyak Yaşam Desteği Modeli

Cardiopulmonary resuscitation after cardiac arrest, independent of its origin, is a regularly encountered medical emergency in hospitals as well as ...

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.

Miyokard İskemisi ve Reperfüzyon Hasarının Geliştirilmiş Kemirgen Modeli

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

Transthoracic Echocardiography to Assess Post-Resuscitation Left Ventricular Dysfunction After Acute Myocardial Infarction and Cardiac Arrest in Pigs

One of the main causes of out-of-hospital cardiac arrest is acute myocardial infarction (AMI). After successful resuscitation from cardiac arrest, approximately 70% of patients die before hospital discharge due to post-resuscitation myocardial and cerebral dysfunction. In experimental models, myocardial dysfunction after cardiac arrest, characterized by an impairment in both left ventricular (LV) systolic and diastolic function, has been described as reversible but very little data are available in cardiac arrest models associated with AMI in pigs. Transthoracic echocardiography is the first-line diagnostic test for the assessment of myocardial dysfunction, structural changes and/or AMI extension. In this pig model of ischemic cardiac arrest, echocardiography was done at baseline and 2-4 and 96 hours after resuscitation. In the acute phase, the examinations are done in anesthetized, mechanically ventilated pigs (weight 39.8 &#177; 0.6 kg) and ECG is recorded continuously. Mono- and bi-dimensional, Doppler and tissue Doppler recordings are acquired. Aortic and left atrium diameter, end-systolic and end-diastolic left ventricular wall thicknesses, end-diastolic and end-systolic diameters and shortening fraction (SF) are measured. Apical 2-, 3-, 4-, and 5-chamber views are acquired, LV volumes and ejection fraction are calculated. Segmental wall motion analysis is done to detect the localization and estimate the extent of myocardial infarction. Pulsed Wave Doppler echocardiography is used to record trans-mitral flow velocities from a 4-apical chamber view and trans-aortic flow from a 5-chamber view to calculate LV cardiac output (CO) and stroke volume (SV). Tissue Doppler Imaging (TDI) of LV lateral and septal mitral anulus is recorded (TDI septal and lateral s&#39;, e&#39;, a&#39; velocities). All the recordings and measurements are done according to the recommendations of the American and European Societies of Echocardiography Guidelines.

Transthoracic echocardiography is the first-line diagnostic test for post-resuscitation left ventricular dysfunction and structural changes in a pig model of cardiac arrest.

Domuzlarda Akut Miyokard Enfarktüsü ve Kardiyak Arrest Sonrası Resüsitasyon Sonrası Sol Ventrikül Disfonksiyonunu Değerlendirmek İçin Transtorasik Ekokardiyografi

One of the main causes of out-of-hospital cardiac arrest is acute myocardial infarction (AMI). After successful resuscitation from cardiac arrest, ...

A Model of Long-Term Ventricular Fibrillation in Isolated Rat Hearts

Ventricular fibrillation (VF) is a fatal arrhythmia with a high incidence in cardiac patients, but VF arrest under perfusion is a neglected method of intraoperative arrest in the field of cardiac surgery. With recent advances in cardiac surgery, the demand for prolonged VF studies under perfusion has increased. However, the field lacks simple, reliable, and reproducible animal models of chronic ventricular fibrillation. This protocol induces long-term VF through alternating current (AC) electrical stimulation of the epicardium. Different conditions were used to induce VF, including continuous stimulation with a low or high voltage to induce long-term VF and stimulation for 5 min with a low or high voltage to induce spontaneous long-term VF. The success rates of the different conditions, as well as the rates of myocardial injury and recovery of cardiac function, were compared. The results showed that continuous low-voltage stimulation induced long-term VF and that 5 min of low-voltage stimulation induced spontaneous long-term VF with mild myocardial injury and a high rate of recovery of cardiac function. However, the low-voltage, continuously stimulated long-term VF model had a higher success rate. High-voltage stimulation provided a higher rate of VF induction but showed a low defibrillation success rate, poor recovery of cardiac function, and severe myocardial injury. On the basis of these results, continuous low-voltage epicardial AC stimulation is recommended for its high success rate, stability, reliability, reproducibility, low impact on cardiac function, and mild myocardial injury.

This protocol presents a model of long-term ventricular fibrillation in rat hearts induced by continuous stimulation with low-voltage alternating current. This model has a high success rate, is stable, reliable, and reproducible, has a low impact on cardiac function, and causes only mild myocardial injury.

İzole Sıçan Kalplerinde Uzun Süreli Ventriküler Fibrilasyon Modeli

Ventricular fibrillation (VF) is a fatal arrhythmia with a high incidence in cardiac patients, but VF arrest under perfusion is a neglected method of ...

Chronic Ovine Model of Right Ventricular Failure and Functional Tricuspid Regurgitation

The pathophysiology of severe functional tricuspid regurgitation (FTR) associated with right ventricular dysfunction is poorly understood, leading to suboptimal clinical results. We set out to establish a chronic ovine model of FTR and right heart failure to investigate the mechanisms of FTR. Twenty adult male sheep (6-12 months old, 62 &#177; 7 kg) underwent a left thoracotomy and baseline echocardiography. A pulmonary artery band (PAB) was placed and cinched around the main pulmonary artery (PA) to at least double the systolic pulmonary artery pressure (SPAP), inducing right ventricular (RV) pressure overload and signs of RV dilatation. PAB acutely increased the SPAP from 21 &#177; 2 mmHg to 62 &#177; 2 mmHg. The animals were followed for 8 weeks, symptoms of heart failure were treated with diuretics, and surveillance echocardiography was used to assess for pleural and abdominal fluid collection. Three animals died during the follow-up period due to stroke, hemorrhage, and acute heart failure. After 2 months, a median sternotomy and epicardial echocardiography were performed. Of the surviving 17 animals, 3 developed mild tricuspid regurgitation, 3 developed moderate tricuspid regurgitation, and 11 developed severe tricuspid regurgitation. Eight weeks of pulmonary artery banding resulted in a stable chronic ovine model of right ventricular dysfunction and significant FTR. This large animal platform can be used to further investigate the structural and molecular basis of RV failure and functional tricuspid regurgitation.

Right ventricular failure and functional tricuspid regurgitation are associated with left-sided heart disease and pulmonary hypertension, which contribute significantly to morbidity and mortality in patients. Establishing a chronic ovine model to study right ventricular failure and functional tricuspid regurgitation will help in understanding their mechanisms, progression, and possible treatments.

Sağ Ventrikül Yetmezliği ve Fonksiyonel Triküspid Yetersizliğinin Kronik Ovine Modeli

The pathophysiology of severe functional tricuspid regurgitation (FTR) associated with right ventricular dysfunction is poorly understood, leading to ...

Kardiyak Arrest Sonrası Hayvan Modelinde Ekstrakorporeal Kardiyopulmoner Resüsitasyon

Pediatric Animal Model of Extracorporeal Cardiopulmonary Resuscitation After Prolonged Circulatory Arrest

Congenital heart disease (CHD) is the most prevalent congenital malformation, with about one million births impacted worldwide per year. Comprehensive investigation of this disease requires appropriate and validated animal models. Piglets are commonly used for translational research due to their analogous anatomy and physiology. This work aimed to describe and validate a neonatal piglet model of cardiopulmonary bypass (CPB) with circulatory and cardiac arrest (CA) as a tool for studying severe brain damage and other complications of cardiac surgery. In addition to including a list of materials, this work provides a roadmap for other investigators to plan and execute this protocol. After experienced practitioners performed several trials, the representative results of the model demonstrated a 92% success rate, with failures attributed to small piglet size and variant vessel anatomy. Furthermore, the model allowed practitioners to select from a wide variety of experimental conditions, including varying times in CA, temperature alterations, and pharmacologic interventions. In summary, this method uses materials readily available in most hospital settings, is reliable and reproducible, and can be widely employed to enhance translational research in children undergoing heart surgery.

Yazar Spotlight: Yenidoğan Domuz Yavrusu Modeli Kullanarak Pediatrik Kalp Cerrahisini Simüle Etme

This protocol describes a neonatal porcine model of cardiopulmonary bypass (CPB), with circulatory and cardiac arrest as a tool for studying severe brain damage and other complications secondary to CPB.

Uzun Süreli Dolaşım Durması Sonrası Ekstrakorporeal Kardiyopulmoner Resüsitasyonun Pediatrik Hayvan Modeli

Congenital heart disease (CHD) is the most prevalent congenital malformation, with about one million births impacted worldwide per year. Comprehensive ...