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.

Critical Steps in the protocol
There are critical steps in the protocol. When mastered, the preparation and protocol proceed as succinctly described below. The surgical preparation is expeditious, advancing catheters rapidly through small incisions triggering minimal or no vessel spasm and positioning the catheter tips as intended, followed by successful tracheal intubation after a single or a few attempt(s); thus, completing the preparation in &#8776; 90 min from the initial pentobar...

Close to 360,000 individuals in the United States1 and many more worldwide2 suffer an episode of sudden cardiac arrest every year. Attempts to restore life require not only that cardiac activity be reestablished but that damage to vital organs be prevented, minimized, or reversed. Current cardiopulmonary resuscitation techniques yield an initial resuscitation rate of approximately 30%; however, survival to hospital discharge is only 5%1. Myocardial dysfunction, neurological dysfunction, systemic inflammation, intercurrent illnesses, or a combination thereof occurring post-resuscitation account for the large proportion of patients who die in spite of initial return of circulation. Thus, greater understanding of the underlying pathophysiology and novel resuscitation approaches are urgently needed to increase the rate of initial resuscitation and subsequent survival with intact organ function.
Animal models of cardiac arrest play a critical role in the development of new resuscitation therapies by providing insights on the pathophysiology of cardiac arrest and resuscitation and offering practical means to conceptualize and test new interventions before they can be tested in humans3. The rat model of closed chest cardiopulmonary resuscitation (CPR) described here has played an important role. The model was developed in 1988 by Irene von Planta &#8211; a research fellow at the time &#8211; and her collaborators4 in the laboratory of late Professor Max Harry Weil M.D., Ph.D. at the University of Health Sciences (renamed Rosalind Franklin University of Medicine and Science in 2004) and has been extensively used in the field of resuscitation predominantly by fellows of Professor Weil and their trainees.
The model simulates an episode of sudden cardiac arrest with resuscitation attempted by conventional CPR techniques and thus includes induction of ventricular fibrillation (VF) by delivering an electrical current to the right ventricular endocardium and provision of closed chest CPR by a pneumatically driven piston device while concomitantly delivering positive pressure ventilation with oxygen-enriched gas. Termination of VF is accomplished by transthoracic delivery of electrical shocks. The rat model strikes a balance between models developed in large animals (e.g., swine) and models developed in smaller animals (e.g., mice) allowing exploration of new research concepts in a well-standardized, reproducible, and efficient manner with access to a robust inventory of pertinent measurements. The model is particularly useful in early stages of research to explore new concepts and examine the effects of confounders before conducting studies in larger animal models that are more costly, but of greater translational impact.
A Medline search for all peer-reviewed articles reporting a similar rat model having VF as the mechanism of cardiac arrest and some form of closed chest resuscitation revealed a total of 69 additional original studies using the model since it was first published in 19884. The research areas include pathophysiological aspects of resuscitation5-17, factors influencing outcomes18-30, the role of pharmacological interventions examining vasopressor agents31-43, buffer agents44, inotropic agents45, agents aimed at myocardial or cerebral protection46-70, and also the effects of mesenchymal stem cells71-73.
The model and protocol described in this article is currently being used at the Resuscitation Institute. Yet, there are multiple opportunities to &#8220;customize&#8221; the model based on the capabilities available to individual investigators and the goals of the studies.

<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.

The rat model described here was recently used to compare the effects of two inhibitors of the sarcolemmal sodium-hydrogen exchanger isoform 1 (NHE-1) on myocardial and hemodynamic function during chest compression and post-resuscitation61. It was previously reported that NHE-1 inhibitors attenuate myocardial reperfusion injury by limiting sodium-induced cytosolic and mitochondrial calcium overload, and thereby help preserve left ventricular distensibility during chest compression and attenuate post-resuscitat...

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.

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

Research

JoVE Journal

Medicine

15.8K Views.  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.

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.

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

Murine Isolated Heart Model of Myocardial Stunning Associated with Cardioplegic Arrest

The following protocol is of use to evaluate impaired cardiac function or myocardial stunning following moderate ischemic insults. The technique is useful for modeling ischemic injury associated with numerous clinically relevant phenomenon including cardiac surgery with cardioplegic arrest and cardiopulmonary bypass, off-pump CABG, transplant, angina, brief ischemia, etc. The protocol presents a general method to model hypothermic hyperkalemic cardioplegic arrest and reperfusion in rodent hearts focusing on measurement of myocardial contractile function. In brief, a mouse heart is perfused in langendorff mode, instrumented with an intraventricular balloon, and baseline cardiac functional parameters are recorded. Following stabilization, the heart is then subject to brief infusion of a cardioprotective hypothermic cardioplegia solution to initiate diastolic arrest. Cardioplegia is delivered intermittently over 2 hr. The heart is then reperfused and warmed to normothermic temperatures and recovery of myocardial function is monitored. Use of this protocol results in reliable depressed cardiac contractile function free from gross myocardial tissue damage in rodents.

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

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

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.

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

Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System

Myocardial infarction (MI) remains the main contributor to morbidity and mortality worldwide. Therefore, research on this topic is mandatory. An easily and highly reproducible MI induction procedure is required to obtain further insight and better understanding of the underlying pathological changes. This procedure can also be used to evaluate the effects or potency of new and promising treatments (as drugs or interventions) in acute MI, subsequent remodeling and heart failure (HF). After intubation and pre-operative preparation of the animal, an anesthetic protocol with isoflurane was performed, and the surgical procedure was conducted&#160;quickly. Using a minimally invasive approach, the left anterior descending artery (LAD) was located and occluded by a ligature. The occlusion can be performed acutely for subsequent reperfusion (ischemia/reperfusion injury). Alternatively, the vessel can be ligated permanently to investigate the development of chronic MI, remodeling or HF. Despite common pitfalls, the drop-out rates are minimal. Various treatments such as remote ischemic conditioning can be examined for their cardioprotective potential pre-, peri- and post-operatively. The post-operative recovery was quick as the anesthesia was precisely controlled and the duration of the operation was short. Post-operative analgesia was administered for three days. The minimally invasive procedure reduces the risk of infection and inflammation. Furthermore, it facilitates rapid recovery. The &#8220;working heart&#8221; measurements were performed ex vivo and enabled precise control of preload, afterload and flow. This procedure requires specific equipment and training for adequate performance. This manuscript provides a detailed step-by-step introduction for conducting these measurements.

This article presents an efficient method to perform myocardial ischemia and subsequent chronic reperfusion in rats using a minimally invasive approach. In addition, left ventricular hemodynamic function of rats is assessed by echocardiography and isolated working heart methods.&#160;

Myocardial infarction (MI) remains the main contributor to morbidity and mortality worldwide. Therefore, research on this topic is mandatory. An easily ...

A New Model of Heart Failure Post-Myocardial Infarction in the Rat

Ligation of the left anterior descending (LAD) coronary artery has been widely used to establish the rat model of heart failure (HF) post myocardial infarction (MI). However, the disadvantages of this model include high mortality rate after ligation and larger variations both in the infarct size and the degree of impaired cardiac function. In addition, a ventilator or exteriorization of the heart is indispensable for the previous models, which complicates the procedure during the ligation. In this study, we developed a reliable and reproducible model without the ventilator or exteriorization of the heart by ligating the LAD coronary artery. Four weeks after the procedure, we found that the serum concentrations of CK-MB, NT-proBNP, and Renin, which were used to assist diagnoses of MI and HF, were significantly higher in the MI group compared to the sham group. In contrast, the value of left ventricle ejection fraction (LVEF) in the MI group was obviously less than in the sham group. Furthermore, the infarct size and cardiac fibrosis area were individually confirmed and quantitatively analyzed by TTC staining and Masson's trichrome staining. Smaller variations were found in either infarct size or fibrosis area in the MI group, which helped to develop a reliable and reproducible model of HF post-MI. This new model of HF post-MI in the rat is vital for studying the potential mechanisms of MI and HF. This new method can be used to develop the new drug for treatment of MI and HF in rats by using pharmacological strategies.

We successfully developed a reliable and reproducible model of heart failure post-myocardial infarction in the rat without ventilation or exteriorization of the heart. This simplifies the procedure and benefits the further studies about the potential mechanisms behind the heart failure.

Ligation of the left anterior descending (LAD) coronary artery has been widely used to establish the rat model of heart failure (HF) post myocardial ...

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.

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

Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats

Animal studies have brought important insights into our understanding regarding atrial fibrillation (AF) pathophysiology and therapeutic management. Reentry, one of the main mechanisms involved in AF pathogenesis, requires a certain mass of myocardial tissue in order to occur. Due to the small size of the atria, rodents have long been considered 'resistant' to AF. Although spontaneous AF has been shown to occur in rats, long-term follow-up (up to 50 weeks) is required for the arrhythmia to occur in those models. The present work describes an experimental protocol of transesophageal atrial burst pacing for rapid and efficient induction of AF in rats. The protocol can be successfully used in rats with healthy or remodeled hearts, in the presence of a wide variety of risk factors, allowing the study of AF pathophysiology, identification of novel therapeutic targets, and evaluation of novel prophylactic and/or therapeutic strategies.

The present work describes an experimental protocol of transesophageal atrial burst pacing for efficient induction of atrial fibrillation (AF) in rats. The protocol can be used in rats with healthy or remodeled hearts, allowing the study of AF pathophysiology, identification of novel therapeutic targets, and evaluation of new therapeutic strategies.

Animal studies have brought important insights into our understanding regarding atrial fibrillation (AF) pathophysiology and therapeutic management. ...

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.

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

Extracorporeal Cardiopulmonary Resuscitation in Animal Model After Cardiac Arrest

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.

Author Spotlight: Simulating Pediatric Cardiac Surgery Using a Neonatal Piglet Model

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.

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