A simpler cardiac arrest model in the mouse

Chen, Menghua; Liu, Tangwei; Xie, Lu; Song, Fengqing; He, Tao; Mo, Shu-Rong; Zeng, Zhiyu

doi:10.1016/j.resuscitation.2007.04.007

Cited by 13 publications

(15 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An important factor for VF inducibility is the size of the heart (so-called “critical mass”): the smaller the size of excitable myocardium the more difficult is VF induction. We used relatively small mice ( ∼ 20 g), whereas in the studies focused on VF induction 40 – 50 g mice were used (Chen et al, 2007). In addition, special interventions to facilitate VF induction have been employed, and include the use of isolated hearts (Vaidya et al, 1999), modification of ionic current, and application of pharmacological agents (Stables and Curtis, 2009).…”

Section: Resultsmentioning

confidence: 99%

Increased Cell–Cell Coupling Increases Infarct Size and Does not Decrease Incidence of Ventricular Tachycardia in Mice

Prestia¹,

Sosunov²,

Anyukhovsky³

et al. 2011

Front. Physio.

View full text Add to dashboard Cite

Increasing connexin43 (Cx43) gap junctional conductance as a means to improve cardiac conduction has been proposed as a novel antiarrhythmic modality. Yet, transmission of molecules via gap junctions may be associated with increased infarct size. To determine whether maintaining open gap junction channels impacts on infarct size and induction of ventricular tachycardia (VT) following coronary occlusion, we expressed the pH- and voltage-independent connexin isoform connexin32 (Cx32) in ventricle and confirmed Cx32 expression. Wild-type (WT) mice injected with adenovirus-Cx32 (Cx32inj) were examined following coronary occlusion to determine infarct size and inducibility of VT. There was an increased infarct size in Cx32inj hearts as compared to WT (WT 22.9 ± 4%; Cx32inj 44.3 ± 5%; p < 0.05). Programmed electrical stimulation showed no difference in VT inducibility in WT and Cx32inj mice (VT was reproducibly inducible in 55% of shams and 50% of Cx32inj mice (p > 0.05). Following coronary occlusion, improving cell–cell communication increased infarct size, and conferred no antiarrhythmic benefit.

show abstract

Section: Resultsmentioning

confidence: 99%

Increased Cell–Cell Coupling Increases Infarct Size and Does not Decrease Incidence of Ventricular Tachycardia in Mice

Prestia¹,

Sosunov²,

Anyukhovsky³

et al. 2011

Front. Physio.

View full text Add to dashboard Cite

show abstract

“…Ear artery blood pressure avoids experimental procedure-related effects on cerebral or limb blood flow, which can alter carotid or femoral artery pressure. 11 The duration of untreated ACCA is decisive for prognosis in both experimental and clinical practice. 8,9 In the first 24 hour after ROSC, postresuscitation myocardial dysfunction is the leading cause of death 12,13 and becomes more severe as the untreated cardiac arrest duration was extended.…”

Section: Discussionmentioning

confidence: 99%

Investigation of the Relationship Between Venticular Fibrillation Duration and Cardiac/Neurological Damage in a Rabbit Model of Electrically Induced Arrhythmia

H²,

Liu³

et al. 2010

Journal of Trauma: Injury, Infection &Amp; Critical Care

View full text Add to dashboard Cite

show abstract

“…An intermediate method consists in the electrical stimulation of the heart through one subcutaneous thoracic electrode and another electrode inserted into the esophagus. This technique has been developed in rodents 38,39 and rabbits 40,41 but canal so be used in swine. 42 For example, a sustained transesophageal alternating current stimulation (50Hz, 18V) during 60seconds has been shown to induce VF in mice.…”

Section: Electrical Induction Of Ventricular Fibrillationmentioning

confidence: 99%

“…42 For example, a sustained transesophageal alternating current stimulation (50Hz, 18V) during 60seconds has been shown to induce VF in mice. 38 In rats and rabbits, VF can be induced with a 50-60Hz current of 1-5mA during 3minutes. 40,43,44 In another study, a rapid pacing with three periods of 5seconds of transesophageal stimulation at 30Hz efficiently induces VF in rats.…”

Section: Electrical Induction Of Ventricular Fibrillationmentioning

confidence: 99%

Untitled

2016

JDVAR

View full text Add to dashboard Cite

Abbreviations: CPR, cardiopulmonary resuscitation; ROSC, resumption of spontenaeous circulation; VF, ventricular fibrillation IntroductionCardiac arrest is an important public health issue in humans in industrialized countries with, e.g., 35,000 to 40,000 new cases each year in France.1,2 Despite increasing implementation of cardiopulmonary resuscitation (CPR) in the field, resumption of spontaneous circulation (ROSC) is typically obtained in less than 35% of these patients. Resuscitated victims often present a post cardiac arrest syndrome with a complex physiopathology combining hemodynamic failure, neurological dysfunction and multi-visceral injury, leading to an additional worsening of the prognosis. Ultimately, less than 8% of the patients survive with favorable neurological function at hospital discharge. [3][4][5] In this context, experimental research is crucial to provide new therapeutic approaches increasing CPR efficiency and initial resuscitation, as well as long term prognosis and neurological recovery. For such investigations, the use of animal models seems unavoidable as cardiac arrest provokes multiple visceral consequences as well as inflammatory response and coagulopathy. These models allow not only a better understanding of the pathophysiology but also the investigation of new treatment strategies to improve CPR efficiency or prevent multi-organ failure. This field of research can also address fundamental questions for veterinary research, beyond the relevance for human medicine. Impact of species-differencesIn general, animal models of cardiac arrest are using rodents, rabbits, pigs or dogs. All these species present anatomical or physiological specificities that should been considered in the design of the study, depending upon the specific goals and corresponding end-points. Cardiac arrest in rodentsAs usual in biomedical research, rodents are widely used in resuscitation sciences due to their relative ease of manipulation, low cost and extensive possibilities of mechanistic investigations with genetically modified animals. Obviously, this use is associated with several limitations related to their cardiovascular anatomy and physiology. On the one hand, rodents present two different cranial venae cavae (right and left) with a coronary sinus formed by the proximal part of the left cranial vena cava.6 This directly modifies the coronary perfusion during cardiac massage through different venous return as compared to large animals.7 In addition, due to their very low body mass, cardiac massage could make blood circulating through direct heart compression, while it is mostly acting through thoracic pumping in large animals. On the other hand, spontaneous heart rate is much higher in rodents than in large animals and humans as usual values average 260-450 or 500-600 beats per minute in awake rats and mice, respectively. 7,8 This directly impacts the required chest compression rate in those species as mice should undergo ≈400 compressions per min to be resuscitated. [9][10][11][12][13][14] Magnetic ...

show abstract

A simpler cardiac arrest model in the mouse

Cited by 13 publications

References 25 publications

Increased Cell–Cell Coupling Increases Infarct Size and Does not Decrease Incidence of Ventricular Tachycardia in Mice

Increased Cell–Cell Coupling Increases Infarct Size and Does not Decrease Incidence of Ventricular Tachycardia in Mice

Investigation of the Relationship Between Venticular Fibrillation Duration and Cardiac/Neurological Damage in a Rabbit Model of Electrically Induced Arrhythmia

Untitled

Contact Info

Product

Resources

About