Abstract
Cardiopulmonary arrest remains as one of the leading causes of death and disability in Western countries. Although ventricular fibrillation (VF) models in rodents mimic the "square wave" type of insult (rapid loss of pulse and pressure) commonly observed in adult humans at the onset of cardiac arrest (CA), they are not popular because of the complicated animal procedure, poor animal survival, and thermal injury. Here, we present a modified, simple, and reliable VF-induced rat model of CA that will be useful in studying the mechanisms of CA-induced delayed neuronal death, as well as the efficacy of neuroprotective drugs. CA was induced in male Sprague Dawley rats using a modified method of von Planta et al. (J Appl Physiol 65:2641-2647, 1988). In brief, VF was induced in anesthetized, paralyzed, and mechanically ventilated rats by an alternating current delivered to the entrance of the superior vena cava into the heart. Resuscitation was initiated by administering a bolus injection of epinephrine and sodium bicarbonate followed by mechanical ventilation and manual chest compressions and countershock with a 10-J direct current. Neurological deficit score was higher in the CA group compared to the sham group during early reperfusion periods, suggesting brain damage. Significant damage in the CA1 hippocampus (21 % normal neurons compared to control animals) was observed following histopathological assessment at 7 days of reperfusion. We propose that this method of VF-induced CA in the rat provides a tool to study the mechanism of CA-induced neuronal death without compromising heart functions.
| Original language | English |
|---|---|
| Pages (from-to) | 571-578 |
| Number of pages | 8 |
| Journal | Translational Stroke Research |
| Volume | 4 |
| Issue number | 5 |
| DOIs | |
| State | Published - Jun 24 2013 |
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Keywords
- Animal model
- Cardiac arrest
- Global cerebral ischemia
- Hippocampus
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
- Cardiology and Cardiovascular Medicine
Cite this
Ventricular Fibrillation-Induced Cardiac Arrest in the Rat as a Model of Global Cerebral Ischemia. / Dave, Kunjan R; Della Morte, David; Saul, Isabel; Prado, Ricardo; Perez-Pinzon, Miguel.
In: Translational Stroke Research, Vol. 4, No. 5, 24.06.2013, p. 571-578.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Ventricular Fibrillation-Induced Cardiac Arrest in the Rat as a Model of Global Cerebral Ischemia
AU - Dave, Kunjan R
AU - Della Morte, David
AU - Saul, Isabel
AU - Prado, Ricardo
AU - Perez-Pinzon, Miguel
PY - 2013/6/24
Y1 - 2013/6/24
N2 - Cardiopulmonary arrest remains as one of the leading causes of death and disability in Western countries. Although ventricular fibrillation (VF) models in rodents mimic the "square wave" type of insult (rapid loss of pulse and pressure) commonly observed in adult humans at the onset of cardiac arrest (CA), they are not popular because of the complicated animal procedure, poor animal survival, and thermal injury. Here, we present a modified, simple, and reliable VF-induced rat model of CA that will be useful in studying the mechanisms of CA-induced delayed neuronal death, as well as the efficacy of neuroprotective drugs. CA was induced in male Sprague Dawley rats using a modified method of von Planta et al. (J Appl Physiol 65:2641-2647, 1988). In brief, VF was induced in anesthetized, paralyzed, and mechanically ventilated rats by an alternating current delivered to the entrance of the superior vena cava into the heart. Resuscitation was initiated by administering a bolus injection of epinephrine and sodium bicarbonate followed by mechanical ventilation and manual chest compressions and countershock with a 10-J direct current. Neurological deficit score was higher in the CA group compared to the sham group during early reperfusion periods, suggesting brain damage. Significant damage in the CA1 hippocampus (21 % normal neurons compared to control animals) was observed following histopathological assessment at 7 days of reperfusion. We propose that this method of VF-induced CA in the rat provides a tool to study the mechanism of CA-induced neuronal death without compromising heart functions.
AB - Cardiopulmonary arrest remains as one of the leading causes of death and disability in Western countries. Although ventricular fibrillation (VF) models in rodents mimic the "square wave" type of insult (rapid loss of pulse and pressure) commonly observed in adult humans at the onset of cardiac arrest (CA), they are not popular because of the complicated animal procedure, poor animal survival, and thermal injury. Here, we present a modified, simple, and reliable VF-induced rat model of CA that will be useful in studying the mechanisms of CA-induced delayed neuronal death, as well as the efficacy of neuroprotective drugs. CA was induced in male Sprague Dawley rats using a modified method of von Planta et al. (J Appl Physiol 65:2641-2647, 1988). In brief, VF was induced in anesthetized, paralyzed, and mechanically ventilated rats by an alternating current delivered to the entrance of the superior vena cava into the heart. Resuscitation was initiated by administering a bolus injection of epinephrine and sodium bicarbonate followed by mechanical ventilation and manual chest compressions and countershock with a 10-J direct current. Neurological deficit score was higher in the CA group compared to the sham group during early reperfusion periods, suggesting brain damage. Significant damage in the CA1 hippocampus (21 % normal neurons compared to control animals) was observed following histopathological assessment at 7 days of reperfusion. We propose that this method of VF-induced CA in the rat provides a tool to study the mechanism of CA-induced neuronal death without compromising heart functions.
KW - Animal model
KW - Cardiac arrest
KW - Global cerebral ischemia
KW - Hippocampus
UR - http://www.scopus.com/inward/record.url?scp=84884904569&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84884904569&partnerID=8YFLogxK
U2 - 10.1007/s12975-013-0267-0
DO - 10.1007/s12975-013-0267-0
M3 - Article
C2 - 24187598
AN - SCOPUS:84884904569
VL - 4
SP - 571
EP - 578
JO - Translational Stroke Research
JF - Translational Stroke Research
SN - 1868-4483
IS - 5
ER -