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 A.
N1 - Funding Information:
Acknowledgments This study was supported by NIH grants NS45676, NS054147, NS34773, NS05820, and NS073779. We would like to thank Dr. Maritza Martinez and Mr. Oleksandr Dashkin for the technical assistance, and Prof. Brant Watson for the critical reading of this manuscript.
PY - 2013
Y1 - 2013
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
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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 -