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J Appl Physiol (June 22, 2006). doi:10.1152/japplphysiol.01487.2005
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Submitted on November 23, 2005
Accepted on June 12, 2006

Cardiopulmonary Resuscitation in a Rat Model of Chronic Myocardial Ischemia

Xiangshao Fang1, Wanchun Tang2*, Shijie Sun3, Lei Huang4, Yun-Te Chang4, Zitong Huang5, and Max Harry Weil3

1 Weil Institute of Critical Care Medicine, Rancho Mirage, California, United States; Emergency Medicine, Second Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China
2 Weil Institute of Critical Care Medicine, Rancho Mirage, California, United States; Keck School of Medicine, USC, Los Angeles, California, United States; Emergency Medicine, Second Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China
3 Weil Institute of Critical Care Medicine, Rancho Mirage, California, United States; Keck School of Medicine, USC, Los Angeles, California, United States
4 Weil Institute of Critical Care Medicine, Rancho Mirage, California, United States
5 Emergency Medicine, Second Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong, China

* To whom correspondence should be addressed. E-mail: drsheart{at}aol.com.

Our group has developed a rat model of cardiac arrest and resuscitation (CPR). However, the current rat model uses healthy adult animals. In an effort to more closely reproduce the event of cardiac arrest and CPR in humans with chronic coronary disease, a rat model of coronary artery constriction was investigated during cardiac arrest and CPR. The left coronary artery constriction was induced surgically in anesthetized, mechanically ventilated Sprague-Dawley rats. Echocardiography was used to measure global cardiac performance before surgery and 4 weeks post surgery. Coronary artery constriction provoked significant decrease in ejection fraction, increases in left ventricular end-diastolic volume, and left ventricular end-systolic volume at 4 weeks post intervention, just prior to induction of ventricular fibrillation (VF). After 6 min of untreated VF, mechanical ventilation and precordial compression were initiated on three groups; 1) coronary artery constriction group, 2) sham-operated group, and 3) control group (without preceding surgery). Defibrillation was attempted after 6 min of CPR. All the animals were resuscitated. Postresuscitation myocardial function as measured by dP/dt40, -dP/dt was more significantly impaired and left ventricular end-diastolic pressure was greater in the coronary artery constriction group compared with the sham-operated group and the control group. In summary, this rat model of chronic myocardial ischemia was associated with ventricular remodeling and left ventricular myocardial dysfunction 4 weeks post intervention, and subsequently severe postresuscitation myocardial dysfunction. This model would suggest further clinically relevant investigation on cardiac arrest and CPR.




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