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RESEARCH PRODUCT

Apoptosis is not involved in the mechanism of myocardial dysfunction after resuscitation in a rat model of cardiac arrest and cardiopulmonary resuscitation.

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OBJECTIVE To investigate the presence of apoptosis after the global myocardial ischemia of cardiopulmonary resuscitation and the regional myocardial ischemia after left anterior descending coronary artery occlusion and relate it to the severity of postresuscitation myocardial dysfunction. DESIGN Prospective animal study. SETTING University-affiliated animal research laboratory. SUBJECTS Male Sprague-Dawley rats. INTERVENTIONS Fifteen male Sprague-Dawley rats weighing 450-550 g were randomized to: (1) 8 mins of untreated cardiac arrest followed by 6 mins of cardiopulmonary resuscitation; (2)left anterior descending coronary artery occlusion for 45 mins followed by 4 hrs of reperfusion; and (3) left anterior descending coronary artery sham group. Cardiac functions, including ejection fraction, analog differentiation of left ventricular pressure at 40 mm Hg, and rate of maximal left ventricular pressure decline were continuously measured for 4 hrs. The hearts were then harvested for the terminal transferase-mediated 2'-deoxyuridine, 5'-triphosphate nick end-labeling assay analysis. MEASUREMENTS AND MAIN RESULTS Myocardial function was significantly impaired after resuscitation from cardiac arrest and reperfusion from left anterior descending coronary artery occlusion(p < .01). There was no difference in the percentage of apoptotic cells between the cardiopulmonary resuscitation animals and sham-operated animals. Fewer apoptotic cells were observed in cardiac arrest/cardiopulmonary resuscitation animals in comparison to left anterior descending coronary artery occlusion animals (p < .05), even though myocardial function was more severely impaired after resuscitation (p < .01). CONCLUSIONS Myocardial function was significantly impaired after cardiac arrest/cardiopulmonary resuscitation and ischemia/reperfusion. However, apoptosis was not involved in the mechanism of postresuscitation myocardial dysfunction in this setting.