| Apoptosis is not involved in the mechanism of myocardial dysfunction after resuscitation in a rat model of cardiac arrest and cardiopulmonary resuscitation. | |
MedLine Citation:
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PMID: 20228676 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
Authors:
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Fengqing Song; Yi Shan; Francesco Cappello; Francesca Rappa; Giuseppe Ristagno; Tao Yu; Giovanni Li Volti; Shijie Sun; Max Harry Weil; Wanchun Tang |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Critical care medicine Volume: 38 ISSN: 1530-0293 ISO Abbreviation: Crit. Care Med. Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-23 Completed Date: 2010-05-14 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0355501 Medline TA: Crit Care Med Country: United States |
Other Details:
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Languages: eng Pagination: 1329-34 Citation Subset: AIM; IM |
Affiliation:
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Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis * Cardiopulmonary Resuscitation / adverse effects* Coronary Occlusion / complications Heart / physiopathology* Heart Arrest / complications, physiopathology, therapy* Male Myocardial Ischemia / etiology, pathology, physiopathology* Myocardial Reperfusion Injury / etiology, pathology, physiopathology* Random Allocation Rats Rats, Sprague-Dawley |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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