title: The difference in myocardial injuries and mitochondrial damages between asphyxial and ventricular fibrillation cardiac arrests.
abstract: BACKGROUND
  Ventricular fibrillation (VF) and asphyxia account for most cardiac arrests but differ in cardiac arrest course, neurologic deficit, and myocardial damage. In VF resuscitation, cardiac mitochondria were known to be damaged via excess generation of reactive oxygen species. This study evaluated the difference of cardiac mitochondrial damages between VF and asphyxial cardiac arrests.
  
  
  METHODS
  In the VF + electrical shock (ES) group, VF was induced and untreated for 5 minutes, followed by 1 minute of cardiopulmonary resuscitation (CPR) and 1 ES of 5 J. Animals were killed immediately after ES. In the asphyxia group, cardiac arrest was induced by airway obstruction, and then pulselessness was maintained for 5 minutes, followed by 1 minute of CPR. The animals were killed immediately after CPR. The histology and ultrastructural changes of myocardium and complex activities and respiration of mitochondria were evaluated. The mitochondrial permeability transition pore opening was measured based on mitochondrial swelling rate.
  
  
  RESULTS
  The histopathologic examinations showed myocardial necrosis and mitochondrial damage in both cardiac arrests. Instead of regional damages of myocardium in the VF + ES group, the myocardial injury in the asphyxia group distributed diffusely. The asphyxia group demonstrated more severe mitochondrial damage than the VF + ES group, which had a faster mitochondrial swelling rate, more decreased cytochrome c oxidase activity, and more impaired respiration.
  
  
  CONCLUSIONS
  Both VF and asphyxial cardiac arrests caused myocardial injuries and mitochondrial damages. Asphyxial cardiac arrest presented more diffuse myocardial injuries and more severe mitochondrial damages than VF cardiac arrest.
authors.affiliation: Department of Emergency Medicine, National Taiwan University Medical College and Hospital, Taipei 100, Taiwan.
authors.forename: Min-Shan
authors.initials: MS
authors.lastname: Tsai
authors.forename: Chien-Hua
authors.initials: CH
authors.lastname: Huang
authors.forename: Shang-Ho
authors.initials: SH
authors.lastname: Tsai
authors.forename: Chia-Ying
authors.initials: CY
authors.lastname: Tsai
authors.forename: Huei-Wen
authors.initials: HW
authors.lastname: Chen
authors.forename: Hsaio-Ju
authors.initials: HJ
authors.lastname: Cheng
authors.forename: Chiung-Yuan
authors.initials: CY
authors.lastname: Hsu
authors.forename: Tzung-Dau
authors.initials: TD
authors.lastname: Wang
authors.forename: Wei-Tien
authors.initials: WT
authors.lastname: Chang
authors.forename: Wen-Jone
authors.initials: WJ
authors.lastname: Chen
mesh_terms: D000818:Animals; D001237:Asphyxia / Q000150:complications / Q000473:pathology*; D006323:Heart Arrest / Q000209:etiology / Q000473:pathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D046529:Microscopy, Electron, Transmission; D008929:Mitochondria, Heart / Q000378:metabolism / Q000473:pathology*; D051336:Mitochondrial Membranes / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D009245:NADH Dehydrogenase / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D013384:Succinate Cytochrome c Oxidoreductase / Q000378:metabolism; D014693:Ventricular Fibrillation / Q000150:complications / Q000473:pathology*
chemical_list: D008315:Malondialdehyde; D013384:Succinate Cytochrome c Oxidoreductase; D009245:NADH Dehydrogenase