title: Protective effects of therapeutic hypothermia in post-resuscitation myocardium.
abstract: OBJECTIVE
  Post-resuscitation therapeutic hypothermia has been recommended because of its neuroprotective effects. However, a few studies have reported the effects of therapeutic hypothermia on the heart, especially in ventricular fibrillation cardiac arrest. The aim of this study was to determine whether therapeutic hypothermia attenuates post-resuscitation myocardial injury in a swine cardiac arrest model.
  
  
  METHODS
  A prospective animal study was performed in the university hospital animal research laboratory. Ventricular fibrillation cardiac arrest was induced in domestic pigs weighing 35-40 kg. After 6 min of no flow time, cardiopulmonary resuscitation was provided to pigs, and the restoration of spontaneous circulation (ROSC) was achieved. The subjects were randomly allocated to a normothermic (NT group, n=5) or hypothermic (HT group, n=5) group. In the HT group, therapeutic hypothermia (core temperature 32-34 °C) was maintained for 24h, and rewarming was performed over a period of 8 h. In the NT group, core temperature was maintained at 37 °C throughout the experiments. Sixty hours after ROSC, blood and myocardial tissues were harvested.
  
  
  RESULTS
  Serum troponin I was not significantly different between the groups. However, myocardial histological damage was attenuated in the HT group. Myocardial ATP contents were higher in the HT group than in the NT group. Immunohistochemistry for apoptosis-related protein showed that survivin expression was higher in the HT group, and XAF1 and cleaved caspase-3 expressions were lower in the HT group than in the NT group.
  
  
  CONCLUSIONS
  Therapeutic hypothermia attenuated histological myocardial injury in ventricular fibrillation cardiac arrest model of pigs while preserving more ATP and decreased apoptosis.
authors.affiliation: Department of Emergency Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea.
authors.forename: Jae Hyuk
authors.initials: JH
authors.lastname: Lee
authors.forename: Gil Joon
authors.initials: GJ
authors.lastname: Suh
authors.forename: Woon Yong
authors.initials: WY
authors.lastname: Kwon
authors.forename: Kyung Su
authors.initials: KS
authors.lastname: Kim
authors.forename: Joong Eui
authors.initials: JE
authors.lastname: Rhee
authors.forename: Min A
authors.initials: MA
authors.lastname: Kim
authors.forename: Myung Hee
authors.initials: MH
authors.lastname: Park
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis; D006323:Heart Arrest / Q000503:physiopathology / Q000628:therapy*; D007036:Hypothermia, Induced / Q000379:methods*; D007150:Immunohistochemistry; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D011446:Prospective Studies; D012151:Resuscitation; D013552:Swine; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood; D014693:Ventricular Fibrillation / Q000503:physiopathology / Q000628:therapy*
chemical_list: D019210:Troponin I; D000255:Adenosine Triphosphate