title: Comparison of Cerebral Metabolism between Pig Ventricular Fibrillation and Asphyxial Cardiac Arrest Models.
abstract: BACKGROUND
  Morbidity and mortality after resuscitation largely depend on the recovery of brain function. Ventricular fibrillation cardiac arrest (VFCA) and asphyxial cardiac arrest (ACA) are the two most prevalent causes of sudden cardiac death. Up to now, most studies have focused on VFCA. However, results from the two models have been largely variable. So, it is necessary to characterize the features of postresuscitation cerebral metabolism of both models.
  
  
  METHODS
  Forty-four Wuzhishan miniature inbred pigs were randomly divided into three groups: 18 for VFCA group, ACA group, respectively, and other 8 for sham-operated group (SHAM). VFCA was induced by programmed electric stimulation, and ACA was induced by endotracheal tube clamping. After 8 min without treatment, standard cardiopulmonary resuscitation (CPR) was initiated. Following neurological deficit scores (NDS) were evaluated at 24 h after achievement of spontaneous circulation, cerebral metabolism showed as the maximum standardized uptake value (SUVmax) was measured by 18 F-fluorodeoxyglucose positron emission tomography/computed tomography. Levels of serum markers of brain injury, neuron specific enolase (NSE), and S100β were quantified with an enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Compared with VFCA group, fewer ACA animals achieved restoration of spontaneous circulation (61.1% vs. 94.4%, P < 0.01) and survived 24-h after resuscitation (38.9% vs. 77.8%, P < 0.01) with worse neurological outcome (NDS: 244.3 ± 15.3 vs. 168.8 ± 9.71, P < 0.01). The CPR duration of ACA group was longer than that of VFCA group (8.1 ± 1.2 min vs. 4.5 ± 1.1 min, P < 0.01). Cerebral energy metabolism showed as SUVmax in ACA was lower than in VFCA (P < 0.05 or P < 0.01). Higher serum biomarkers of brain damage (NSE, S100β) were found in ACA than VFCA after resuscitation (P < 0.01).
  
  
  CONCLUSIONS
  Compared with VFCA, ACA causes more severe cerebral metabolism injuries with less successful resuscitation and worse neurological outcome.
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Emergency, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
authors.forename: Chun-Sheng
authors.initials: CS
authors.lastname: Li
authors.forename: Cai-Jun
authors.initials: CJ
authors.lastname: Wu
authors.forename: Jun
authors.initials: J
authors.lastname: Yang
authors.forename: Chen-Chen
authors.initials: CC
authors.lastname: Hang
mesh_terms: D000818:Animals; D001237:Asphyxia / Q000150:complications / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism*; D016887:Cardiopulmonary Resuscitation; D006323:Heart Arrest / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D049268:Positron-Emission Tomography; D013552:Swine; D014693:Ventricular Fibrillation / Q000378:metabolism* / Q000473:pathology / Q000628:therapy