title: Hyperoxemic reperfusion after prolonged cardiac arrest in a rat cardiopulmonary bypass resuscitation model.
abstract: BACKGROUND
  The effect of hyperoxygenation at reperfusion, particularly in the setting of cardiac arrest, remains unclear. This issue was studied in a prolonged cardiac arrest model consisting of 25 min cardiac arrest in a rat resuscitated with cardiopulmonary bypass (CPB). The objective of this study was to determine the effect of hyperoxygenation following prolonged cardiac arrest resuscitation on mitochondrial and cardiac function.
  
  
  METHODS
  Male Sprague-Dawley rats (400-450 g) were anesthetized with ketamine and xylazine and instrumented for closed chest cardiopulmonary bypass (CPB). Following a 25-min KCl-induced cardiac arrest, the animals were resuscitated by CPB with 100% oxygen. Three minutes after successful return of spontaneous circulation (ROSC), the animals received either normoxemic reperfusion (CPB with 40-50% oxygen) or hyperoxemic reperfusion (CPB with 100% oxygen) for 1 h. Post-resuscitation hemodynamics, cardiac function, mitochondrial function and immunostaining of 3-nitrotyrosine were compared between the two different treatment groups.
  
  
  RESULTS
  At 1 h after ROSC, the hyperoxemic reperfusion group had a significant higher mean arterial pressure, less metabolic acidosis and better diastolic function than the normoxemic reperfusion group. Cardiac mitochondria from the hyperoxemic reperfusion group had a higher respiratory control ratio (RCR) and cardiac tissue showed less nitroxidative stress compared to the normoxemic reperfusion group.
  
  
  CONCLUSIONS
  One hour of hyperoxemic reperfusion after 25 min of cardiac arrest in an in vivo CPB model resulted in significant short-term improvement in myocardial and mitochondrial function compared with 1h of normoxemic reperfusion. This myocardial response may differ from previously reported post-arrest hyperoxia mediated effects following shorter arrest times.
authors.affiliation: Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA.
authors.forename: Steve T
authors.initials: ST
authors.lastname: Yeh
authors.forename: Sverre E
authors.initials: SE
authors.lastname: Aune
authors.forename: Traci A
authors.initials: TA
authors.lastname: Wilgus
authors.forename: Allison E
authors.initials: AE
authors.lastname: Parent
authors.forename: Mark G
authors.initials: MG
authors.lastname: Angelos
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis; D002315:Cardiopulmonary Bypass / Q000379:methods*; D006323:Heart Arrest / Q000503:physiopathology / Q000628:therapy*; D006439:Hemodynamics; D018496:Hyperoxia; D007150:Immunohistochemistry; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D010102:Oxygen Inhalation Therapy / Q000379:methods*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014443:Tyrosine / Q000031:analogs & derivatives / Q000032:analysis
chemical_list: C002744:3-nitrotyrosine; D014443:Tyrosine