title: Hyperoxia during early reperfusion does not increase ischemia/reperfusion injury.
abstract: OBJECTIVE
  Oxygen is routinely administered to patients undergoing acute myocardial infarction as well as during revascularization procedures and cardiac surgery. Because reactive oxygen species are mediators of ischemia/reperfusion injury, increased oxygen availability might theoretically aggravate myocardial injury during reperfusion. We hypothesized that ventilation with a hyperoxic gas at start of reperfusion might increase ischemia/reperfusion injury.
  
  
  METHODS
  Rats were anesthetized with isoflurane and ventilated with 40% oxygen. The animals were subjected to 40 min of regional myocardial ischemia and 120 min of reperfusion. In the test group, rats (n=11) were ventilated with a normobaric hyperoxic gas (95% O2) during the last 10 min of ischemia and the first 10 min of reperfusion. Control rats (n=14) were ventilated with 40% O2 throughout the experiments. Due to irreversible reperfusion arrhythmias, one animal in the hyperoxia group and six animals in the control group were excluded. Hearts (n=8 in the control group and n=10 in the test group) were harvested for measurement of infarct size.
  
  
  RESULTS
  The incidence of lethal arrhythmias was 1/11 in the test group and 6/14 in the control group (p=0.06). Reperfusion with normobaric hyperoxia did not influence infarct size (20±8% of area at risk) compared with the normoxia group (24±8% and of area at risk), respectively (mean±SD, p>0.2).
  
  
  CONCLUSIONS
  Normobaric hyperoxia during early reperfusion did not increase ischemia/reperfusion injury.
authors.affiliation: Faculty of Medicine, Department of Molecular Biosciences, University of Oslo, and Institute for Experimental Medical Research, Department of Surgery, Oslo University Hospital, Oslo, Norway. l.h.mariero@medisin.uio.no
authors.forename: Lars Henrik
authors.initials: LH
authors.lastname: Mariero
authors.forename: Arkady
authors.initials: A
authors.lastname: Rutkovskiy
authors.forename: Kåre-Olav
authors.initials: KO
authors.lastname: Stensløkken
authors.forename: Jarle
authors.initials: J
authors.lastname: Vaage
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D018496:Hyperoxia / Q000097:blood / Q000150:complications*; D008297:Male; D009203:Myocardial Infarction / Q000097:blood / Q000209:etiology / Q000473:pathology; D015425:Myocardial Reperfusion / Q000379:methods*; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000209:etiology* / Q000473:pathology; D010100:Oxygen / Q000097:blood; D010102:Oxygen Inhalation Therapy / Q000009:adverse effects; D010313:Partial Pressure; D051381:Rats; D017208:Rats, Wistar
chemical_list: D010100:Oxygen