title: Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction.
abstract: OBJECTIVE
  The purpose of the study was to test the hypothesis that intracoronary aqueous oxygen (AO) hyperbaric reperfusion reduces myocardial injury after prolonged coronary occlusion. Background. Attenuation of ischemia/reperfusion injury by the use of hyperbaric oxygen (HBO) administered during reperfusion has been demonstrated for a wide variety of tissues, including myocardium. We have recently developed a more practical, catheter-based, site-specific method for delivery of oxygen at hyperbaric levels with aqueous oxygen infusion.
  
  
  METHODS
  Following a 60-minute balloon occlusion of the left anterior descending coronary artery in swine, intracoronary AO hyperoxemic perfusion (50 mL blood/minute; 1.5 mL AO/minute; mean pO2 = 834   104 mmHg) was performed for 90 minutes after a 15-minute period of normoxemic autoreperfusion (physiologic reperfusion). Control groups consisted of autoreperfusion alone; active normoxemic perfusion (50 mL/minute) for 90 minutes; and hyperoxemic perfusion with a hollow fiber oxygenator (HFO) for 90 minutes. Results. A significant improvement in left ventricular ejection fraction was noted by ventriculography at 105 minutes of reperfusion (ANOVA, p < 0.05), compared to the 15-minute autoreperfusion period, only in the AO and HFO groups. Mean percent infarct size (area of necrosis)/(area at risk), quantitative post-mortem hemorrhage score, and myocardial myeloperoxidase levels at 3 hours of reperfusion were significantly less in the AO group (ANOVA, p < 0.05), but not in the HFO group, compared to normoxemic groups. Conclusions. The results demonstrate that intracoronary hyperbaric reperfusion with AO, but not with a membrane oxygenator, attenuates myocardial ischemia/reperfusion injury.
authors.affiliation: Cardiovascular Research Laboratory, Wayne State University, Detroit, MI 48201, USA. aa1811@wayne.edu
authors.forename: J Richard
authors.initials: JR
authors.lastname: Spears
authors.forename: Cassandra
authors.initials: C
authors.lastname: Henney
authors.forename: Petar
authors.initials: P
authors.lastname: Prcevski
authors.forename: Rui
authors.initials: R
authors.lastname: Xu
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Giles J
authors.initials: GJ
authors.lastname: Brereton
authors.forename: Marcello
authors.initials: M
authors.lastname: DiCarli
authors.forename: Ali
authors.initials: A
authors.lastname: Spanta
authors.forename: Richard
authors.initials: R
authors.lastname: Crilly
authors.forename: Abdulbaset M
authors.initials: AM
authors.lastname: Sulaiman
authors.forename: Samir
authors.initials: S
authors.lastname: Hadeed
authors.forename: Steven
authors.initials: S
authors.lastname: Lavine
authors.forename: William R
authors.initials: WR
authors.lastname: Patterson
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Creech
authors.forename: Richard
authors.initials: R
authors.lastname: Vander Heide
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D006931:Hyperbaric Oxygenation / Q000379:methods*; D007261:Infusions, Intra-Arterial; D023421:Models, Animal; D009203:Myocardial Infarction / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000379:methods*; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D013552:Swine