Abstract
Ischemia-reperfusion injury (IRI) is a paradoxical tissue response following reoxygenation of an ischemic organ. The predominant role of oxidative stress (OS) in IRI is well established. In humans, hyperpoxia exacerbates myocardial infarction (MI) size in the setting of STEMI (AVOID study. Circulation 2015). This is not seen in experimental studies in young and healthy animals. Effects of hyperoxia on OS during myocardial reperfusion (MR) in STEMI are unknown in mature rodents. To test the hypothesis that hyperoxic myocardial reperfusion (HMR) in mature Wistar rats increases IRI in comparison to normoxic reperfusion (NMR). Twenty-nine mature male Wistar rats (35–40vweeks old) underwent myocardial ischemia by LAD ligation for 60 minutes. Animals were randomised either in the HMR (receiving 100% oxygen, n = 13) or the NMR (ambient air, n = 16) groups. MR lasted for 3 hours after LAD reopening. The SHAM group underwent surgery without LAD ligation ( n = 7) and was ventilated with ambient air for 4 hours after surgery. Blood samples were collected before ischemia and after reperfusion. Troponin T was measured as a surrogate of MI size. Plasma superoxide dismutase (SOD) and total thiols (TT) were measured as antioxidant biomarkers. Plasma malondialdehyde (MDA) and 3-chlorotyrosine (3-ClT) (myeloperoxidase surrogate) were measured as oxidant biomarkers. Pre-ischemia troponin, plasma SOD, TT, MDA and 3-ClT were similar in the 3 groups (HMR, NMR and SHAM). There was a difference in the post-reperfusion troponin measurement between SHAM and HMR, and SHAM and NMR, P = 0.01 and 0.03 respectively. Post-reperfusion troponin levels did not differ between HMR and NMR ( P -value = 0.178). Post-reperfusion OS biomarkers did also not differ between HMR and NMR. HMR after STEMI in mature Wistar rats increased neither infarct size nor oxidative stress. Aging only may thus not explain the deleterious effect of HMR in humans.
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