Effects of hyperoxia and cardiovascular risk factors on myocardial ischemia reperfusion injury: a randomized, sham and placebo controlled parallel study

Recent studies on O2 supplementation in acute coronary syndrome patients are equivocal. We tested the hypothesis that oxidative stress (OS) is increased in rodents with cardiovascular risk factors and enhances ischemia reperfusion injury in the presence of hyperoxia.
Forty-three Wistar rats (WR), 30 spontaneous hypertensive rats (SHR) and 33 obese Zucker rats (ZR) were randomized in a sham procedure (1/3rd) or a left anterior descending ligation for 60 minutes (2/3rd). This was followed by 3 hours of reperfusion while animals were randomised either in a hyperoxic (HR) or a normoxic reperfusion group (NR). Baseline troponin (cTnT) was larger in SHR and ZR than WR (both p < 0.001). HR was associated with a lesser troponin rise in SHR and ZR than in NR (both p < 0.001); while the reverse occurred in WR (p < 0.001). In SHR, HR limited total MPO (myeloperoxydase) increase as compared to NR (p = 0.0056) to the contrary of total MPO in WR (p = 0.013). NR was associated with a drastic reduction of total thiols as compared to HR both in SHR and in ZR (both p < 0.001).
Despite a heightened baseline OS, HR rather restrained myocardial necrosis and anti/pro-oxidant imbalance in SHR and ZR, to the reverse of healthy WR.