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Table 1 Summary of hypoxemic reperfusion studies

From: Hypoxemic reperfusion of ischemic states: an alternative approach for the attenuation of oxidative stress mediated reperfusion injury

Study Type of study Model of ischemia Reperfusion protocol Outcome
Perry et al. [40] Experimental Celiac artery ischemia through adjustable screw clamp Pa O2 = 34 mmHg for 1 h before return to normal perfusion ↓gastric mucosal bleeding
Douzinas et al. [41] Experimental SMA clamping Pa O2 = 30–35 mmHg with gradual return to normoxemia over a 2 h period ↓intestinal mucosa and lung injury
↓inflammatory response
Douzinas et al. [42] Experimental SMA clamping Pa O2 = 30–35 mmHg with gradual return to normoxemia over a 2 h period ↑hemodynamic profile
↓oxidative response
↓myocardial injury
Burda et al. [43] Experimental Clamping of left subclavian artery and brachiocephalic trunk Pa O2 = 37.5 mmHg with gradual return to normoxemia over a 15–30 minute period ↑cerebral protein synthesis
Douzinas et al. [44] Experimental Global cerebral ischemic insult through decrease of MAP, bilateral clamping of carotid arteries and cessation of respiration FiO2 = 0.12 with gradual increase to achieve PaO2 = 100 mmHg over a 1 h period ↑neurological outcome
↓oxidative response
Douzinas et al. [45] Experimental Global cerebral ischemic insult through decrease of MAP, bilateral clamping of carotid arteries and cessation of respiration Pa O2 = 30–35 mmHg with gradual increase to achieve PaO2 = 100 mmHg over a 1 h period ↓cerebral injury
Hickey et al. [46] Experimental Deep hypothermic circulatory arrest Pa O2 = 40–50 mmHg throughout the reperfusion period ↑cerebral injury
Abdel-Rahman et al. [47] Experimental Aortic clamping and cardioplegic arrest Pa O2 = 40–50 mmHg gradually increased towards normoxemia over a 10 minute period ↑hemodynamic profile
↓myocardial injury
↓oxidative response
Abdel-Rahman et al. [48] Clinical CPB for CABG Pa O2 = 50 mmHg with return to normoxemia over a 5 minute period ↓oxidative response
Fercakova et al. [49] Experimental Infrarenal aortic occlusion Graded postischemic reoxygenation ↑neuroprotection
Daxnerova et al. [50] Experimental Infrarenal aortic occlusion Graded postischemic reoxygenation ↑neuroprotection
Marsala et al. [51] Experimental Infrarenal aortic occlusion Graded postischemic reoxygenation ↓neuropathological damage
Orendacova et al. [52] Experimental Infrarenal aortic occlusion Pa O2 = 48 mmHg with gradual return to normoxemia over a 15 minute period ↑neuroprotection
Lukacova et al. [53] Experimental Infrarenal aortic occlusion Pa O2 = 48 ± 12 mmHg with gradual return to normoxemia over a 30 minute period ↑neuroprotection
Lehmann et al. [54] Experimental Supraceliac aortic clamp Pa O2 = 25–35 mmHg for 30 minutes with gradual return to normoxemia over a 90 minute period ↓hemodynamic profile
Douzinas et al. [55] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.12 with gradual increase to FiO2 = 0.21 over a 40 minute period ↑hemodynamic profile
↓oxidative response
↓inflammatory response
Douzinas et al. [3] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.08–0.10 with gradual increase to FiO2 = 0.21 over a 60 minute period ↑hemodynamic profile
↓oxidative response
↓inflammatory response
Douzinas et al. [56] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.08–0.10 with gradual increase to FiO2 = 0.21 over a 60 minute period ↓oxidative response
↓inflammatory response
Douzinas et al. [57] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.08-0.10 with gradual increase to FiO2 = 0.21 over a 60 minute period ↑vascular homeostasis
Douzinas et al. [58] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.08-0.10 with gradual increase to FiO2 = 0.21 over a 60 minute period ↓oxidative response
↓lung injury
Douzinas et al. [59] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.08-0.10 with gradual increase to FiO2 = 0.21 over a 60 minute period ↓oxidative response
↓inflammatory response
↓lung injury
Douzinas et al. [60] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.08-0.10 with gradual increase to FiO2 = 0.21 over a 60 minute period ↓oxidative response
↓inflammatory response
↓liver injury
Luo et al. [61] Experimental Hemorrhagic shock - exsanguination FiO2 = 0.11 with gradual increase to FiO2 = 0.21 over a 60 minute period ↓hemodynamic profile
─oxidative response
─inflammatory response
  1. Table summarizes the data of the available studies of hypoxemic reperfusion presenting the setting, the model of ischemia – reperfusion injury studied, the reperfusion protocol and the main outcomes
  2. P a O 2 partial arterial oxygen pressure, SMA superior mesenteric artery, FiO 2 fraction of inspired oxygen, MAP mean arterial pressure, CPB cardio-pulmonary bypass, CABG coronary artery bypass grafting