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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