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The "Normobaric Oxygen Paradox" (NOP) is a physiologic mechanism that induces an increase of endogenous erythropoietin (EPO) production by creating a state of relative hypoxia in subjects previously exposed to hyperoxia, followed by a rapid return to normoxia. Oxygen exposure duration and inspired oxygen fraction required to observe a significant increase in EPO or hemoglobin are not clearly defined. Consequently, we here study the effect of one model of relative hypoxia on EPO, reticulocytes and hemoglobin stimulation in patients after surgery. Patients were prospectively randomized in two groups. The O2 group (n = 10) received 100% oxygen for 1 h per day for eight consecutive days, via a non-rebreathing mask. The control group (n = 12) received no oxygen variation. Serum EPO, hemoglobin and reticulocyte count were measured on admission and postoperatively on days seven and nine. Percentage EPO at day nine with respect to the baseline value was significantly elevated within the groups [O2 group: 323.7 (SD ± 139.0); control group: 365.6 (SD± 162.0)] but not between them. No significant difference was found between the groups in terms of reticulocytes count and hemoglobin. Our NOP model showed no difference on EPO increase between the two groups. However, both groups expressed separately significant EPO elevation. [ABSTRACT FROM AUTHOR]

The “Normobaric Oxygen Paradox” (NOP) is a physiologic mechanism that induces an increase of endogenous erythropoietin (EPO) production by creating a state of relative hypoxia in subjects previously exposed to hyperoxia, followed by a rapid return to normoxia. Oxygen exposure duration and inspired oxygen fraction required to observe a significant increase in EPO or hemoglobin are not clearly defined. Consequently, we here study the effect of one model of relative hypoxia on EPO, reticulocytes and hemoglobin stimulation in patients after surgery. Patients were prospectively randomized in two groups. The O2 group (n = 10) received 100% oxygen for 1 h per day for eight consecutive days, via a non-rebreathing mask. The control group (n = 12) received no oxygen variation. Serum EPO, hemoglobin and reticulocyte count were measured on admission and postoperatively on days seven and nine. Percentage EPO at day nine with respect to the baseline value was significantly elevated within the groups [O2 group: 323.7 (SD ± 139.0); control group: 365.6 (SD± 162.0)] but not between them. No significant difference was found between the groups in terms of reticulocytes count and hemoglobin. Our NOP model showed no difference on EPO increase between the two groups. However, both groups expressed separately significant EPO elevation.

As we all know that stroke is still a leading cause of death and acquired disability. Etiological treatment and brain protection are equally important. This review aimed to summarize the advance of normobaric-hyperoxia (NBHO) on brain protection in the setting of experimental stroke and brain trauma. We analyzed the data from relevant studies published on PubMed Central (PMC) and EMBASE, about NBHO on brain protection in the setting of experimental ischemic and hemorrhagic strokes and brain trauma, which revealed that NBHO had important value on improving hypoxia and attenuating ischemia damage. The mechanisms of NBHO involved increasing the content of oxygen in brain tissues, restoring the function of mitochondria, enhancing the metabolism of neurons, alleviating blood-brain barrier (BBB) damage, weakening brain cell edema, reducing intracranial pressure, and improving cerebral blood flow, especially in the surrounding of injured area of the brain, to make the neurons in penumbral area alive. Compared to hyperbaric oxygen (HBO), NBHO is more safe and more easily to transform to clinical use, whereby, further studies about the safety and efficacy as well as the proper treatment protocol of NBHO on human may be still needed.

As we all know that stroke is still a leading cause of death and acquired disability. Etiological treatment and brain protection are equally important. This review aimed to summarize the advance of normobaric-hyperoxia (NBHO) on brain protection in the setting of experimental stroke and brain trauma. We analyzed the data from relevant studies published on PubMed Central (PMC) and EMBASE, about NBHO on brain protection in the setting of experimental ischemic and hemorrhagic strokes and brain trauma, which revealed that NBHO had important value on improving hypoxia and attenuating ischemia damage. The mechanisms of NBHO involved increasing the content of oxygen in brain tissues, restoring the function of mitochondria, enhancing the metabolism of neurons, alleviating blood-brain barrier (BBB) damage, weakening brain cell edema, reducing intracranial pressure, and improving cerebral blood flow, especially in the surrounding of injured area of the brain, to make the neurons in penumbral area alive. Compared to hyperbaric oxygen (HBO), NBHO is more safe and more easily to transform to clinical use, whereby, further studies about the safety and efficacy as well as the proper treatment protocol of NBHO on human may be still needed. [ABSTRACT FROM AUTHOR]