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In both animal and human studies,11,36,37 hyperoxia is an important driver for the arrest of vascular growth in phase 1.
Even room air can lead to hyperoxia compared with the intrauterine environment, where mean oxygen pressure is less than 50 mm Hg during the second half of pregnancy.38 More importantly, supplemental oxygen given to premature infants with respiratory distress can lead to abnormally high oxygen saturation.
Hyperoxia leads to suppression of oxygen-regulated angiogenic growth factors, particularly erythropoietin39,40 and vascular endothelial growth factor (VEGF),41 which in turn causes both cessation of retinal vessel growth and loss of some existing retinal vessels42 (a process that has been partly reversed in mice with the replacement of VEGF and erythropoietin).39-42 Some investigators43 speculate that in more mature infants, exposure to high oxygen concentrations causes loss of existing vessels not seen with controlled oxygen delivery, which mainly causes cessation of vessel growth.
After the first wave of retinopathy of prematurity, when the use of 100% oxygen made even some mature preterm babies blind, oxygen was restricted to 50% of inspired O2, which resulted in about 16 deaths per case of blindness prevented.54 What constitutes the best oxygen saturation at different gestational ages and in each phase of disease is unknown, although hyperoxia can have different effects during phase 2 (when vascular proliferation is taking place) than it does in phase 1.
Strict management of oxygen to minimise alternating hypoxia and hyperoxia and avoidance of undesired high oxygen saturations in phase 1 seem to be the most promising strategies to prevent retinopathy of prematurity, although this outcome has to be balanced against the effect on other morbidities such as cerebral palsy and death.69,70
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