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Bronchopulmonary Dysplasia (BPD) was described as secondary injuries due to long exposure to high FiO2 levels and high pressures during mechanical ventilation. Therefore, the treatment of RDS which is high O2 levels and high pressures over time is the primary cause of BPD on infants. Oxygen toxicity, barotrauma, presence of PDA, and fluid overload are the four factors that are linked to appear in BPD. High concentrations levels of oxygen heads to inflammation, edema, and thickening of the alveolar membrane. As time passes this leads to the necrosis and hemorrhage of the alveolar tissues. As well, the lungs become fibrotic or stiff as the disease advances. Thus in this literature review a research is being done on premature rabbits that are exposed to high levels of oxygen. Their hypothesis states is “hyperoxia will cause progressive changes to the vascular compartment of the developing lung that will result in a phenotype of PH”. As well, treatment is mentioned for BPD. 
Rabbits were chosen to make this study for the reason being that these animals have a short pregnancy and a large litter size, however they have similar lung development as humans.  Adding to that they show histological changes such as inflammatory responses when exposed to high levels of oxygen, and lung function impairment. The study on the rabbits had a control were the preterm rabbits on normoxia and the others on hyperoxia for a total time of 7 days. Several parameters were taken to see the changes between the rabbits exposed to hyperoxia and the rabbits on normoxia. Those parameters are pulmonary artery acceleration time, pulmonary artery acceleration/ ejection time ratio, media thickness, total lung capacity, airway resistance, tissue elastance.
The following will be the vascular changes that happen in the 7 day study of the rabbits exposed high levels of oxygen and normoxia. Thus resulting in Pulmonary Hypertension. Pulmonary artery acceleration time in days 3 and 5 did not make much of difference. However on day seven it significant decreased on the hyperoxia group. Going from 33.5 on day three to 25.03 on day 7. As expected the normoxia group PAAT only increased slightly.
Pulmonary artery acceleration/ ejection time ratio decreased over time which it decreased from 30.58 on day 3 to 26.03 on day 5 to 24.19 on day 7 on the hyperoxia group. In normoxia group PAAT/PAET did not change.
Media thickness is one of the most visible changes in the lungs of the rabbits. Increasing significantly from 13.12 on day three to 16.58 on day seven to the rabbits exposed to hyperoxia. However in the normoxia group the media thickness only increased ever so slightly from 12.57 on day three to 12.83 on day 7.
  The following are the functional parenchymal changes on the lung parenchyma of the preterm rabbits that were in this study.
One interesting outcome on this study is that airway resistance was not affected on the rabbits in the hyperoxia group. Going from 0.082 on day three to 0.124 on day seven. As stated there was no dramatic change in airway resistance. 
Tissue elastance significantly increased on the hyperoxia group going from 8.55 on day three to 49.25 on day seven. However in the normoxia group the elastence decreased from 10.40 on day 3 to 5.97 on day 7 not dramatic change like the other group.
Total lung capacity extremely decreased on the hyperoxia group going from 1.2 on the third day to 0.545 on the seventh day. In the normal group TLC increased from 1.1 on the third day and 2.5 on the seventh day. We can see that the TLC worsen in high levels of oxygen.
 The following will be the changes in the  structure of the lung parenchyma.
The hyperoxia group had a thickening of the alveolar walls going from 8.441 on day 3 to 22.76 on day 7. On the normal group the thickening actually decrease just slightly. 
The radial alveolar count decreased in the hyperoxia group from 5.71 on the third day to 4.71 on the seventh day. The normal group had an increased RAC.
Acute lung inflammation increased on both groups however, it significantly increased more on the hyperoxia group. 0.305 on the third day to 0.659 on the seventh day.
All of these parameters show how the high levels of oxygen changes the lungs of the preterm rabbits making clear that medical professionals have to considerate all the factors affecting BPD on preemies this is only one factor which is hyperoxia. However significant improvements are made during prenatal care such as administration of corticosteroids, preterm birth prevention, and surfactant therapy and better mechanical ventilation strategies. Even though all these factors improve survival it does not decrease the incidence of chronic lung disease.
With the revealing tests above increased levels of FiO2 given to premature rabbits caused progressive functional and structural vascular damage in the lungs. Therefore since the rabbits mimics the disease process in humans, medical professionals that have premature babies as patients have to maintain oxygen levels as low as possible if given any. In the incidence of BPD in the infant the overall treatment is first to prevent it from happening with special considerations such as prevent prematurity and the administration of prenatal glucocorticoids, single course. However the patient can still get BPD if the neonate is delivered premature and no prevention matters are taken. Surfactant replacement will decrease a possibility of BPD and oxygen therapy but has to be monitored because of the risks known of excessive oxygen therapy. High frequency ventilation is a possible benefit effect for BPD. Other measures are taken too that are not in this text. BPD can be a ferocious disease if not treated properly and taking preventive measures can help decrease the possibly of BPD.

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