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首页> 外文期刊>Journal of Perinatal Medicine >Bronchopulmonary dysplasia and early prophylactic inhaled nitric oxide in preterm infants: current concepts and future research strategies in animal models.
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Bronchopulmonary dysplasia and early prophylactic inhaled nitric oxide in preterm infants: current concepts and future research strategies in animal models.

机译:早产儿支气管肺发育不良和早期预防性吸入一氧化氮:动物模型的当前概念和未来研究策略。

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摘要

Abstract We reviewed the literature on the use of inhaled nitric oxide and the influence of supplemental oxygen on bronchopulmonary dysplasia (BPD), and the role of endogenous nitric oxide-synthase, vascular endothelial growth factor, the interplay of nitric oxide and superoxide, protein nitration and the nuclear factor kappa B-pathway. BPD is a major cause of neonatal mortality and morbidity leading to arrested lung development in newborns. Several studies indicate that inhaled nitric oxide (iNO) improves pulmonary angiogenesis, lung alveolarization, distal lung growth and pulmonary function in preterm infants. Given the inconclusive results of clinical studies, however, it is unclear which subpopulations of infants might benefit. Moreover, data on iNO are conflicting whether exogenous nitric oxide is protective or damaging in the presence of hyperoxia. The toxicology of iNO is poorly understood and its potential interaction with oxygen has to be considered given that infants treated with iNO are alsosupplemented with oxygen. The underlying mechanisms of the effects of iNO in the newborn lung need further analysis. New data clarifying the role of endogenous nitric oxide-synthases, vascular endothelial growth factor (VEGF), the interplay of nitric oxide and superoxide, and protein nitration with concurrent iNO-therapy might answer some of these questions.
机译:摘要我们综述了吸入一氧化氮的使用和补充氧对支气管肺发育不良(BPD)的影响,内源性一氧化氮合酶,血管内皮生长因子的作用,一氧化氮与超氧化物的相互作用,蛋白质硝化的文献。以及核因子κB通路。 BPD是导致新生儿死亡和发病的主要原因,导致新生儿的肺部发育停滞。多项研究表明,吸入一氧化氮(iNO)可改善早产儿的肺血管生成,肺泡形成,远端肺生长和肺功能。然而,鉴于临床研究尚无定论,目前尚不清楚婴儿的哪些亚群可能会受益。此外,关于iNO的数据在高氧存在下是外源性一氧化氮是保护性还是破坏性的也存在矛盾。鉴于对iNO的毒理学了解甚少,并且考虑到iNO治疗的婴儿也需要补充氧气,因此必须考虑其与氧气的潜在相互作用。 iNO对新生肺的影响的潜在机制需要进一步分析。新数据阐明了内源性一氧化氮合酶,血管内皮生长因子(VEGF),一氧化氮和超氧化物的相互作用以及同时进行iNO治疗的蛋白质硝化作用可能会回答其中一些问题。

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