Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exogenous or inhaled NO (iNO) has been successfully used, as a selective pulmonary vasodilator, in a wide variety of clinical situations especially in the management of persistent pulmonary hypertension in the newborn. A better understanding of the role of endogenous and exogenous NO in the lungs of surfactant-deficient animals exposed to hyperoxia could result in novel strategies for the better management of RDS in premature babies with the ultimate aim to decrease chronic lung disease in these infants. This review will focus on the effects of NO, when used in combination with hyperoxia, on lung injury; information on the effects on cell culture systems and animal models will be used to highlight the unique responses of the developing lung. Most of the data from cell culture systems and adult animal models of hyperoxia-induced lung injury suggests that endogenous NO has a protective role. In the newborn animal, endogenous NO appeared to be harmful, had no effect or was protective in hyperoxia-induced lung injury. The data are conflicting on the issue of whether exogenous NO is protective or damaging in the presence of hyperoxia on lung cells and animal models. Despite the variability in the studies, it would appear that low dose exogenous NO for short duration is beneficial in hyperoxic lung injury in adult and newborn animals. In the human newborn, use of iNO in infants< 34 weeks of gestation should be considered experimental, pending results of ongoing trials.
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PMID:The role of nitric oxide in hyperoxia-induced injury to the developing lung. 1270 92

Treatment of neonatal RDS in premature infants with intratracheal administration of natural surfactant has become gold standard therapy. Natural surfactant preparations mainly contain, apart from phospholipids, the surfactant associated proteins B and C (SP-B and SP-C). Both proteins are synthesized mainly in alveolar type-II cells and Clara-cells, SP-B, also in the gastrointestinal tract and the auditive tube. SP-B is encoded on chromosome 2 over a region with 11 exons, whereas the SP-C gene is localized on chromosome 8 in a region containing 6 exons. Transcription of both SP-B and SP-C is induced by TTF-1. Furthermore SP-1 and SP-3 are known as transcription factors for SP-B. The main function of SP-B and SP-C is to maintain physiologic surface properties enabeling adequate lung mechanics. A complete SP-B deficiency following homozygous mutations in the SP-B gene (e. g. 121-ins 2-mutation) therefore leads to severe respiratory failure postnatally, due to the lack of functional surfactant. On the other hand complete deficiency of SP-C causes chronic interstitial pneumonitis as well in infants as in adults depending on disease-modifiers yet unknown. Besides the surface tension lowering property, SP-B reveals immunological functions regarding its interaction with different proinflammatory cellular systems as well as other inflammatory mediators, e. g. following hyperoxia. For SP-C first studies have described modulation of inflammatory reactions in macrophages, suggesting similar immune-modulatory effects. Whereas basic effects on lung mechanisms of both lipophilic surfactant proteins seem to be well understood, their immunologic local pulmonary functions and effects on surfactant metabolism require further investigations.
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PMID:[Surfactant-associated proteins B and C: molecular biology and physiologic properties]. 1522 16