ALTERED URINARY-EXCRETION OF ELASTIN CROSS-LINKS IN PREMATURE-INFANTS WHO DEVELOP BRONCHOPULMONARY DYSPLASIA
ALTERED URINARY-EXCRETION OF ELASTIN CROSS-LINKS IN PREMATURE-INFANTS WHO DEVELOP BRONCHOPULMONARY DYSPLASIA
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DOI：
10.1164/arrd.1985.131.4.568
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发表时间：
1985-01-01
期刊：
影响因子：
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通讯作者：
FANAROFF, AA
中科院分区：
文献类型：
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作者：
BRUCE, MC;WEDIG, KE;FANAROFF, AA
为了确定是否弹性蛋白降解增加的婴儿呼吸功能不全，需要通气与高浓度的O2，弹性蛋白降解产物（锁链素）排泄在尿中的14个早产男婴在前3周的生活进行了定量的氨基酸分析。其中8名婴儿，即“低氧”婴儿，没有严重的肺部疾病，在出生后的前8小时内不需要超过40%的O2。其他6名婴儿，回顾性选择，因为他们发展支气管肺发育不良（BPD），通气超过60%的氧气至少在第一个72小时的生活。在出生后的前3周内，BPD婴儿的锁链素排泄模式与“低氧”婴儿的排泄模式有显著差异（P < 0.05）。在出生后第1周末，BPD发生较晚的婴儿的锁链素排泄量显著高于无严重肺部疾病的“低氧”婴儿（P < 0.05）。从第7-9天到第20-22天，锁链素排泄在“低氧”婴儿中从6.9 . ±. 1.7μ g/kg至9.0 ±。3.5μ g/kg。相比之下，锁链素排泄在BPD婴儿中没有保持升高，从10.6 ± 0.5降低。2.2μ g/kg至6.1 ±。2.9. μ g/kg。在BPD婴儿中，到第9天锁链素排泄升高可能反映肺损伤，而超过第9天锁链素排泄降低表明弹性蛋白合成和周转受损，可能是营养缺乏的结果。在“低氧”和BPD婴儿中所观察到的锁链素排泄模式之间的差异强烈地表明了两组婴儿中弹性蛋白代谢的差异。弹性蛋白可能在肺泡间隔发育中起关键作用;因此，弹性蛋白的破坏和/或合成受损可能是与BPD相关的肺生长受损的原因。
To determine whether elastin degradation is increased in infants whose respiratory insufficiency required ventilation with high concentrations of O2, the elastin degradation products (desmosines) excreted in the urine of 14 premature male infants during the first 3 wk of life were quantitated by amino acid analysis. Eight of these infants, the "low-O2" infants, did not have severe lung disease and did not require more than 40% O2 beyond the first 8 h of life. The other 6 infants, selected retrospectively because they developed bronchopulmonary dysplasia (BPD), were ventilated with more than 60% O2 for at least the first 72 h of life. The pattern of desmosine excretion observed in infants who developed BPD differed significantly (P < 0.05) from the excretion pattern seen in "low-O2" infants during the first 3 wk of life. At the end of the 1st wk of life, desmosine excretion was significantly greater (P < 0.05) in the infants who later developed BPD than in the "low-O2" infants without severe lung disease. From days 7-9 to 20-22, desmosine excretion increased in the "low-O2" infants from 6.9 .+-. 1.7 .mu.g/kg to 9.0 .+-. 3.5 .mu.g/kg. In contrast, desmosine excretion did not remain elevated in the BPD infants, decreasing from 10.6 .+-. 2.2 .mu.g/kg to 6.1 .+-. 2.9 .mu.g/kg during the same period. In the BPD infants, elevated desmosine excretion through day 9 is likely to reflect lung injury, whereas decreased desmosine excretion beyond day 9 suggests that elastin synthesis and turnover is impaired, possibly as a result of nutritional deficiencies. The observed differences between desmosine excretion patterns in the "low-O2" and BPD infants strongly suggests differences in elastin metabolism in the 2 groups of infants. Elastin may play a critical role in alveolar septal development; therefore, destruction and/or impaired synthesis of elastin might be a causal factor in the impaired lung growth associated with BPD.