TY - JOUR
T1 - Altered urinary excretion of elastin cross-links in premature infants who develop bronchopulmonary dysplasia
AU - Bruce, M. C.
AU - Wedig, K. E.
AU - Jentoft, N.
AU - Martin, R. J.
AU - Cheng, P. W.
AU - Boat, T. F.
AU - Fanaroff, A. A.
PY - 1985
Y1 - 1985
N2 - In order to determine whether elastin degradation is increased in infants whose respiratory insufficiency requires ventilation with high concentrations of O2, we quantitated, by amino acid analysis, the elastin degradation products (desmosines) excreted in the urine of 14 premature male infants during the first 3 wk of life. 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 first week 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 μg/kg to 9.0 ± 3.5 μg/kg. In contrast, desmosine excretion did not remain elevated in the BPD infants, decreasing from 10.6 ± 2.2 μg/kg to 6.1 ± 2.9 μg/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 is thought to 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.
AB - In order to determine whether elastin degradation is increased in infants whose respiratory insufficiency requires ventilation with high concentrations of O2, we quantitated, by amino acid analysis, the elastin degradation products (desmosines) excreted in the urine of 14 premature male infants during the first 3 wk of life. 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 first week 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 μg/kg to 9.0 ± 3.5 μg/kg. In contrast, desmosine excretion did not remain elevated in the BPD infants, decreasing from 10.6 ± 2.2 μg/kg to 6.1 ± 2.9 μg/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 is thought to 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.
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U2 - 10.1164/arrd.1985.131.4.568
DO - 10.1164/arrd.1985.131.4.568
M3 - Article
C2 - 3994150
AN - SCOPUS:0021882165
SN - 0003-0805
VL - 131
SP - 568
EP - 572
JO - American Review of Respiratory Disease
JF - American Review of Respiratory Disease
IS - 4
ER -