Endogenous surfactant metabolism in critically ill infants measured with stable isotope labeled fatty acids

被引:43
|
作者
Cogo, PE
Carnielli, VP
Bunt, JEH
Badon, T
Giordano, G
Zacchello, F
Sauer, PJJ
Zimmermann, LJI
机构
[1] Univ Padua, Dept Paediat, I-35128 Padua, Italy
[2] Erasmus Univ, Sophia Childrens Hosp, Div Neonatol, Dept Paediat, NL-3015 GJ Rotterdam, Netherlands
[3] Univ Groningen, Dept Paediat, NL-9700 RB Groningen, Netherlands
关键词
D O I
10.1203/00006450-199902000-00015
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Little is known about endogenous surfactant metabolism in infants, because radioactive isotopes used for this purpose in animals cannot be used in humans. We developed a novel and safe method to measure the endogenous surfactant kinetics in vivo in humans by using stable isotope labeled fatty acids. We infused albumin-bound [U-C-13]palmitic acid (PA) and [U-C-13]linoleic acid (LLA) for 24 h in eight critically ill infants (mean +/- SD; weight. 3.7 +/- 1.3 kg; age: 51.3 +/- 61.6 d) who required mechanical ventilation, The C-13 enrichment of PA and LLA in surfactant phosphatidylcholine (PC), obtained from tracheal aspirates, was measured by gas chromatography combustion interface-isotope ratio mass spectrometry. We measured a significant incorporation of both C-13-PA and C-13-LLA into surfactant PC. PC-PA and PC-LW became enriched after 8.7 +/- 4.9 h (range: 3.4-17.3) and 10.0 +/- 7.2 h (range: 3.0-22.4), respectively; the times at maximum enrichment were 49.2 +/- 8.9 and 45.6 +/- 19.3 h, respectively. The fractional synthesis rate of surfactant PC-PA ranged from 0.4 to 3.4% per h, whereas the fractional synthesis rate of PC-LLA ranged from 0.5 to 3.8% per h. The surfactant PC-PA and PC-LLA half-lives ranged from 16.8 to 177.7 and 23.8 to 144.4 h, respectively. This method provides new data on surfactant metabolism in infants requiring mechanical ventilation. We found that synthesis of surfactant from plasma PA and LLA is a slow process and that there were marked differences in PC kinetics among infants. This variability could be related to differences in lung disease and could affect the clinical course of the respiratory failure.
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收藏
页码:242 / 246
页数:5
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