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• W2034232698 abstract "Summary: Plasminogen, total protein, and surface-active material were measured in antniotic fluid in 112 pregnancies at 11–42 weeks' gestation. In 65 of these pregnancies, cord blood was also analyzed for serum plasminogen and total protein. Plasminogen was detected in 25 of 114 amniotic fluid samples, and 23 came from pregnancies of less than 37 weeks' gestation. Plasminogen was found in 15 of 32 amniotic fluid samples from pregnancies with complications, but only in 10 of 80 “uncomplicated” pregnancies. The mean cord serum plasminogen was relatively constant in births or abortuses of 17 to 30 weeks' gestation, but was present in increasing amounts in births of gestational ages from 30 to 40 weeks. The concentration of plasminogen in cord serum was directly related to the cord total protein (r = 0.7513, P < 0.001). The cord plasminogen concentration was significantly higher in infants with a positive foam stability test (5.6 ± 0.3 mg/100 ml) than in the combined group of infants with negative and intermediate tests (4.3 ± 0.16, P < 0.005). However, infants with a positive foam stability also had a significantly greater gestational age than infants with a negative or intermediate foam stability test. With one exception, infants with a low cord plasminogen (below 4 mg/100 ml) developed respiratory distress syndrome (RDS) only if amniotic fluid surfactant was low. The data suggest that low levels of serum plasminogen are correlated with severe lung disease only in the presence of surfactant deficiency. Speculation: In infants that develop the respiratory distress syndrome, many serum proteins are found in diminished concentration in the umbilical cord blood. Interest has naturally focused on the antiproteinases because a functional deficiency in these could contribute to fibrin deposition, a characteristic finding in hyaline membranes. However, it has been difficult to determine whether antiproteinases are low because of increased consumption or as a result of nonspecific leakage of many proteins from the blood. Even the evidence of a selectively greater depletion of α1-antitrypsin than the larger molecule, plasminogen, or other cord serum proteins may simply represent a preferential molecular sieving of small molecules. If another serum protein of similar or lesser molecular weight than the relatively small α1-antitrypsin were simultaneously studied in the cord blood, it should be possible to answer the question of a selective depletion. If a greater deficiency of serum α1-antitrypsin than of the second protein of similar size were found in RDS, this would favor a specific depletion of the antiproteinase. If the two proteins were equally deficient or if a smaller protein were more deficient, there would be little evidence for a specific deficiency of α1-antitrypsin." @default.
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• W2034232698 date "1977-02-01" @default.
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• W2034232698 title "Serum Plasminogen and Lung Surfactant in the Respiratory Distress Syndrome" @default.
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• W2034232698 doi "https://doi.org/10.1203/00006450-197702000-00008" @default.
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