ELASTASE AND ALPHA-1-PROTEINASE INHIBITOR ACTIVITY IN TRACHEAL ASPIRATES DURING RESPIRATORY-DISTRESS SYNDROME - ROLE OF INFLAMMATION IN THE PATHOGENESIS OF BRONCHOPULMONARY DYSPLASIA
ELASTASE AND ALPHA-1-PROTEINASE INHIBITOR ACTIVITY IN TRACHEAL ASPIRATES DURING RESPIRATORY-DISTRESS SYNDROME - ROLE OF INFLAMMATION IN THE PATHOGENESIS OF BRONCHOPULMONARY DYSPLASIA
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DOI:
10.1172/jci111015
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发表时间:
1983-01-01
影响因子:
15.9
通讯作者:
GLUCK, L
中科院分区:
文献类型:
--
作者:
MERRITT, TA;COCHRANE, CG;GLUCK, L
Pulmonary effluent samples were obtained from 26 preterm or term [human] infants throughout the period of endotracheal intubation. Infants with respiratory distress syndrome, infants with this disorder developing bronchopulmonary dysplasia and intubated infants without lung disease were compared daily in terms of lung effluent cellularity, albumin, elastase activity, .alpha.1-proteinase content and activity, and elastase inhibitory capacity. Elastase activity was determined to be neutrophilic in origin. Polyacrylamide gel electrophoresis of pulmonary effluents from 2 infants with respiratory distress syndrome and exposed to FiO2 [inspired O2 fraction] > 0.6-6 d [day] revealed cleavage of .alpha.1-proteinase inhibitor to a 47,000-MW fragments suggestive of oxidation. Pulmonary effluent neutrophils, macrophages and elastase activity were increased by day 3 of life in infants with respiratory distress syndrome eventually developing bronchopulmonary dysplasia. Elastase inhibitory capacity and .alpha.1-proteinase inhibitor activity were reduced in infants developing chronic lung disease. Bronchopulmonary dysplasia developed in infants with enhanced inflammatory response, but with less or inhibited antiprotease activity.