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
GLUCK, L
中科院分区:
医学1区
文献类型:
--
作者:
MERRITT, TA;COCHRANE, CG;GLUCK, L

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在整个气管插管期间,从 26 名早产儿或足月婴儿身上获取了肺流出物样本。每天比较患有呼吸窘迫综合征的婴儿、患有这种疾病的发展为支气管肺发育不良的婴儿和没有肺部疾病的插管婴儿的肺流出物细胞结构、白蛋白、弹性蛋白酶活性、α1-蛋白酶含量和活性以及弹性蛋白酶抑制能力。弹性蛋白酶活性被确定为起源于中性粒细胞。对来自 2 名患有呼吸窘迫综合征并暴露于 FiO2 [吸入的 O2 分数] > 0.6-6 天 [天] 的婴儿的肺流出物进行聚丙烯酰胺凝胶电泳,显示 α1-蛋白酶抑制剂裂解为 47,000-MW 的碎片,表明氧化。患有呼吸窘迫综合征的婴儿出生后第 3 天,肺流出物中性粒细胞、巨噬细胞和弹性蛋白酶活性增加,最终发展为支气管肺发育不良。患有慢性肺病的婴儿中弹性蛋白酶抑制能力和α1-蛋白酶抑制剂活性降低。婴儿中出现支气管肺发育不良,炎症反应增强,但抗蛋白酶活性较低或受到抑制。
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.