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呼吸窘迫综合征后慢性肺病婴儿气管支气管吸出物中的白细胞介素8与粒细胞弹性蛋白酶α1蛋白酶抑制剂复合物

Interleukin 8 and granulocyte elastase alpha 1 proteinase inhibitor complex in the tracheobronchial aspirate of infants with chronic lung disease following respiratory distress syndrome.

作者信息

Takasaki J, Ogawa Y

机构信息

Department of Pediatrics, Saitama Medical Center, Saitama Medical School, Japan.

出版信息

Acta Paediatr Jpn. 1996 Oct;38(5):434-9. doi: 10.1111/j.1442-200x.1996.tb03522.x.

Abstract

In order to elucidate the role of interleukin 8 (IL-8) on the development of chronic lung disease (CLD) in neonates following an episode of respiratory distress syndrome (RDS), serial and simultaneous measurements of the concentration of IL-8 and granulocyte elastase alpha 1 proteinase inhibitor complex (E-alpha 1 PI) in the tracheobronchial aspirate of very low birthweight infants with RDS were conducted. The concentration of IL-8 and E-alpha 1 PI in infants with CLD was low in the first 48 h of life, but dramatically increased after 48 h. The concentration of IL-8 between 48 h of life and day 5 was significantly correlated to the fraction of inspired oxygen concentration (FiO2) within 48 h of age, but not to the mean airway pressure. Interleukin 8 seemed to stimulate neutrophils to release granulocyte elastase which, in turn, caused lung tissue injury, resulting in the development of CLD. It is suggested that high FiO2 is an important factor causing IL-8 production in the lung.

摘要

为了阐明白细胞介素8(IL-8)在新生儿呼吸窘迫综合征(RDS)发作后慢性肺病(CLD)发展中的作用,对患有RDS的极低出生体重儿的气管支气管吸出物中IL-8浓度和粒细胞弹性蛋白酶α1蛋白酶抑制剂复合物(E-α1 PI)进行了系列和同步测量。患有CLD的婴儿在出生后的头48小时内IL-8和E-α1 PI浓度较低,但在48小时后显著增加。出生后48小时至第5天的IL-8浓度与出生后48小时内的吸入氧浓度(FiO2)显著相关,但与平均气道压力无关。白细胞介素8似乎刺激中性粒细胞释放粒细胞弹性蛋白酶,进而导致肺组织损伤,从而导致CLD的发展。提示高FiO2是导致肺中IL-8产生的重要因素。

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