Contreras M, Hariharan N, Lewandoski J R, Ciesielski W, Koscik R, Zimmerman J J
Division of Critical Care Medicine, Children's Hospital, University of Wisconsin, Madison 53792-4108, USA.
Crit Care Med. 1996 Jan;24(1):29-37. doi: 10.1097/00003246-199601000-00008.
To quantify oxyradical inflammatory markers in serial endotracheal tube aspirates obtained from premature neonates at risk for developing bronchopulmonary dysplasia, and to correlate these parameters with clinical manifestations of the disease.
Prospective cohort study.
Tertiary neonatal intensive care unit.
Twenty-eight intubated, premature infants, with 15 infants displaying simple respiratory distress syndrome and 13 infants eventually developing bronchopulmonary dysplasia.
Endotracheal tube aspirates were collected and clinical severity scores were calculated longitudinally from an inception cohort during the first week of life. Diagnosis of bronchopulmonary dysplasia by standard criteria was recorded at 30 days of life. Various biochemical analyses related to pulmonary oxyradical stress were determined on endotracheal tube aspirates and were normalized according to the magnitude of serum/aspirate urea ratios. The demographic, illness severity, and biochemical characteristics of infants with simple respiratory distress syndrome and those characteristics of infants developing bronchopulmonary dysplasia were evaluated by masked comparison.
Populations of respiratory distress syndrome and bronchopulmonary dysplasia infants could be differentiated during the first week of life by means of the following parameters: gestational age; birth weight; Score of Neonatal Acute Physiology; Neonatal Therapeutic Intervention Scoring System; epithelial lining fluid leukocytes; elastase; myeloperoxidase; xanthine oxidase and catalase enzyme activities; and total sulfhydryls.
Infants with simple respiratory distress syndrome could be segregated from those infants who developed bronchopulmonary dysplasia by the magnitude of the epithelial lining fluid oxyradical inflammation markers. While infants developing bronchopulmonary dysplasia typically exhibited increased concentrations of these markers during the first week of life, those infants with simple respiratory distress syndrome displayed low, uniform, or decreasing values of these markers over this interval. Infants developing bronchopulmonary dysplasia demonstrate an early pulmonary inflammatory response, and one key aspect of this response involves various oxyradical-generating systems.
对有发生支气管肺发育不良风险的早产儿系列气管内吸出物中的氧自由基炎症标志物进行定量，并将这些参数与该疾病的临床表现相关联。
前瞻性队列研究。
三级新生儿重症监护病房。
28名插管的早产儿，其中15名婴儿表现为单纯呼吸窘迫综合征，13名婴儿最终发展为支气管肺发育不良。
收集气管内吸出物，并在出生后第一周从起始队列纵向计算临床严重程度评分。在出生30天时记录根据标准标准诊断的支气管肺发育不良情况。对气管内吸出物进行与肺氧自由基应激相关的各种生化分析，并根据血清/吸出物尿素比值的大小进行标准化。通过盲法比较评估单纯呼吸窘迫综合征婴儿的人口统计学、疾病严重程度和生化特征以及发展为支气管肺发育不良的婴儿的这些特征。
呼吸窘迫综合征和支气管肺发育不良婴儿群体在出生后第一周可通过以下参数进行区分：胎龄；出生体重；新生儿急性生理学评分；新生儿治疗干预评分系统；上皮衬液白细胞；弹性蛋白酶；髓过氧化物酶；黄嘌呤氧化酶和过氧化氢酶活性；以及总巯基。
单纯呼吸窘迫综合征婴儿可通过上皮衬液氧自由基炎症标志物的大小与发展为支气管肺发育不良的婴儿区分开来。虽然发展为支气管肺发育不良的婴儿在出生后第一周通常表现出这些标志物浓度升高，但单纯呼吸窘迫综合征婴儿在该时间段内这些标志物的值较低、一致或下降。发展为支气管肺发育不良的婴儿表现出早期肺部炎症反应，这种反应的一个关键方面涉及各种产生活氧自由基的系统。
