Singhal K K, Parton L A
Department of Pediatrics, SUNY at Stony Brook School of Medicine 11794-8111, USA.
Pediatr Res. 1996 Feb;39(2):229-35. doi: 10.1203/00006450-199602000-00007.
Respiratory distress syndrome (RDS) is characterized by the presence of fibrin-rich exudates in the alveoli. Fibrin and its degradation products may play an important role in the pathogenesis of bronchopulmonary dysplasia (BPD). The purpose of this study was to test the hypothesis that preterm neonates with RDS have depressed alveolar fibrinolytic activity and that those with RDS progressing to BPD have an even greater impairment in alveolar fibrinolysis. Serial tracheal aspirate (TA) samples from intubated neonates--9 control and 46 with RDS--were analyzed for fibrinolytic activity. In neonates with RDS, 26 resolved, 18 progressed to BPD, and 2 died before 28 d. Plasminogen activator (PA) and its inhibitor (PAI) were identified in TA by reverse fibrin autography and immunoblotting. Net PA/plasmin activity in TA was significantly depressed on d 1 of life in patients with self-resolved RDS (median = 20.85 ng/mL, p < 0.05) and RDS progressing to BPD (median = 4.97 ng/mL, p < 0.001) compared with control patients (median = 87.1 ng/mL). In addition, neonates progressing to BPD had significantly lower PA/plasmin activity on day one of life compared with neonates with self-resolved RDS (p < 0.001). ELISA for specific PA and PAI were not significantly different. We speculate that depressed fibrinolytic activity may place preterm neonates at risk for RDS and that the degree of this depression may predict the progression to BPD. In infants < or = 30 wk of gestation at birth with RDS, a PA/plasmin activity < or = 10.0 ng/mL on the 1st d of life had a positive predictive value of 80% (12/15) and a negative predictive value of 82% (9/11) for the progression to BPD.
呼吸窘迫综合征（RDS）的特征是肺泡内存在富含纤维蛋白的渗出物。纤维蛋白及其降解产物可能在支气管肺发育不良（BPD）的发病机制中起重要作用。本研究的目的是检验以下假设：患有RDS的早产儿肺泡纤溶活性降低，而那些RDS进展为BPD的早产儿肺泡纤溶功能受损更严重。对插管新生儿的系列气管吸出物（TA）样本——9例对照和46例患有RDS的新生儿——进行纤溶活性分析。在患有RDS的新生儿中，26例病情缓解，18例进展为BPD，2例在28天前死亡。通过反向纤维蛋白自显影和免疫印迹在TA中鉴定纤溶酶原激活剂（PA）及其抑制剂（PAI）。与对照患者（中位数 = 87.1 ng/mL）相比，自行缓解的RDS患者（中位数 = 20.85 ng/mL，p < 0.05）和RDS进展为BPD的患者（中位数 = 4.97 ng/mL，p < 0.001）在出生第1天时TA中的净PA/纤溶酶活性显著降低。此外，与自行缓解的RDS新生儿相比，进展为BPD的新生儿在出生第一天的PA/纤溶酶活性显著更低（p < 0.001）。特异性PA和PAI的ELISA检测无显著差异。我们推测纤溶活性降低可能使早产儿面临患RDS的风险，并且这种降低的程度可能预测进展为BPD的情况。在出生时胎龄≤30周且患有RDS的婴儿中，出生第1天时PA/纤溶酶活性≤10.0 ng/mL对进展为BPD的阳性预测值为80%（12/15），阴性预测值为82%（9/11）。
