新生儿肺疾病的纤溶改变及其与肺动脉压力的关系

Changes of Fibrinolysis and Their Relationship with Pulmonary Artery Pressures in Neonates with Lung Diseases

目的 研究新生儿肺疾病的纤溶改变及其与肺动脉压力的关系。方法 用发色底物法测定 2 7例新生儿肺疾病患儿 (病例组 )及 2 5例正常新生儿 (对照组 )血浆组织纤溶酶原激活剂 (TPA)和纤溶酶原激活抑制物(PAI)活性变化 ;用超声多普勒方法测定肺动脉血流加速时间 (TPV)与右室射血时间 (RVET)之比值 (TPV/RVET) ,以此估计新生儿肺动脉压力 (TPV/RVET比值与肺动脉压力成反比 )。结果 病例组PAI活性 [(9.3±4 .1)AU× 10 -1/ml]明显高于对照组 [(5 .5± 3.0 )AU× 10 -1/ml],P <0 .0 1,TPV/RVET比值 (0 .2 9± 0 .0 5 )明显低于对照组 (0 .34± 0 .0 8) ,(P <0 .0 5 ) ;发生肺出血者肺动脉压力 [TPV/RVET (0 .2 3± 0 .0 2 ) ]显著升高 ,P <0 .0 5。肺出血恢复期新生儿TPA [(3.7± 1.7)IU× 10 -1/ml]及血小板 [(180± 30 )× 10 9/L]明显高于肺出血发生时 [TPA (1.8± 0 .7)IU× 10 -1/ml,血小板 (98± 39)× 10 9/L],(P <0 .0 1)。结论 新生儿肺疾病时由于肺动脉压力增高 ,肺血管内皮细胞破坏 ,导致TPA释放减少 ,PAI活性增高 ,纤溶活性降低。

Objective To study changes in plasma fibrinolysis and their relationship with pulmonary artery pressures in neonates with lung diseases. Methods Plasma activities of the tissue plasminogen activator (TPA) and tissue plasminogen activator inhibitor (PAI) were measured by chromogenic substrate methods in 27 newborns with lung diseases [10 with the respiratory distress syndrome (RDS), 12 with the meconium aspiration syndrome (MAS) and 5 with pneumonia] and in 25 normal newborns (controls). The ratio of the time of peak velocity (TPV) to the right ventricular ejection time (RVET) was determined using an Aloka SSD650 ultrasound system incorporating pulse waves to evaluate pulmonary artery pressures. Results PAI activity was significantly higher in infants with lung diseases [( 9.3 ± 4.1 ) AU×10 -1 /ml] than in the controls [( 5.5 ± 3.0 ) AU×10 -1 /ml] (P< 0.01 ). The ratio of TPV to RVET was lower in the newborns with lung diseases ( 0.29 ± 0.05 ) than in the controls ( 0.34 ± 0.08 )(P< 0.05 ). Elevated pulmonary artery pressures appeared to be involved in the fibrinolytic dysfunction in the infants with lung diseases. In 10 infants who developed pulmonary hemorrhage, TPA activity [( 1.8 ± 0.7 ) IU×10 -1 /ml)] and platelet counts [( 98 ±39)×10 9/L] in the acute phase of injury were significantly lower than those recorded during the recovery stage [( 3.7 ± 1.7 ) IU×10 -1 /ml and (180±30)×10 9/L, respectively] (P< 0.01 ). Conclusions Following pulmonary hypertension, endothelial cell injury results in a lower release of TPA and increased PAI activity.