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目的 研究新生儿呼吸窘迫综合征 (RDS)肺动脉压力动态变化及其与血清内皮素 1(endothelin 1,ET 1)、一氧化氮 (nitricoxide ,NO )的关系。方法 对 13例确诊为新生儿RDS患儿 (实验组 )和 2 0例正常新生儿 (对照组 )用脉冲超声多谱勒分别于生后 2、12、2 4、4 8、72h测定肺动脉血流加速时间 (TPV)及右心室射血时间 (RVET) ,以TPV/RVET比值反映肺动脉压力。用硝酸还原酶法和放射免疫法分别测定实验组和对照组新生儿生后 2 4、72h血清ET 1和NO的水平。结果 实验组和对照组新生儿肺动脉压力在生后 2、12及 72h差异无显著意义 (t值分别为 1 2 5、1 84、0 94 ,P均 >0 0 5 ) ;实验组 2 4、4 8hTPV/RVET比值为 0 2 77± 0 0 76、0 2 78± 0 0 2 7,对照组分别为 0 32 1± 0 0 5 1、0 32 9± 0 0 6 2 ,两组相比差异有显著意义 (t值分别为 2 86、2 2 0 ,P <0 0 1、 <0 0 5 ) ;实验组和对照组在生后 2 4h时ET 1[(6 2± 2 3)ng/L、(47± 8)ng/L]、NO[(11± 10 ) μmol/L、(32± 2 2 ) μmol/L]水平相比 ,差异有显著意义 (t值分别为 2 33、2 37,P均 <0 0 5 ) ;而 72h时差异无显著意义 (t值分别为 0 87、1 93,P均 >0 0 5 ) ,与肺动脉压力变化相一致。死亡组肺动脉压力 (0 2 5± 0 0 2 )明显高于
Objective To study the dynamic changes of pulmonary artery pressure in neonatal respiratory distress syndrome (RDS) and its relationship with serum endothelin 1 (ET 1) and nitric oxide (NO). Methods Pulmonary arterial blood was measured in 13 children diagnosed as neonatal RDS (experimental group) and 20 normal neonates (control group) by pulsed sonography at 2,12,2,4,48 and 72 h Flow acceleration time (TPV) and right ventricular ejection time (RVET), pulmonary artery pressure to reflect the TPV / RVET ratio. Nitric acid reductase and radioimmunoassay were used to determine the levels of serum ET 1 and NO at 24, 72 hours after birth in the experimental group and the control group respectively. Results There was no significant difference in neonatal pulmonary artery pressure between the experimental group and the control group at 2, 12 and 72 hours after birth (t values were 1 2 5,1 84,0 94, P both> 0 05) 4 8hTPV / RVET ratio of 0 2 77 ± 0 0 76,0 2 78 ± 0 0 2 7, the control group were 0 32 1 ± 0 0 5 1,0 32 9 ± 0 0 6 2, the difference between the two groups (P <0.01, <0.05). The ET 1 [(62 ± 2 3) ng / ml) in the experimental group and the control group at 24 h after birth were significantly higher than those in the control group L, (47 ± 8) ng / L] and NO [(11 ± 10) μmol / L, (32 ± 2 2) μmol / L] 37, P <0.05). However, there was no significant difference at 72h (t = 0 87, 93, P> 0.05), which was consistent with changes of pulmonary artery pressure. Pulmonary artery pressure (0 2 5 ± 0 0 2) in the death group was significantly higher than that in the control group