Thibeault D W, Kilbride H K
Department of Pediatrics, Children's Mercy Hospital, University of Missouri-Kansas City School of Medicine, USA.
Am J Perinatol. 1997 Sep;14(8):457-60. doi: 10.1055/s-2007-994179.
Pulmonary hypoplasia (PH), secondary to premature rupture of fetal membranes (PROM), is a frequent cause of pulmonary insufficiency in preterm infants. Pulmonary hypoplasia of diverse causes is usually associated with pulmonary hypertension. The objective of this study was to quantitate the acinar arterial wall thickness and muscularization in preterm infants with PROM that died with PH in comparison to age-matched controls. The left lung and pulmonary vasculature were perfused and fixed in a standard method in 16 infants with PROM and PH, and in 16 controls. In infants with PH, the alveolar ductal artery walls were nearly twice as thick as those of controls, 15.1 +/- 5.1% versus 7.4 +/- 1.3%, p < 0.0001. Ninety-one percent had muscle in the wall compared to 18% of controls. We conclude that infants with PROM and PH have increased pulmonary arterial muscularization, placing them at significant risk to have pulmonary hypertension. For these infants, therapy to reduce pulmonary vascular resistance should be instituted early.
继发于胎膜早破（PROM）的肺发育不全（PH）是早产儿肺功能不全的常见原因。多种原因引起的肺发育不全通常与肺动脉高压有关。本研究的目的是定量分析死于肺发育不全的胎膜早破早产儿与年龄匹配的对照组相比，腺泡动脉壁厚度和肌化程度。对16例胎膜早破合并肺发育不全的婴儿和16例对照组婴儿的左肺和肺血管进行标准方法的灌注和固定。在肺发育不全的婴儿中，肺泡导管动脉壁几乎是对照组的两倍厚，分别为15.1±5.1%和7.4±1.3%，p<0.0001。91%的婴儿动脉壁有肌肉，而对照组为18%。我们得出结论，胎膜早破合并肺发育不全的婴儿肺动脉肌化增加，使其患肺动脉高压的风险显著增加。对于这些婴儿，应尽早开始降低肺血管阻力的治疗。
