Wild Y K, Piasecki G J, De Paepe M E, Luks F I
Department of Pathology, Brown University School of Medicine and Hasbro Children's Hospital, Providence, RI, USA.
J Pediatr Surg. 2000 May;35(5):775-9. doi: 10.1053/jpsu.2000.6067.
BACKGROUND/PURPOSE: Prolonged tracheal occlusion (TO) accelerates lung growth but impairs surfactant production. Short-term TO results in less lung growth but preserves type II cell function. The authors studied the effects of short-term TO on lung physiology in diaphragmatic hernia.
Diaphragmatic hernia was created in 9 fetal lambs at 90 to 95 days. Five were left uncorrected (CDH), 4 underwent 2-week TO (108 to 122 days; CDH + TO). Five unoperated lambs served as controls. Near-term (136 days) fetuses were ventilated for 90 to 150 minutes. Pulmonary arterial pressure, postductal blood gases, quasistatic compliance, total lung capacity (TLC), and lung weight to body weight (LW/BW) were measured.
There was an overall survival rate of 89% at full term. Short-term occlusion did not induce lung growth (TLC and LW/BW, 6.07 +/- 2.92 mL/kg and 0.022 +/- 0.008 in CDH, 4.86 mL/kg and 0.019 +/- 0.005 in CDH + TO, 10.81 +/- 3.55 mL/kg and 0.036 +/- 0.006 in controls, respectively). However, pulmonary hypertension in CDH (47.4 +/- 12.32/35.8 +/- 12.19 torr) was corrected by short-term occlusion (20.2 +/- 4.0/16.0 +/- 4.8 torr in CDH + TO, P< .05, single-factor analysis of variance [ANOVA]; similar to control). Best pO2 and pCO2 improved after occlusion (CDH, 48.6 +/- 6.7 torr and 107.1 +/- 34.3 torr, respectively; CDH + TO, 101.5 +/- 16.3 torr and 81.9 +/- 2.4 torr; control, 291.4 +/- 4.7 torr and 37.7 +/- 17.3), as did oxygenation index (P < .05, CDH vCDH + TO; CDH, 97.2 +/- 23.0; CDH + TO, 28.7 +/- 3.1; control, 5.6 +/- 0.6).
Short-term TO corrects pulmonary hypertension and improves gas exchange in fetal lambs with diaphragmatic hernia despite failure to produce accelerated lung growth. Inducing lung maturation and correcting the physiological derangement in diaphragmatic hernia may be more important than achieving lung growth alone.
背景/目的:长时间气管阻塞(TO)可加速肺生长,但会损害表面活性剂的产生。短期TO导致肺生长较少,但保留II型细胞功能。作者研究了短期TO对膈疝肺生理的影响。
在90至95日龄的9只胎羊中制造膈疝。5只未矫正(CDH),4只接受2周TO(108至122日龄;CDH + TO)。5只未手术的胎羊作为对照。接近足月(136日龄)的胎儿通气90至150分钟。测量肺动脉压、导管后血气、准静态顺应性、肺总量(TLC)以及肺重量与体重之比(LW/BW)。
足月时总体存活率为89%。短期阻塞未诱导肺生长(TLC和LW/BW,CDH组分别为6.07±2.92 mL/kg和0.022±0.008,CDH + TO组分别为4.86 mL/kg和0.019±0.005,对照组分别为10.81±3.55 mL/kg和0.036±0.006)。然而,CDH组的肺动脉高压(47.4±12.32/35.8±12.19托)通过短期阻塞得到纠正(CDH + TO组为20.2±4.0/16.0±4.8托,P<0.05,单因素方差分析[ANOVA];与对照组相似)。阻塞后最佳pO2和pCO2有所改善(CDH组分别为48.6±6.7托和107.1±34.3托;CDH + TO组分别为第101.5±16.3托和81.9±2.4托;对照组分别为291.4±4.7托和37.7±17.3),氧合指数也有所改善(P < 0.05,CDH与CDH + TO比较;CDH组为97.2±23.0;CDH + TO组为28.7±3.1;对照组为5.6±0.6)。
尽管未能促进肺加速生长,但短期TO可纠正膈疝胎羊的肺动脉高压并改善气体交换。诱导肺成熟和纠正膈疝的生理紊乱可能比单纯实现肺生长更重要。