Egberts J, Clark C, Kodack L, Brumley G
Respir Physiol. 1984 Aug;57(2):213-23. doi: 10.1016/0034-5687(84)90094-x.
Prenatal asphyxia resulting in hypoxia, hypercarbia and amniotic fluid aspiration reduces the synthesis of the pulmonary surfactant. Using 135-day fetal lambs we studied the in utero effects of hypercarbic acidosis alone on fetal breathing activity, excised lung pressure-volume relationships and lamellar body (LB) surfactant disaturated phosphatidylcholine (DSPC) pool size and specific activity for [14C]palmitate. Fetal PaCO2 levels greater than 125 mm Hg for 30 min were associated with pH values less than 7.0 and very vigorous breathing activity. Analysis 22 h after the period of hypercarbic acidosis demonstrated no differences in pressure-volume relationships or the quantity of lamellar body surfactant DSPC. The specific activity of lamellar body DSPC also was not different although total label (dpm) per gram dry weight was higher and label was detected in the lavage fluid earlier in the acidotic lambs than controls. We conclude from these data that hypercarbic acidosis does not influence the synthesis or function of the pulmonary surfactant as assessed in this system. From these results and prior work from our laboratory we can infer that hypoxia remains the most probable cause for reduced surfactant synthesis in the asphyxiated fetus.
产前窒息导致缺氧、高碳酸血症和羊水吸入,会减少肺表面活性物质的合成。我们使用135日龄的胎羊,研究了单纯高碳酸血症酸中毒对胎儿呼吸活动、离体肺压力-容积关系以及板层小体(LB)表面活性物质二饱和磷脂酰胆碱(DSPC)池大小和[14C]棕榈酸酯比活性的子宫内影响。胎儿PaCO2水平高于125 mmHg持续30分钟与pH值低于7.0以及非常剧烈的呼吸活动相关。在高碳酸血症酸中毒期后22小时进行的分析表明,压力-容积关系或板层小体表面活性物质DSPC的量没有差异。板层小体DSPC的比活性也没有差异,尽管酸中毒胎羊每克干重的总标记(dpm)更高,且在灌洗液中比对照组更早检测到标记。从这些数据我们得出结论,在这个系统中评估,高碳酸血症酸中毒不会影响肺表面活性物质的合成或功能。从这些结果以及我们实验室之前的工作中,我们可以推断,缺氧仍然是窒息胎儿表面活性物质合成减少的最可能原因。