Intrauterine hypercarbia and lamb lung surfactant synthesis.
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.
D000142:Acidosis, Respiratory / Q000209:etiology / Q000503:physiopathology; D000818:Animals; D006935:Hypercapnia / Q000150:complications / Q000196:embryology* / Q000378:metabolism; D010713:Phosphatidylcholines / Q000032:analysis; D010743:Phospholipids / Q000032:analysis; D011312:Pressure; D011663:Pulmonary Surfactants / Q000032:analysis / Q000096:biosynthesis*; D012119:Respiration; D012756:Sheep / Q000196:embryology / Q000378:metabolism
D010713:Phosphatidylcholines; D010743:Phospholipids; D011663:Pulmonary Surfactants; C017463:lecithins, disaturated