ExtractTracheal ligation was performed in 16 fetal lambs at 74-129 days of gestation (normal term, 138-157 days). Operated lambs were subsequently delivered spontaneously at term. Postmortem procedures were performed on the same day and revealed lungs enormously distended with fluid, weighing approximately 10 times more than those found in normal lambs, and displacing the diaphragm to the [joint where it was concave downward, bulging into the abdominal cavity. To measure the rate of lung fluid formation in fetal lambs, catheters were placed in the trachea of three fetuses borne by three ewes near term. Periodic aspiration of fluid following the operation revealed rates of lung fluid formation of 0.015, 0.030, and 0.055 ml/kg/min. The day after surgery pressure measurements of lung fluid made via the catheter in two of these animals revealed an initial pressure of 12 and 19 cm saline. This pressure rose only moderately after injecting 150 ml 0.85% NaCl in 20-ml increments into the fetal lung. The injected fluid was readily recoverable, indicating that it had been accommodated by expansion of the fetal lung and had not passed across lung-lining cells into the fetal circulation. Gestation times were within the normal range. SpeculationFetal lung fluid contains surfactant, which has been biochemically characterized as a phospholipid and as a lecithin. Soya bean phospholipids containing a predominance of lecithins arc capable of sensitizing the rabbit uterus to oxytocin and precipitating premature delivery. The fetus is known to participate in the timing of its own birth, and we speculated whether lung phospholipids formed near term in the fetal lung could reacli the amniotic fluid and precipitate labor. Tracheal occlusion, however, did not alter gestation time in our animals. Other mechanisms of fetal participation in the precipitation of labor must be sought. IntroductionRecent work [5,9, 14, 18] has indicated that fetal lungs secrete fluid. The fluid was thought to flow via the trachea to the oral pharynx, where it was either swallowed or passed via the nose or mouth into the amniotic fluid. Reynolds [17], however, published observations suggesting that with relatively minor pressure changes fluid would move in the reverse direction. He concluded that "it is clear that ... the fetal lung is a
The mammalian fetus affixed to the uterine wall in some ways resembles a homograft, but maternal homograft immunity even when specifically directed against her fetuses fails to destroy them. The placental barrier appears to be critical in protecting the fetus against maternal immunologic attack. In order to evaluate the means by which it affords protection, we have measured in rabbits the transfer of cytotoxic antibody from mother to fetus. When the offspring were not the specific targets for maternal antibody, we found titers of cytotoxic antibody in the newborn animals at or near maternal levels in 16 of 18 cases (89 per cent), demonstrating the ability of this antibody to cross the rabbit placenta. When the offspring were appropriate targets for antibody, however, 11 of 18 newborn animals (61 per cent) had no demonstrable titer. We believe that in these latter cases, antibody had become fixed to antigenic sites and thereby had been removed from the fetal circulation. There was, however, no evidence of harm to any of the fetuses, either in survival (as demonstrated in a previous study) or in spleen or thymus weights or peripheral leukocyte and mononuclear cell counts. Cytotoxic antibody appears to reach the embryo early in gestation, since we found antibody in 8-day-old blastocyst fluid in each of 2 trials. We conclude that the fetus neither receives nor requires protection against cytotoxic antibody, and believe that fetal protection against maternal homograft immunity is afforded by a placental barrier to maternal mononuclear leukocytes.
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