Experimental production of the pulmonary hyaline membrane syndrome

Abstract

<h2>Summary</h2> Eighty-seven adult guinea pigs receivedintratracheal injections of a mixture of human amniotic fluid and human plasma. Ten of them developed the thoracic retraction which is seen in newborn infants who have the pulmonary hyaline membrane syndrome, and post-mortem examination of their lungs revealed findings similar to those in the human disease. The lungs were firm, deep red, and sank in formalin solution; they showed extensive atelectasis, vascular engorgement, and eosinophilic hyaline membrane which lined occasional dilated aveolar ducts and alveoli. One hundred seventeen control animalsreceived intratracheal injections of human amniotic fluid, human plasma, or cold normal saline. In general, the amniotic fluid produced extensive atelectasis and pulmonary vascular engorgement; the plasma produced pulmonary edema and hemorrhage and, in one animal, scattered areas of eosinophilic hyaline membrane without accompanying atelectasis; the saline produced patchy atelectasis, emphysema, and hemorrhage. The present experiments suggestthat the injected plasma caused an intrapulmonary exudation of fluid and pulmonary vascular engorgement. The injected amniotic fluid created atelectasis. Its thromboplastin-like activity may have aided in clotting the exudate to form a membrane although one animal accomplished this with massive pulmonary edema due to plasma alone. It is suggested that the pulmonary hyaline membrane syndrome in the human infant may be the result of a similar mechanism when aspirated amniotic fluid mixes with a pulmonary exudate. The etiologies of the exudate are probably diverse and future investigation into the pathogenesis of the human syndrome might well endeavor to elucidate the etiologies of pulmonary edema in the neonatal period.