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Perinatal reactions of the rabbit lung to maternal endotoxemia
The reactions of the fetal and newborn lung to in utero injury were investigated in rabbits using as a model maternal administration of Escherichia coli endotoxin, 2 to 4 mug per kg. of body weight, injected intravenously at the 29th gestational day. At 6 hours after endotoxin injection, the lung revealed diffuse alveolar damage-sparing type II cells which appeared resistant to injury but more mature than type II cells from control lungs. These changes were followed by a reparative phase which over a 2-day period resulted in increased interstitial cellularity, replacement of the damaged type I cells by proliferated type II cells, and marked intraalveolar accumulation of myelin figures. The above reactions were associated with an average increase of 100 per cent in the phospholipid content of the surfactant fraction isolated from lung washing. Postnatally, the lungs showed structural changes resembling those seen in hyaline membrane disease of the newborn. The findings suggest that the response of the alveolar epithelim to injury inudced late in gestation follows a pattern similar to that described previously in adult lung, and is assoicated with in utero increased release of surfactant. It is proposed that alveolar injury and repair, including reduction of the intracellular surfactant reservoir occurring prior to breathing, may interfere postnatally with formation and maintenance of a normal surfactant layer, thereby predisposing to respiratory distress.
The reactions of the fetal and newborn lung to in utero injury were investigated in rabbits using as a model maternal administration of Escherichia coli endotoxin, 2 to 4 mug per kg. of body weight, injected intravenously at the 29th gestational day. At 6 hours after endotoxin injection, the lung revealed diffuse alveolar damage-sparing type II cells which appeared resistant to injury but more mature than type II cells from control lungs. These changes were followed by a reparative phase which over a 2-day period resulted in increased interstitial cellularity, replacement of the damaged type I cells by proliferated type II cells, and marked intraalveolar accumulation of myelin figures. The above reactions were associated with an average increase of 100 per cent in the phospholipid content of the surfactant fraction isolated from lung washing. Postnatally, the lungs showed structural changes resembling those seen in hyaline membrane disease of the newborn. The findings suggest that the response of the alveolar epithelim to injury inudced late in gestation follows a pattern similar to that described previously in adult lung, and is assoicated with in utero increased release of surfactant. It is proposed that alveolar injury and repair, including reduction of the intracellular surfactant reservoir occurring prior to breathing, may interfere postnatally with formation and maintenance of a normal surfactant layer, thereby predisposing to respiratory distress.