Morris G S, Thliveris J A, Faridy E E
Respir Physiol. 1980 Dec;42(3):263-85. doi: 10.1016/0034-5687(80)90119-x.
Pregnancies were prolonged by daily subcutaneous injection of progesterone to the maternal rats from day 20 through 24 of gestation (Term is 22 days). The fetuses were harvested by cesarean section on gestation days (GD) 21 through 25. In spite of reduction in placental weight the fetal body weight increased during prolonged gestation. Both lung wet and dry weights decreased resulting in smaller lung per body weight. Compared to term fetuses, post term fetuses (GD 25) exhibited a 10% reduction in lung cell numbers, and a 90% reduction in lung glycogen. Lung disaturated phosphatidyl choline expressed per lung increased up to GD 23 and subsequently decreased by GD 25. Surface tension of lung extracts and pulmonary lavage fluids increased with prolongation of gestation. Histological studies revealed a decrease in the number of lamellar bodies in the Type II cells and a gradual reduction in the size of terminal sacs leading to areas of complete atelectasis at GD 25. It is suggested that lung hypocellularity, depletion of lung glycogen, reduction in intracellular reserve of phospholipids, loss of pulmonary fluid leading to atelectasis, and loss of surface activity of pulmonary fluid may be predisposing factors for the development of respiratory distress in postmaturity.
从妊娠第20天至24天,每天给孕鼠皮下注射孕酮以延长孕期(孕期为22天)。在妊娠第21天至25天通过剖宫产取出胎儿。尽管胎盘重量减轻,但在延长的孕期中胎儿体重增加。肺的湿重和干重均下降,导致每体重的肺变小。与足月胎儿相比,过期胎儿(妊娠第25天)的肺细胞数量减少10%,肺糖原减少90%。每肺表达的肺二饱和磷脂酰胆碱在妊娠第23天之前增加,随后在妊娠第25天下降。随着孕期延长,肺提取物和肺灌洗液的表面张力增加。组织学研究显示,II型细胞中板层小体数量减少,终末囊大小逐渐减小,导致妊娠第25天出现完全肺不张区域。提示肺细胞减少、肺糖原耗竭、细胞内磷脂储备减少、肺液丧失导致肺不张以及肺液表面活性丧失可能是过期产儿发生呼吸窘迫的易感因素。