Oxytocin-induced labor augments IL-1 -stimulated lung fluid absorption in fetal guinea pig lungs

Nair, Prem K., Tianbo Li, Reshma Bhattacharjee, Xin Ye, and Hans G. Folkesson. Oxytocin-induced labor augments IL-1 -stimulated lung fluid absorption in fetal guinea pig lungs. Am J Physiol Lung Cell Mol Physiol 289: L1029–L1038, 2005. First published August 5, 2005; doi:10.1152/ajplung.00256.2004.—We tested the hypothesis that oxytocin-induced labor augmented IL-1 -induced/ -stimulated lung fluid absorption in preterm guinea pig fetuses. IL-1 was administered subcutaneously daily to timed-pregnant guinea pigs for 3 days with and without simultaneous cortisol synthesis inhibition by metyrapone. At day 3, oxytocin was administered, and fetuses were delivered by abdominal hysterotomy at 61 and by oxytocin-induced birth at 68 days gestation. Delivered fetuses were instilled with isosmolar 5% albumin into the lungs, and lung fluid movement was measured over 1 h by mass balance. Lung fluid absorption was induced in 61-day and stimulated in 68-day gestation lungs by IL-1 . Labor induction by oxytocin augmented IL-1 -induced/-stimulated lung fluid absorption. Metyrapone pretreatment did not affect oxytocin-induced/-stimulated lung fluid absorption, while completely blocking IL-1 -induced/-stimulated fluid absorption. Fetal lung fluid absorption, when present, was always propranolol and amiloride sensitive, suggesting that -adrenoceptor stimulation and amiloridesensitive sodium channels were critical for fluid absorption. Epithelial sodium channel and Na-K-ATPase subunit expressions were both increased by IL-1 , but not further by oxytocin. Our results indicate that IL-1 release into the maternal blood circulation positively affects lung maturation due to the IL-1 -induced release of cortisol and thus prepares the lungs for the epinephrine surge associated with labor.