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Am J Physiol Lung Cell Mol Physiol 289: L1029-L1038, 2005. First published August 5, 2005; doi:10.1152/ajplung.00256.2004
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Oxytocin-induced labor augments IL-1{beta}-stimulated lung fluid absorption in fetal guinea pig lungs

Prem K. Nair, Tianbo Li, Reshma Bhattacharjee, Xin Ye, and Hans G. Folkesson

Department of Physiology and Pharmacology, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio

Submitted 7 July 2004 ; accepted in final form 28 July 2005

We tested the hypothesis that oxytocin-induced labor augmented IL-1{beta}-induced/-stimulated lung fluid absorption in preterm guinea pig fetuses. IL-1{beta} 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{beta}. Labor induction by oxytocin augmented IL-1{beta}-induced/-stimulated lung fluid absorption. Metyrapone pretreatment did not affect oxytocin-induced/-stimulated lung fluid absorption, while completely blocking IL-1{beta}-induced/-stimulated fluid absorption. Fetal lung fluid absorption, when present, was always propranolol and amiloride sensitive, suggesting that {beta}-adrenoceptor stimulation and amiloride-sensitive sodium channels were critical for fluid absorption. Epithelial sodium channel and Na-K-ATPase subunit expressions were both increased by IL-1{beta}, but not further by oxytocin. Our results indicate that IL-1{beta} release into the maternal blood circulation positively affects lung maturation due to the IL-1{beta}-induced release of cortisol and thus prepares the lungs for the epinephrine surge associated with labor.

{beta}-adrenoceptors; cortisol; epinephrine; prenatal lung development; sodium transport



Address for reprint requests and other correspondence: H. G. Folkesson, Dept. of Physiology and Pharmacology, Northeastern Ohio Univs., College of Medicine, 4209 State Rte. 44, PO Box 95, Rootstown, OH 44272-0095 (e-mail: hgfolkes{at}neoucom.edu)




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