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 three 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 amiloride-sensitive 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 may 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.