Effect of hydration on spontaneous labor outcomes in nulliparous pregnant women: a multicenter randomized controlled trial comparing three methods.

OBJECTIVE: To evaluate the effect of mode and amount of fluid hydration during labor. STUDY DESIGN: The authors conducted a randomized controlled trial of uncomplicated nulliparous women in spontaneous labor at 36 weeks or more gestational age. Women were randomized to receive lactated Ringer solution with 5% dextrose at (1) 125 mL/h intravenously with limited oral intake, (2) 250 mL/h intravenously with limited oral intake, or (3) 25 mL/h intravenously with ad libitum oral intake of clear liquids. Results were analyzed by intent-to-treat analysis. RESULTS: A total of 311 out of 324 women were available for analysis. Groups 1 (n = 105), 2 (n = 105), and 3 (n = 101) above did not differ significantly for mean labor duration (11.6 ± 5.9, 11.4 ± 5.5, and 11.5 ± 5.9 hours, respectively; p = 0.998), proportion of women in labor > 12 hours (all groups 41%; p = 0.998), proportion receiving oxytocin augmentation (59, 60, and 57%, respectively; p = 0.923), or proportion delivered by cesarean (22, 17, and 17%, respectively; p = 0.309). Indications for cesarean were similar between groups. No cases of pulmonary edema, maternal aspiration, or perinatal mortality occurred. CONCLUSION: Although apparently safe, neither increased intravenous hydration nor oral hydration during labor improves labor performance.

ATP depletion of tubular cells causes dissociation of the zonula adherens and nuclear translocation of beta-catenin and LEF-1.

This study examined the events associated with the reversible disruption of the structural and functional integrity of the zonula occludens (ZA) induced by ATP depletion of renal tubular cells. It shows that loss of the ZA after ATP depletion is associated with the withdrawal of E-cadherin, alpha-catenin, and beta-catenin, probably as intact cadherin-catenin complexes from the basolateral membrane of tubular cells. The relative amounts of all three proteins increased in the Triton X-100-insoluble fraction of cell lysates and decreased in the Triton X-100-soluble pool. These changes were reversed with repletion of cell ATP. It is additionally shown that ATP depletion induces nuclear translocation of beta-catenin and T cell factor (TCF)/lymphoid enhancer factor-1 (LEF-1), a transcriptional factor with which beta-catenin associates. The redistribution of the ZA proteins as intact E-cadherin-catenin complexes from the plasma membrane facilitates the rapid recovery of the ZA after sublethal ischemic injury. The translocation of beta-catenin and TCF/LEF-1 to the nucleus indicates that ATP depletion may activate the wnt/wingless signal transduction pathway. Thus, entirely novel evidence is provided that both of the known roles of beta-catenin, as a structural part of the ZA and as a component of the wnt/wingless pathway, play a role after sublethal ischemic injury to tubular cells. It is also speculated that the nuclear translocation of beta-catenin and TCF/LEF-1 modulates gene expression after ischemic injury and may contribute to events necessary for renal regeneration and repair after ischemic injury.