Aim: To determine the levels of RBC HbSNO and HbFe(II)NO using chemiluminescence in very low birth weight infants breathing room air, during the first 2 days of life.
Method: RBC NO values were compared to the levels obtained in cord blood at birth from infants of similar gestational age. Five infants ranging from 25 to 27 weeks of gestation were sampled between 12 and 24 h after birth.
Stimulation of freshly isolated rat hepatocytes with lysophosphatidic acid (LPA) resulted in LPA1 receptor-mediated and nitricoxide-dependent up-regulation of the immediate early genes iNOS (inducible nitric-oxide synthase (NOS)) and mPGES-1 (microsomal prostaglandin E synthase-1). Because LPA is a ligand for both cell surface and intracellular receptor sites and a potent endothelial NOS (eNOS) activator, we hypothesized that NO derived from activated nuclearized eNOS might participate in gene regulation. Herein we show, by confocal microscopy performed on porcine cerebral endothelial cells expressing native LPA1-receptor and eNOS and on HTC4 rat hepatoma cells co-transfected with recombinant human LPA1-receptor and fused eNOS-GFP cDNA, a dynamic eNOS translocation from peripheral to nuclear regions upon stimulation with LPA.
View Article and Find Full Text PDFObjective: To compare the levels of S-nitrosohemoglobin (HbSNO) at different gestational ages in newborn infants and correlate the levels of HbSNO with HbA and HbF.
Method: Cord blood samples of 22 newborn infants of different gestational ages (25-41 weeks) were analyzed. The levels of HbF and HbA were determined by HPLC and of HbSNO by chemiluminescence.
S-nitrosohemoglobin (HbSNO), where hemoglobin (Hb) is nitrosated at Cysbeta93, presumably controls delivery of the vasorelaxant nitric oxide (NO) to hypoxic tissues in an oxygen-sensitive manner. Little is known about how Hb regulates NO bioavailability during fetal development. A study was planned to determine the levels of HbSNO and HbFe(II)NO (NO bound to FeII of heme) in the cord blood of newborn infants of different gestational ages and establish their relationship with the levels of fetal Hb (HbF).
View Article and Find Full Text PDFObjective: Fetal hemoglobin (HbF) levels in the hemolysates obtained from infants who died from sudden infant death syndrome (SIDS) are reported to be markedly increased compared with controls. This finding could have been explained by increased HbF synthesis caused by episodes of hypoxemia in the SIDS infants. A prospective study in a group of infants being monitored at home after an apparent life-threatening event (ALTE) and considered at increased risk for SIDS was conducted with an improved ribonuclease protection assay.
View Article and Find Full Text PDFA study was conducted during the first week of life to determine the changes in P50 (PO2 required to achieve a saturation of 50% at pH 7.4 and 37 degrees C) and the proportions of fetal hemoglobin (HbF) and adult hemoglobin (HbA) prior to and after transfusion in very early preterm infants. Eleven infants with a gestational age < or = 27 weeks have been included in study.
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