vasoactive-intestinal-peptide and Fetal-Growth-Retardation

Topics: Acid-Base Equilibrium; Adrenocorticotropic Hormone; Amino Acids; Catecholamines; Cordocentesis; Female; Fetal Blood; Fetal Growth Retardation; Fetus; Growth Hormone; Hemoglobins; Humans; Hydrocortisone; Insulin; Insulin-Like Growth Factor I; Lactates; Pregnancy; Thyroid Hormones; Triglycerides; Vasoactive Intestinal Peptide

Glucose uptake by the placenta and its transfer to the fetus is a finely regulated process required for placental and fetal development. Deficient placentation is associated with pregnancy complications such as fetal growth restriction (FGR). The vasoactive intestinal peptide (VIP) has embryotrophic effects in mice and regulates human cytotrophoblast metabolism and function. Here we compared glucose uptake and transplacental transport in vivo by VIP-deficient placentas from normal or VIP-deficient maternal background. The role of endogenous VIP in placental glucose and amino acid uptake was also investigated. Wild type C57BL/6 (WT) or VIP

Topics: Animals; Biological Transport; Female; Fetal Growth Retardation; Glucose; Glucose Transporter Type 1; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Placenta; Pregnancy; Pregnancy Complications; TOR Serine-Threonine Kinases; Trophoblasts; Vasoactive Intestinal Peptide

Intrauterine growth retardation and neurodevelopmental handicaps are common among infants born to HIV-positive mothers and may be due to the actions of virions and/or maternally derived viral products. The viral envelope protein, gp120, is toxic to neurons, induces neuronal dystrophy, and retards behavioral development in neonatal rats. Vasoactive intestinal peptide, a neuropeptide regulator of early postimplantation embryonic growth, and the neuroprotective protein, activity-dependent neurotrophic factor, prevent gp120-induced neurotoxicity. Whole embryo culture of gestational day 9.5 mouse embryos was used to assess the effect of gp120 on growth. Embryos treated with gp120 exhibited a dose-dependent inhibition of growth. gp120-treated embryos (10(-8) M) grew 1.2 somites in the 6-h incubation period, compared with 3.9 somites by control embryos. Embryos treated with gp120 were significantly smaller in cross-sectional area and had significantly less DNA and protein than controls. Growth inhibition induced by gp120 was prevented by cotreatment with vasoactive intestinal peptide or activity-dependent neurotrophic factor. gp120 may play a role in the growth retardation and developmental delays experienced by infants born to HIV-positive mothers. Vasoactive intestinal peptide and related factors may provide a therapeutic strategy in preventing developmental deficits.

Topics: Animals; Culture Media; Culture Techniques; DNA; Embryo, Mammalian; Embryonic and Fetal Development; Fetal Growth Retardation; HIV Envelope Protein gp120; Male; Mice; Nerve Growth Factors; Nerve Tissue Proteins; Neuropeptides; Neuroprotective Agents; Oligopeptides; Pituitary Adenylate Cyclase-Activating Polypeptide; Proteins; Rats; Rats, Sprague-Dawley; Vasoactive Intestinal Peptide

The objectives of this study were (1) to detect vasoactive intestinal polypeptide in fetal blood obtained by cordocentesis (2) to examine possible changes in growth retarded fetuses and to establish relationships between its levels and fetal blood acid-base status as well as fetal haemodynamics as assessed by Doppler ultrasonography. Vasoactive intestinal polypeptide was measured in umbilical vein blood obtained at cordocentesis in 12 growth retarded fetuses and in 13 control fetuses. Umbilical vein pH and PO2 values were determined in all the cases. Before the procedure, Doppler indices were calculated from umbilical artery, middle cerebral artery, renal artery, cardiac outflow tracts and inferior vena cava. Simple and multiple stepwise regression analysis were performed to examine the relationships between Doppler indices, acid-base status and vasoactive intestinal polypeptide levels. In control fetuses, vasoactive intestinal polypeptide was always detectable in cord blood and its levels did not change with gestational age. In growth retarded fetuses, vasoactive intestinal polypeptide levels were higher and significantly related to umbilical vein PO2 levels, Pulsatility Index in umbilical artery, middle cerebral artery and renal artery, while no relationship was found with umbilical vein pH, cardiac and venous Doppler indices. Stepwise multiple regression demonstrated middle cerebral artery Pulsatility Index to be the best explanatory variable for vasoactive intestinal polypeptide levels. In conclusion, vasoactive intestinal polypeptide blood levels are increased in growth retarded fetuses and this increase is inversely related to the Doppler measured impedance to flow in middle cerebral artery.

Topics: Acid-Base Equilibrium; Adult; Arteries; Blood Flow Velocity; Cordocentesis; Female; Fetal Growth Retardation; Gestational Age; Hemodynamics; Humans; Hydrogen-Ion Concentration; Laser-Doppler Flowmetry; Oxygen; Pregnancy; Umbilical Veins; Vasoactive Intestinal Peptide