Fetal organ growth in response to oesophageal infusion of amniotic fluid, colostrum, milk or gastrin-releasing peptide: a study in fetal sheep.
The hypothesis of the present study was that the infusion of the biological fluids to which the developing gut is normally exposed (i.e. amniotic fluid, colostrum, milk) and a single growth factor (gastrin-releasing peptide), which is found in high concentrations in fetal fluids and milk, could ameliorate the altered growth induced by the elimination of swallowed input secondary to ligation of the oesophagus. At 108-110 days of gestation the fetal oesophagus was ligated and a catheter inserted towards the stomach (32 fetuses). At 117-119 days of gestation saline (n = 5), amniotic fluid (n = 5), colostral whey (n = 5), milk whey (n = 5) or gastrin-releasing peptide (3.6 nmol day(-1), n = 6), was infused for 7 days (4 x 20 mL day(-1)), or no infusion was given (ligated group, n = 6). A further 15 fetuses were not ligated (normal group, n = 15). All fetuses had carotid artery and/or jugular vein catheters implanted. At 124-126 days of gestation the fetus was delivered and fetal body and organ weights recorded. Analysing the results by ANOVA, there were no effects of either ligation alone or infusion after ligation on fetal weight, crown-rump length, or weight relative to bodyweight of heart, adrenal, pancreas, large intestine and cecum. There were significant differences between the infusion groups for lungs, kidney, pancreas, total gut, abomasum, small intestine, spleen, chest and neck thymus, and mesenteric lymph nodes. Ligation alone significantly reduced small intestinal growth and increased kidney and spleen growth. Colostrum infusion enhanced growth of most organs. Gastrin-releasing peptide significantly increased growth of all the immune organs studied. It was concluded that at an age when premature delivery could be encountered, the fetal gut is capable of significant adaptive growth, to varying degrees, depending on the enteral diet. Growth effects in organs distant to the gut suggest that either gastrointestinal uptake and transport of growth factors or altered nutrient uptake and/or availability can affect the growth of other major fetal organs.
Trahair
J F
JF
Department of Anatomical Sciences, University of Adelaide, South Australia, Australia. jeff.trahair@adelaide.edu.au
Sangild
P T
PT
D000653:Amniotic Fluid; D000818:Animals; D003126:Colostrum; D004064:Digestive System / Q000196:embryology; D005314:Embryonic and Fetal Development; D004750:Enteral Nutrition; D004947:Esophagus / Q000196:embryology* / Q000601:surgery; D005260:Female; D005325:Fetal Organ Maturity; D020567:Fetal Weight; D019886:Gastrin-Releasing Peptide / Q000008:administration & dosage*; D005865:Gestational Age; D007668:Kidney / Q000196:embryology; D008026:Ligation; D008198:Lymph Nodes / Q000196:embryology; D008892:Milk; D009929:Organ Size; D011247:Pregnancy; D012756:Sheep / Q000196:embryology*; D013950:Thymus Gland / Q000196:embryology
D019886:Gastrin-Releasing Peptide