The nutrition of the fetus with intestinal atresia: studies in the chick embryo model.
This article examines the effects of experimental prenatal intestinal obstruction on the growth and blood composition of chick embryos. Intestinal atresia (IA) was produced by bipolar bowel electrocoagulation in fertile eggs on the 14th day of incubation. The chicks killed on the 19th day were measured, weighed, and blood-sampled. Twenty-three control, 10 sham-operated, and 11 IA chicks were studied. Animals with IA were severely undernourished by weight (43.4 +/- 4.7 v 70.3 +/- 7.6% of egg weight, P < .001) and length (15.3 +/- 1.1 v 18.1 +/- 0.9 mm tibial length, P < .001) in comparison with sham-operated ones. Their hematocrit was slightly lower, and total protein increased. Prealbumin was absent in their sera and albumin, alpha and beta globulins were significantly decreased, whereas gamma-globulin was greatly increased. Sodium, potassium chloride, urea, and glucose remained within normal limits. The lack of placenta in the avian embryo precludes any supply of nutrients by this route and the ingestion of amniotic fluid, which is protein-rich after the 13th day of incubation, when the opening of the seroamniotic connection allows albumen to be mixed with it, becomes the main source of nutrients until hatching. Obstruction of the main incoming avenue by IA induces severe malnutrition in this model which relies on this route to a greater extent than the human fetus. In spite of the obvious biological differences between the avian embryo and the human fetus, the present evidence supports the hypothesis that prenatal interruption of the amniotic fluid transit contributes to fetal undergrowth in IA.
Lopez de Torre
B
B
Pediatric Surgery Services, Universidad del País Vasco, Hospital Na. Sa. de Aranzazu, San Sebastián, Spain.
Tovar
J A
JA
Uriarte
S
S
Aldazabal
P
P
D000653:Amniotic Fluid / Q000378:metabolism; D000818:Animals; D001798:Blood Proteins / Q000378:metabolism; D002642:Chick Embryo; D004195:Disease Models, Animal; D005314:Embryonic and Fetal Development / Q000502:physiology*; D005260:Female; D005317:Fetal Growth Retardation / Q000196:embryology*; D006801:Humans; D007231:Infant, Newborn; D007409:Intestinal Atresia / Q000196:embryology*; D011247:Pregnancy
D001798:Blood Proteins