Effect of maternal hyperalimentation on intrauterine growth retardation.

The effect of maternal hyperalimentation on intrauterine growth retardation was studied by performing unilateral uterine vessel ligation on day 17 in Wistar rats. Test animals were given food supplements by gavage for three days postoperatively whereas control animals received saline. The caloric intake and weight gain of the test dams was significantly greater than that of the controls from days 17 to 20 but not over the longer period, day 14 to 23. The survival and growth of fetuses in the unoperated horn were similar in test and control rats. Fetal survival in the ligated horn was doubled by maternal food supplementation but the growth and development of the survivors were not improved.

Reduced plasma somatomedin activity and costal cartilage sulfate incorporation activity during experimental growth retardation in the fetal rat.

In this study, the experimental model of Wigglesworth was used to limit the maternal blood supply to the rat fetus and induce intrauterine growth retardation. The associated changes in plasma somatomedin activity, insulin, glucose, and cartilage metabolic activity are reported. The mean body weight (+/- SEM) of 108 fetuses in ligated uterine horns was significantly lower than that of 146 control fetuses (ligated, 2820 +/- 50 mg; control, 3180 +/- 50 mg; p less than 0.001), as was mean nose-tail tip length (ligated, 55.6 +/- 0.4 mm; control, 59.4 +/- 0.3 mm; p less than 0.001) and mean liver weight (ligated, 222 +/- 5 mg; control, 274 +/- 5 mg; p less than 0.001). The uptake of [35S]sulfate by fetal costal cartilage in basal culture medium was significantly lower in growth-retarded fetuses than in controls. Plasma somatomedin activity measured by fetal rat cartilage bioassay was significantly lower in growth-retarded than in control fetuses (p less than 0.001). The growth-retarded fetuses were relatively hypoinsulinemic and hypoglycemic compared to control animals. These studies suggest that nutrient supply may become a limiting factor in the release of insulin and the circulating levels of somatomedin activity in the rat fetus, and hence in its growth.

Thrombosis of the right umbilical artery, presumably related to the shortness of the umbilical cord: an unusual cause of fetal distress.

This case report concerns a late pregnancy complication, clinically apparent as severe variable decelerations in the first stage of labor. Emergency cesarean section delivered a mildly asphyxiated full-term newborn infant. Examination of the umbilical cord revealed a thrombus of the right umbilical artery, near the fetal side, confirmed by histological examination. The total length of the umbilical cord, only 30 cm, was below the limit necessary for uncomplicated delivery of the fetus near term. Transient stretching during fetal descent is thought to be responsible for constriction of the umbilical arteries, blood flow sludging and thrombosis. Although only a few cases have been reported, thrombosis of the umbilical vessels has to be considered whenever the fetal heart rate pattern shows unexplained variable decelerations.

Intrauterine growth retardation and development of endocrine pancreas in the experimental rat.

Intrauterine growth retardation (IUGR) was induced in rats by uterine artery ligation according to Wigglesworth. Control and growth-retarded animals were studied at days 21 and 22 of fetal life and 2 h after spontaneous birth. Fetuses with IUGR, when compared to controls, showed significantly lower glycemia and insulinemia levels. Newborn rats with IUGR had reduced glycemia levels but identical insulin values in comparison to controls. Dysmature and control animals had significantly different absolute weights of endocrine pancreas, but they had equal amounts of endocrine pancreatic tissue in proportion to their total body weight. Within the endocrine pancreas the same number of islet cells was counted in dysmature and control animals, but the animals with IUGR ended up with a reduced percentage of insulin-containing granulated B cells after birth.

Insulin levels in amniotic fluid and fetal growth.

Insulin concentrations in amniotic fluid were correlated with fetal age and with fetal weight in order to test the hypothesis that fetal insulin regulates fetal growth. No significant correlation could be detected. Insulin levels in amniotic fluid in diabetics, however, were significantly higher than in nondiabetics. In the same samples of amniotic fluid C-peptide proved to be very unstable during long term storage.

A morphological study of the endocrine pancreas in human pregnancy.

During human pregnancy an enlargement of the islets of Langerhans and hyperplasia of the beta cells is present. These morphological changes indicate that the endocrine pancreas is able to adapt to the metabolic changes of pregnancy.

The endocrine pancreas in small-for-dates infants.

In a small series of pregnancies complicated by severe fetal growth retardation we found reduction of fetal endocrine pancreatic tissues and of the insulin producing beta cells.