Abstract:A method is described for the simultaneous estimation of uterine and umbilical blood flows and oxygen uptakes. A test stubstance, antipyrine, was infused at constant rate in the fetal circutlation. About 50 min. after starting the infusion a steady state was attained in which the rate of transplacental diffusion of the test substance was equal, blut for small corrections, to the rate of infusion. During the steady state, blood samples were collected from uterine and umbilical arteries and veins and analyzed fo… Show more
“…2). The transport fractions reported for antipyrine in sheep (Meschia et al, 1966) were between 35 and 45 p. 100 at the same flow ratio. A value of 30 p. 100 was found in goat (Rankin and Peterson, 1969).…”
“…2). The transport fractions reported for antipyrine in sheep (Meschia et al, 1966) were between 35 and 45 p. 100 at the same flow ratio. A value of 30 p. 100 was found in goat (Rankin and Peterson, 1969).…”
“…Uterine and umbilical blood flows were calculated according to the antipyrine steady-state diffusion method (Meschia et al 1966). Uptakes of metabolites for mother and fetus were calculated by application of the Fick principle: uterine uptake=uterine blood flow (maternal artery uterine vein concentration); fetal uptake= umbilical blood flow (umbilical vein femoral artery concentration); placental uptake=uterine uptake fetal uptake.…”
It has been shown that IGF-I has an anabolic effect in the normal fetus. However, there is evidence to suggest that there may be IGF-I resistance in the growth retarded fetus. Therefore, we investigated the effects of acute IGF-I infusion to chronically catheterised fetal sheep. At 128 days gestation, fetuses underwent a 4 h infusion of IGF-I (50 µg/kg/h). Three groups of animals were studied. Nine normally grown fetuses were studied as controls. Embolised animals (n=8) received microspheres into the uterine vasculature, and animals with spontaneous intra-uterine growth retardation (IUGR animals) (n=6) were fetuses found at post mortem to be spontaneously growth restricted.The effects of IGF-I infusion on feto-placental carbohydrate and protein metabolism were similar in our control group to previous similar experiments. IGF-I infusion decreased fetal blood glucose, oxygen, urea and aminonitrogen concentrations, and inhibited placental lactate production. The same fetal blood metabolite concentrations also fell during IGF-I infusion in the embolised fetuses, but the effect on placental lactate production was not seen. The only effect of IGF-I infusion in the spontaneous IUGR animals was a fall in fetal blood amino-nitrogen concentrations. We conclude that fetal IGF-I infusion does not have the same anabolic effects in the growth retarded fetus as the normal fetus. In addition, the effects of IGF-I were different in the two growth retarded groups. Our data support previous evidence that the growth retarded fetus has altered IGF-I sensitivity, and this may vary depending on the cause, severity and duration of growth retardation.
“…The collected fractions of arginine metabolites were measured for 3 H activity by liquid scintillation counting. Calculations Umbilical and uterine blood flows (ml/min) were calculated from measured antipyrine concentrations according to the Fick principle, as the quotient of the infusion rate and the arterio-venous concentration difference across the placenta (Meschia et al, 1966). Plasma flows were calculated as the product of the blood flow and (1 -fractional haematocrit).…”
Urea production may be impaired in intrauterine growth restriction (IUGR), increasing the risk of toxic hyperammonaemia after birth. Arginine supplementation stimulates urea production, but its effects in IUGR are unknown. We aimed to determine the effects of IUGR and arginine supplementation on urea production and arginine metabolism in the ovine foetus. Pregnant ewes and their foetuses were catheterised at 110 days of gestation and randomly assigned to control or IUGR groups. IUGR was induced by placental embolisation. At days 120 and 126 of gestation, foetal urea production was determined from [ 14 C]-urea kinetics and arginine metabolism was determined from the appearance of radioactive metabolites from [ 3 H]-arginine, both at baseline and in response to arginine or an isonitrogenous mixed amino acid supplementation. Urea production decreased with gestational age in the embolised animals (13.9^3.1 to 11.2^3.0 mmol/kg per min, P # 0.05) but not in the controls (13.3^3.5 to 14.8^6.0 mmol/kg per min). Arginine supplementation increased urea production in both groups, but only at 126 days of gestation (control: 15.0^8.5 to 17.0^9.4 mmol/kg per min; embolised: 11.7^3.1 to 14.3^3.1 mmol/kg per min, P # 0.05). Embolisation reduced foetal arginine concentrations by 20% ( P # 0.05) while foetal arginine consumption was reduced by 27% ( P # 0.05). The proportions of plasma citrulline and hydroxyproline derived from arginine were reduced in the embolised animals. These data suggest that foetal urea production and arginine metabolism are perturbed in late gestation after placental embolisation.
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