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PubMed2001

Analysis of heart rate variability of an anencephalic fetus using a new method to determine a fractal dimension of non-stationary time-serial data.

Human fetal heart rate (HR) variabilities were analyzed using the QIS-A, which we devised to determine a fractal dimension of non-stationary time series. Fifteen 10-min HR data of an anencephalic fetus at 23 weeks and 3 days of gestation and those of 10 normal fetuses at the same weeks of gestation were obtained by ultrasonic cardiography. The anencephalus preserved the spinal cord, medulla and partial anterior hypothalamus. The fractal scaling exponent alpha of the anencephalus was compared with that of each normal fetus by Student's t-test. In results, the scaling relationship in each case had a crossover pattern characterized by alpha(s) and alpha(l), which were slopes above and below a crossover point, respectively. Differences in mean alpha(s) and mean alpha(l) between the anencephalus and each normal fetus were significant (P < 0.01): mean alpha(s), 1.0 +/- 0.1 (+/-SD) (1/f fluctuation) and 1.6 +/- 0.2 (+/-SEM); mean alpha(l), 1.6 +/- 0.2 (+/-SD) and 1.4 +/- 0.1 (+/-SEM). There were six significant differences in mean crossover point between the anencephalus and each normal fetus: 13.8 +/- 5.7 s (+/-SD) and 15.3 +/- 5.6 s (+/-SEM). These results reveal the relationship between fractal structure of fetal HR variability and the developing central nervous system (CNS). In particular, the 1/f fluctuation of HR variability in an anencephalic fetus from the 1.25 to 13.8 s time scale might have a strong relation to the defect of the CNS.

Algorithms↗
PubMed1978

Developmental aspects of the pituitary-adrenal axis response to hemorrhagic stress in lamb fetuses in utero.

Plasma ACTH and corticosteroid concentrations were measured by radioimmunoassay in chronically catheterized fetuses of 32 pregnant sheep. Fetal plasma ACTH levels 38+/-5 pg/ml (means+/-SEM) were slightly (P < 0.05) lower than maternal 54+/-4 pg/ml levels. No general rise in fetal plasma ACTH concentration was noted before 140 days gestation; however, fetal plasma corticoid levels began to increase after about 125 days. This suggested that an increase in fetal adrenal responsiveness to endogenous ACTH occurred during gestation. Hemorrhage of 15% of estimated blood volume decreased mean arterial pressure from 54+/-3 to 36+/-3 torr and increased plasma ACTH from 30+/-5 to 130+/-30 pg/ml in fetuses older than 0.80 gestation. In fetuses younger than 0.67 gestation, 15% hemorrhage caused no change in plasma ACTH levels despite a significant fall in mean arterial pressure. This suggests that system(s) subserving the ACTH response to mild hemorrhage are either absent or nonfunctional in the younger fetuses. The hemorrhage-induced increase in plasma ACTH levels was associated with a small rise in plasma corticoids in fetuses younger than 0.94 gestation. In older fetuses, a similar increase in plasma ACTH was associated with a pronounced increase in plasma corticoid levels. This also suggests that an increase in adrenal responsiveness to endogenous ACTH occurs during gestation. No detectable changes in maternal plasma ACTH or corticoids were found in response to fetal hemorrhage, thus the fetal pituitary-adrenal axis can autonomously respond to stress.

Adrenal Cortex Hormones↗
PubMed1999

Plasma from human mothers of fetuses with severe arthrogryposis multiplex congenita causes deformities in mice.

Arthrogryposis multiplex congenita (AMC) is characterized by fixed joint contractures and other deformities, sometimes resulting in fetal death. The cause is unknown in most cases, but some women with fetuses affected by severe AMC have serum antibodies that inhibit fetal acetylcholine receptor (AChR) function, and antibodies to fetal antigens might play a pathogenic role in other congenital disorders. To investigate this possibility, we have established a model by injecting pregnant mice with plasma from four anti-AChR antibody-positive women whose fetuses had severe AMC. We found that human antibodies can be transferred efficiently to the mouse fetus during the last few days of fetal life. Many of the fetuses of dams injected with AMC maternal plasmas or Ig were stillborn and showed fixed joints and other deformities. Moreover, similar changes were found in mice after injection of a serum from one anti-AChR antibody-negative mother who had had four AMC fetuses. Thus, we have confirmed the role of maternal antibodies in cases of AMC associated with maternal anti-AChR, and we have demonstrated the existence of pathogenic maternal factors in one other case. Importantly, this approach can be used to look at the effects of other maternal human antibodies on development of the fetus.

Animals↗
PubMed1980

Porcine fetuses with pulmonary hypoplasia resulting from experimental swine influenza virus infection.

Porcine fetuses between 51 and 57 days of gestation were inoculated intraallantoically with swine influenza virus and examined 3, 7, 13, 28 and 58 days after inoculation. At 3 and 7 days, severe epithelial necrosis was seen in most bronchial buds and there was moderate epithelial necrosis in more fully differentiated major bronchi. As a result of the epithelial injury, bronchial buds did not develop further and the surrounding mesoderm failed to differentiate. By 28 days, the lungs of inoculated fetuses were about one-half the size of the normal control lungs. Microscopically, the lungs of the inoculated fetuses were composed of major bronchi surrounded by multiple islands of cartilage, medium to large arteries and a few small, incompletely developed lobules. Influenza virus was isolated most consistently and in greatest quantity from the lung, trachea and chorion of inoculated fetuses. Influenza viral antigen was shown in the epithelium of bronchial buds, bronchi and the trachea by direct fluorescent antibody staining. Hemagglutination inhibiting antibodies to influenza virus were first found in the serum of an inoculated fetus at 13 days and in the sera of all inoculated fetuses at 28 and 58 days.

Animals↗
PubMed1991

Brucella abortus-associated meningitis in aborted bovine fetuses.

Granulomatous meningitis was present in 6/33 bovine fetuses from which Brucella abortus (B. abortus) had been isolated. Meningitis was severe in three fetuses, moderate in one fetus, and mild in the remaining two fetuses. The meningitis was characterized by the infiltration of a mixed population of lymphocytes, plasma cells, and macrophages in the leptomeninges. Vasculitis characterized by the infiltration of lymphocytes and plasma cells in the vascular wall was observed in the vessels of the cerebral cortices of 4/6 fetuses. Gram negative coccobacilli were present in the cytoplasm of the leptomeningeal macrophages and extracellularly. Brucellar antigens labeled by the avidin-biotin-peroxidase complex method were present in massive amounts in leptomeningeal macrophages and in small foci of stained cells in the choroid plexus and ependyma. The findings indicate that B. abortus is one of pathogens capable of inducing meningitis in bovine fetuses.

Abortion, Veterinary↗
PubMed1996

Gross and microscopic lesions in porcine fetuses infected with porcine reproductive and respiratory syndrome virus.

Diagnosis of porcine reproductive and respiratory syndrome virus (PRRSV)-induced reproductive failure in swine is difficult because of the rapid inactivation of virus in fetuses that have died prior to abortion or farrowing. In this report, we describe gross and microscopic lesions of diagnostic value found in fetuses transplacentally infected with PRRSV during late gestation. Seven sows free of PRRSV-specific antibody and 1 sow (#8) that had been previously infected with PRRSV were oronasally exposed to a PRRSV inoculum at or about 90 days of gestation (DG). One control sow (#9) was oronasally exposed to a sham inoculum at 90 DG. Sows were euthanized 21 days postexposure, and fetuses were tested for virus. Transplacental infection was detected in litters 1-7, and gross lesions of the umbilical cord were observed in some fetuses in 6 of the 7 litters. No transplacental infection or fetal lesions were found in litters 8 and 9. The gross lesions in the umbilical cords ranged from segmental hemorrhagic areas 1-2 cm in length to a full length involvement of the cord, which was grossly distended with frank hemorrhage. All live fetuses that had gross lesions in the umbilical cord were viremic, and histopathologic examination revealed a necrotizing umbilical arteritis with periarterial hemorrhage. This was the most consistent microscopic lesion in fetuses infected with PRRSV. Sows 1-7 had endometritis and myometritis of various degrees, suggesting PRRSV also may induce these lesions. Careful gross and microscopic examination of the umbilical cord may aid in the diagnosis of PRRSV-induced reproductive failure.

Animals↗
PubMed1977

Magnesium deficiency anemia in the rat fetus.

Magnesium-deficient fetuses exhibited malformations (44%), anemia, and edema. Maternal plasma magnesium levels at day 21 of pregnancy reflected the level of dietary magnesium (2.43 +/- 0.09 mg Mg/100 ml, control; 0.74 +/- 0.02 mg Mg/100 ml, deficient). Plasma magnesium levels of deficient fetuses showed similar decreases although all fetal magnesium values at term were hihger than maternal values from the same group (3.29 +/- 0.22 mg Mg/100 ml, control; 1.78 +/- 0.07 mg Mg/100 ml, deficient). Magnesium deficiency did not appear to affect the maternal blood parameters. However, when fetal blood was examined, all of the parameters measured were altered in magnesum-deficient fetuses (Table 2). No abnormalities in hemoglobin bands or plasma proteins were seen between any groups by electrophoresis. Measurement of total protein contents showed no differences between maternal blood protein contents, but total plasma protein from magnesium-deficient fetuses was significantly lower than controls (2.00 +/- 0.14 versus 2.62 +/- 0.13 g/100 ml), thus establishing a factor in fetal edema production. Morphologic data showed that in magnesium-deficient fetuses, fetal erythropoiesis was significantly greater in liver, adrenal glands, and spleen than in controls and that maturation was normoblastic. Stained and unstained peripheral blood smears of magnesium-deficient fetuses showed and obvious macrocytosis and at least 50% of the red cells stained abnormally, exhibiting pale areas. Erythrocytic morphology seen in fetal magnesium deficiency is consistent with inadequate filling of the cell by hemoglobin as suggested by Cohlan et al. (5), a probable cause of membrane collapse. The inadequate filling of magnesium-deficient red blood cells (RBC) with hemoglobin might be explained by a reduction in hemoglobin synthesis which is consistent with the reduced mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) of the deficient fetal red cells. The role of magnesium in protein synthesis is also compatible with a reduction in hemoglobin synthesis, yet may not completely explain the abnormalities and resultant shortened lifespan of the red cells.

Anemia↗
PubMed1979

Potassium: aldosterone relationships in pregnant ewes and chronically cannulated ovine fetuses.

UNLABELLED: As maternal hyperkalemia quickly induces fetal hyperkalemia, it was decided to investigate the effect of small elevations of plasma [K+] on the peripheral blood aldosterone concentration in chronically catheterized ovine fetuses and to compare this response to that obtained in the adult ewe both pregnant and nonpregnant. Fol elevations of plasma [K+] of 0.1 to 0.3 mmole/liter blood aldosterone concentrations were elevated by 6.7 +/- 4.9 (9) ng/dl in nonpregnant sheep, 6.3 +/- 5.0 (6) in pregnant ewes, but only 0.3 +/- 1.7 (4) in fetal sheep. For increments in plasma [K+] of 0.4--1.0 mmole/liter aldosterone increments in nonpregnant ewes were 9.5 +/- 4.5 (4) ng/dl compared with 10.1 +/- 4.7 (5) in pregnant ewes and 1.5 +/- 2.6 (7) in fetuses. There was no obvious correlation between the age of the fetus and the response to increased plasma [K+]. In effect, the blood aldosterone concentration of the fetus was not elevated by increasing plasma plasma [K+]. SPECULATION: The ovine fetus is not able to cope with hyperkalemia by increasing blood aldosterone concentration. Until the fetus is close to term, hyperkalemia may jeopardize the pregnancy by causing placental hemorrhages.

Aldosterone↗
PubMed2006

The effects of maternal betamethasone administration on the intrauterine growth-restricted fetus.

Intrauterine growth restriction (IUGR) is associated with altered fetal cardiovascular function to ensure adequate perfusion of essential organs. IUGR fetuses are at risk of preterm delivery and so are likely to receive antenatal glucocorticoids to promote lung maturation. Because glucocorticoids alter vascular tone, we questioned whether such treatment may induce fetal cardiovascular alterations. Using pregnant sheep carrying twins, we induced IUGR at approximately 0.7 gestation by single umbilical artery ligation in one twin, using the other twin as a control. In each fetus, we monitored carotid blood flow and arterial blood gases. We administered 11.4 mg betamethasone (n = 5) or vehicle (n = 4) to the ewe on d 5 (BM1) and 6 (BM2) postsurgery. On d 7, fetal brains were collected for immunohistochemistry. In control fetuses, carotid blood flow decreased 3.5 h post-BM1 by 24% (P < 0.001), returning to baseline at 5.5 h. In IUGR fetuses, carotid flow decreased 2.5 h post-BM1 by 27% and then increased by 25% over baseline, peaking at 11 h (P < 0.001). Compared to control + saline, we observed a significant increase in oxidative damage (4-hydroxynonenal-positive cells) in the fetal hippocampus and subcallosal area of all treatment groups (IUGR + BM > IUGR + saline = control + BM). There was a significant correlation between carotid blood flow reperfusion after betamethasone and the number of 4-hydroxynonenal-positive cells in the cortex and hippocampus. These data suggest that antenatal betamethasone may induce brain injury in the IUGR fetus but not in the normally grown fetus.

Animals↗
PubMed1988

Transfer of thyroxine from the mother to the rat fetus near term: effects on brain 3,5,3'-triiodothyronine deficiency.

It has recently been shown that thyroid hormones are transferred from the mother to the developing rat embryo early in gestation, before the onset of fetal thyroid function. We have now studied whether there is transfer of T4 from the mother to the fetus late in gestation when the fetal thyroid is impaired. Normal and thyroidectomized females were mated, given a goitrogen [methimazole (MMI)], starting before the onset of fetal thyroid function and until term, alone or together with a constant infusion of T4 (1.8 micrograms/100 g BW.day). T4 and T3 were determined by RIA in several maternal samples and in tissues from 21-day-old fetuses. The administration of MMI blocked the fetal thyroid, as assessed from the decreased thyroid concentrations of T4 and T3. The concentrations of both iodothyronines also decreased in placenta, thyroid, plasma, brain, liver, lung, and carcass of fetuses from MMI-treated dams. Infusion of T4 into such MMI-treated mothers partly avoided this decrease, and T4 levels increased in all fetal tissues to 41-57% of those in normal fetuses. In contrast to this, T4 infusion affected the concentration of T3 to varying degrees in different tissues. The T3 concentration in plasma and lung increased very little when the MMI-treated mother was infused with T4, but in the brain T3 reached concentrations comparable to those in normal fetuses. Results not only show transfer of T4 from the mother to the fetus near term, at least when the fetal thyroid is impaired, but also suggest that it might mitigate, or avoid, the adverse effects of such failure on the developing brain.

Animals↗
PubMed1997

Effects of maternal thyroid status on thyroid hormones and growth in congenitally hypothyroid goat fetuses during the second half of gestation.

Congenital hypothyroidism in Dutch goats is due to a thyroglobulin (TG) synthesis defect that is inherited in an autosomal recessive manner. Minute amounts of mutated TG messenger RNA are translated into glycosylated TG fragments that contain the N-terminal hormonogenic site and are able to form T4, albeit less efficiently. We analyzed the effects of maternal thyroid status on fetal plasma thyroid hormones and growth during the second half of gestation (E90-E150). Maternal hypothyroidism, present from midgestation, resulted in decreased brain and cerebellum weights of affected goitrous fetuses, most evident at term gestation (E150). Brain and cerebellum weights of affected fetuses from unaffected mothers were not decreased. T4 and FT4 levels in affected fetuses were dependent on the maternal phenotype, as was the degree of enlargement of the goiter at E150. Newborn unaffected lambs from affected mothers had plasma T4 levels within the normal range. The present data show that in late gestation, fetal goats have to rely on their own thyroidal T4 production. The results suggest that affected fetuses are able to maintain sufficiently high T4 and T3 levels to prevent severe adverse effects of thyroid hormone deficiency on the brain if maternal iodide supply is adequate, although a possible increased transfer of maternal T4 to affected fetuses cannot be excluded. Under normal conditions, sufficient amounts of iodine are provided by the efficient iodine metabolism in euthyroid mothers. In affected mothers, much iodine is wasted because the thyroid also iodinates proteins other than the aberrant TG, resulting in insufficient iodine provision of the fetus and, consequently, in severe hypothyroidism.

Animals↗
PubMed1990

[The arterial distribution to the abdominal digestive organs in human fetuses].

The arterial supply of the abdominal digestive organs and the developmental process were studied in 25 Japanese fetuses from 3 months to 9 months old into whose arteries latex rubber was injected. The results were as follows: 1) The branching patterns of the celiac trunk were classified into 5 types. The most common type or the complete celiac trunk was found in 18 cases (72%). Four variation types or incomplete celiac trunks were found in 7 cases (28%). 2) The rates at which the following arteries were observed in the stomach were as follows: 100% for the left gastric artery, 100% for the left and right gastroepiploic artery, 100% for the short gastric artery, 100% for the gastroduodenal artery, 92% for the right gastric artery, 24% for the branch of the left inferior phrenic artery, and 16% for the posterior gastric artery arising from the splenic artery. The left gastric artery was better developed than the other arteries in 3-month-old fetuses. 3) The rates at which the following arteries were observed in the liver were as follows: 100% for the proper hepatic artery, 28% for the accessory left hepatic artery and 8% for the accessory right hepatic arteries. The accessory left hepatic artery in 3-month-old fetuses was better developed than in older fetuses. 4) The rates at which the following arteries were observed in the pancreas were follows: 100% for the branches of the splenic artery, 100% for the branches of the gastroduodenal artery and 100% for the branches of the superior mesenteric artery. Further, dorsal pancreatic arteries not arising from the splenic artery were found in 20% of cases. The dorsal and great pancreatic arteries branching from the splenic artery could not be distinguished from one another in younger fetuses. 5) The rates at which the following arteries were observed in the duodenum were as follows: 100% for the branches of the superior and the inferior pancreaticoduodenal arteries. This arterial supply was the same in all the fetuses. 6) The arterial supply of the jejunum and the ileum were as follows: the jejunum and the ileum were supplied only by the branches of the superior mesenteric artery. The minimum number of the branches was 7 and the maximum 12. 7) The arterial supply of the large intestine was as follows: the caecum was supplied only by the ileocolic artery.(ABSTRACT TRUNCATED AT 400 WORDS)

Arteries↗
PubMed2005

Pregnancy outcome of euploid fetuses with increased nuchal translucency: how bad is the news?

AIMS: The number of fetuses with an abnormal increased first trimester nuchal translucency (NT), but confirmed normal karyotype and anatomy is relatively small and therefore a challenge for prenatal counseling. Universal guidelines are still needed for a systematic work-up, how to decide on the rewarding cut-off for this policy as well as how to counsel patients with an increased NT but with euploid fetuses. The current review aims to address some of these issues. RESULTS: Eleven studies reporting on the pregnancy outcome of 2,128 euploid fetuses with increased NT (>or=3 mm or >or=95 centile) were retrieved by our previously reported literature search. 2.2-10.6% of the fetuses has miscarried and 0.5-15.8% ended in perinatal death. There was an overall rate of 0.5-13% neurodevelopmental problems, and 2-8% of the malformations were undiagnosed before birth, the most common being cardiac anomalies. Nevertheless, 70-90% fetuses had normal outcomes. CONCLUSION: For those euploid fetuses with increased NT>2 MoM or >or=1.5 mm delta NT we recommend a detailed two-step anomaly scan including midgestation fetal echocardiography. Maternal age as well as data on relevant family history and persistence of nuchal edema provides additional relevant information for counseling and planning pregnancy management.

Congenital Abnormalities↗
PubMed1989

The vanishing fetus. A report of 17 cases of triplets and quadruplets.

The incidence of multiple conceptions is higher than the incidence of multiple deliveries. The "vanishing fetus" is a relatively new concept being a direct result of the advent of ultrasonography. Early first trimester loss of one or more conceptuses accounts for this phenomenon. The patient may be symptomatic (bleeding, pain, abdominal cramps) but in most instances, the finding is fortuitous. We report 17 cases of a vanishing fetus in a multiple gestation of greater than twins. In 13 patients one fetus vanished in the course of pregnancy while in four cases two fetuses disappeared from each gestation. The phenomenon was observed up to the 16th week of pregnancy. It is our feeling that the finding of a vanishing fetus should be recorded early, as the prognosis for pregnancy bleeding is different than in the singleton pregnancy. Thus information regarding this phenomenon should be given to couples who consider artificial reduction of fetuses in the multiple gestation.

Female↗
PubMed2005

Study of global left atrial shortening in fetuses of diabetic mothers.

OBJECTIVE: To test the hypothesis that left atrial shortening fraction is lower in fetuses of diabetic mothers than in fetuses of mothers with no systemic disease. METHODS: Forty-two fetuses of mothers with previous diabetes or gestational diabetes and 39 healthy fetuses of mothers with no systemic disease (controls) underwent echocardiographic examination. Their gestational ages ranged from 25 weeks to term. The left atrial shortening fraction was obtained with the following formula: (left atrial maximum diameter - left atrial minimum diameter)/left atrial maximum diameter. Data were compared using the Student t test, with an alpha level of 0.05. RESULTS: Mean left atrial shortening fractions in fetuses of diabetic mothers and in those in the control group were 0.39 +/- 0.15 and 0.51 +/- 0.11, respectively. This difference was significant with P < 0.001. CONCLUSION: Left atrial dynamics, with a reduction in global left atrial shortening, is increased in fetuses of diabetic mothers. We speculate that this parameter may be useful in assessing fetal left ventricular diastolic function.

Diabetes, Gestational↗
PubMed1996

The effects of cortisol on the growth rate of the sheep fetus during late gestation.

Using indwelling crown-rump length (CRL)-measuring devices, the growth rate of sheep fetuses was monitored during late gestation and after experimental manipulation of fetal plasma cortisol by exogenous infusion and fetal adrenalectomy. In intact control fetuses, the increment in CRL declined progressively during the last 20-25 days of gestation: mean +/- S.E.M. values fell from 5.5 +/- 0.4 mm/day (n = 12) at 21-25 days before delivery to 2.5 +/- 0.3 mm/day (n = 12) in the last 5 days before birth (P < 0.01). These changes closely parallelled the normal prepartum increase in fetal plasma cortisol which rose from 19.3 +/- 3.3 nmol/l (n = 10) at 21-25 days before birth to 177.4 +/- 19.0 nmol/l (n = 10) in the final 5 days before delivery (P < 0.01). When this cortisol surge was prevented by fetal adrenalectomy, there was no decrease in CRL increment towards normal term: mean CRL increment in the 5 days before normal term (4.8 +/- 0.6 mm/day, n = 5) was similar to that observed at 21-25 days before term (4.7 +/- 0.4 mm/day, n = 5). At delivery at term, the body weight (4.116 +/- 0.280 kg, n = 5) and CRL (51.9 +/- 1.7 cm, n = 5) of the adrenalectomized fetuses were significantly greater than the corresponding values in their sham-operated controls (2.877 +/- 0.070 kg and 47.1 +/- 1.6 cm, n = 6, respectively). In contrast with the sham-operated controls, plasma glucose and insulin levels in the adrenalectomized fetuses decreased towards term. Infusion of cortisol into the preterm fetus for 5 days increased fetal plasma cortisol to term levels and decreased the CRL increment to a value (1.8 +/- 0.5 mm/day, n = 8) which was similar to that observed in untreated controls during the last 5 days before spontaneous delivery at term (2.1 +/- 0.3 mm/day, n = 6). There were no significant alterations in the fetal arterial concentrations of plasma glucose or insulin in response to fetal cortisol infusion. When all the data were combined irrespective of treatment or proximity to delivery, the fetal plasma concentrations of cortisol (P < 0.001) and glucose (P < 0.04), but not insulin (P > 0.05), had a significant effect on the fetal CRL increment measured over 5-day periods during the last 25-30 days of gestation. These findings show that cortisol inhibits growth of the axial skeleton in the sheep fetus during late gestation. They also indicate that the prepartum cortisol surge may be responsible for the normal decline in fetal growth rate observed towards term in this species.

Adrenalectomy↗
PubMed2001

Insulin-like growth factor-binding protein-1 in umbilical artery and vein of term fetuses with signs suggestive of distress during labor.

Insulin-like growth factor-binding protein-1 (IGFBP-1) is believed to be an inhibitory factor for fetal growth. The regulation of IGFBP-1 secretion in the fetus is uncertain, although insulin and oxygen tension (PO2) and saturation are thought to play a role. We studied IGFBP-1 levels in umbilical cord artery (UA) and vein (UV) of 98 singleton fetuses at term with clinical signs of distress during labor, i.e. meconium-stained liquor or/and an abnormal fetal heart rate tracing. Blood gas values and serum C-peptide and IGFBP-1 concentrations were measured in both UA and UV. Twenty-five fetuses had an UA pH<7.20. The concentrations of IGFBP-1 were similar in UA and UV and were highly correlated (r=0.98). IGFBP-1 levels were inversely correlated with birth weight, with increased concentrations in small-for-gestational age fetuses (< or =10th weight percentile). IGFBP-1 levels were negatively correlated with C-peptide concentrations, and remained so after correction for birth weight (r=-0.37 for both UA and UV; P<0.001); more specifically, IGFBP-1 levels were increased in the lowest C-peptide quartile (<0.23 nmol/l) compared with the other quartiles. In addition, IGFBP-1 levels were inversely correlated with PO(2) values (r=-0.39 in UA and r=-0.34 in UV; P<0.001); quartiles of UA and UV PO2 showed a gradual increase in IGFBP-1 concentrations with lower PO2 values. A regression model with C-peptide and PO2 values as independent variables predicted IGFBP-1 concentrations (R2 of model was 0.25 and 0.22 for UA and UV respectively; P<0.001). Other blood gas values (pH, PCO2, HCO3- and base deficit) did not correlate with IGFBP-1 levels. The data of this study indicate that serum IGFBP-1 levels in term fetuses are determined by both insulin and PO2 levels, and suggest that acute hypoxemia stimulates IGFBP-1 secretion in the fetus.

Analysis of Variance↗
PubMed1991

Effect of number of corpora lutea and fetuses on concentrations of progesterone in blood of goats.

The objectives of this study were to assess relationships between 1) number of corpora lutea (CL) and concentrations of progesterone (P) in plasma of goats from onset of estrus (d 0) to d 45 of pregnancy and 2) concentration of P and number of fetuses on d 45. Blood from 79 pregnant goats was obtained on d 0 and 1 and at 48-h intervals thereafter to d 25 of gestation. Additional samples were collected every 5 d from d 25 to d 45. Plasma samples were analyzed for P by RIA. Fetuses and CL were counted at laparotomy on d 45 +/- 3. Six does had one CL, 47 had two and 26 had three or four. Concentrations of P were compared for 1) animals with different numbers of CL and 2) animals with the same number of CL but different numbers of fetuses on d 45. Concentration of P increased in all animals from d 3 to a maximum of 8.5 +/- .3 ng/ml on d 13, then P declined to 5 +/- .3 ng/ml by d 35. Goats with multiple CL had higher P than goats with one CL (P less than .01) from d 7 to d 30. Of goats with two CL, those with two fetuses at d 45 had higher P on d 13 than those with one fetus (P less than .01). The number of CL or fetuses did not influence the concentration of P after d 30.

Animals↗