Fetal Brain Weight Research Articles

Magnesium sulfate protection of fetal rat brain from severe maternal hypoxia

Objective: To determine whether severe maternal hypoxia affects fetal rat physical characteristics and causes neuronal damage, and whether magnesium sulfate can decrease these effects. Methods: At 17 days gestation, rats were randomly assigned to one of four groups that received saline injections and room air ( n = 6), magnesium sulfate and room air ( n = 5), saline and hypoxia ( n = 5) or magnesium sulfate and hypoxia ( n =5). Maternal magnesium sulfate or saline injections were given for 4 hours. In groups 3 and 4 this was followed by a hypoxia chamber protocol that included a gas mixture of 9% oxygen and 3% carbon dioxide for 2 hours. After 72 hours of recovery, fetuses were delivered abdominally, perfused transcardially, and brains removed intact. Fetal body and brain weight and size were measured. Brains were embedded in paraffin, sectioned, and stained. A neuropathologist masked to the protocol performed histologic grading of brain regions. Results: Exposure to the hypoxia chamber resulted in decreased maternal oxygen tension and pH (from 82.8 ± 20.0 to 49.2 ± 14.4 mmHg, and from 7.37 ± 0.05 to 7.20 ± 0.04, respectively; P < .005). Magnesium sulfate administration resulted in higher magnesium levels in blood (from 1.52 ± 0.2 to 3.77 ± 0.7 mg/dL; P < .001). The hypoxia protocol resulted in a significant decrease in fetal body and brain size, but not weight. Hypoxia also caused an increase in the proportion of fetal rats that had brain injury, including shrinkage of cells and karyorrhexis in the hippocampus and thalamus (from 0% to 38.1% and 38.9%, respectively; P < .05). Magnesium sulfate reduced these effects on fetal brain histopathology and size. Conclusion: Severe maternal rat hypoxia resulted in significant fetal neuronal damage and decreased fetal body and brain size. Maternal magnesium sulfate administration reduced the effect of hypoxia on fetal brain histopathology and size without affecting body size.

Effects of dietary mixtures of amino acids on fetal growth and maternal and fetal amino acid pools in experimental maternal phenylketonuria

Branched-chain amino acids have been reported to improve fetal brain development in a rat model in which maternal phenylketonuria (PKU) is induced by the inclusion of an inhibitor of phenylalanine hydroxylase, DL-p-chlorophenylalanine, and L-phenylalanine in the diet. We studied whether a dietary mixture of several large neutral amino acids (LNAAs) would improve fetal brain growth and normalize the fetal brain amino acid profile in a rat model of maternal PKU induced by DL-alpha-methylphenylalanine (AMPhe). Long-Evans rats were fed a basal diet or a similar diet containing 0.5% AMPhe + 3.0% L-phenylalanine (AMPhe + Phe diet) from day 11 until day 20 of gestation in experiments to test various mixtures of LNAAs. Maternal weight gains and food intakes to day 20, fetal body and brain weights at day 20, and fetal brain and fetal and maternal plasma amino acid concentrations at day 20 were measured. Concentrations of phenylalanine and tyrosine in fetal brain and in maternal and fetal plasma were higher and fetal brain weights were lower in rats fed the AMPhe + Phe diet than in rats fed the basal diet. However, fetal brain growth was higher and concentrations of phenylalanine and tyrosine in fetal brain and in maternal and fetal plasma were lower in rats fed the AMPhe + Phe diet plus LNAAs than in rats fed the diet containing AMPhe + Phe alone. LNAA supplementation of the diet improved fetal amino acid profiles and alleviated most, but not all, of the depression in fetal brain growth observed in this model of maternal PKU.

Chronic Ethanol Exposure Alters MK-801 Binding Sites in the Cerebral Cortex of the Near-Term Fetal Guinea Pig

The mechanism of ethanol central nervous system (CNS) teratogenesis, resulting from chronic maternal ingestion of high-dose ethanol during pregnancy, is not clearly understood. One of the target sites for ethanol-induced damage in the developing brain is the cerebral cortex. It has been proposed that chronic prenatal ethanol exposure alters NMDA receptors in the developing cerebral cortex. To test this hypothesis, timed pregnant guinea pigs were administered one of the following oral treatments throughout gestation: 4 g ethanol/kg maternal body weight/day; isocaloric sucrose/pair-feeding; water; or no treatment (ad lib). Near-term fetuses were studied at gestational day (GD) 63 (term, about GD 68). This ethanol regimen produced a maternal blood ethanol concentration of 66 ± 4 mM (304 ± 19 mg/dl) at 1 h after the daily dose on GD 58. The chronic ethanol regimen decreased near-term fetal body weight (12–26% decrease), brain weight (23% decrease), and cerebral cortical weight (21% decrease), compared with the isocaloric sucrose/pair-feeding, and combined water/ad lib experimental groups. Saturation analysis of near-term fetal cerebral cortical membranes using a [ 3H]MK-801 radioligand binding assay demonstrated a decreased affinity and increased number of MK-801 binding sites for the chronic ethanol regimen compared with the control treatments. These data support the suggestion that upregulation of NMDA receptors in the cerebral cortex after chronic prenatal ethanol exposure could lead to NMDA receptor-mediated excitotoxicity in this brain region.

Intra-uterine growth restriction differentially regulates perinatal brain and skeletal muscle glucose transporters

Employing Western blot analysis, we investigated the effect of maternal uterine artery ligation causing uteroplacental insufficiency with asymmetrical intrauterine growth restriction (IUGR) upon fetal (22d) and postnatal (1d, 7d, 14d and 21d) brain (Glut 1 and Glut 3) and skeletal muscle (Glut 1 and Glut 4) glucose transporter protein concentrations. IUGR was associated with a ∼42% decline in fetal plasma glucose ( p<0.05) and a ∼25% decrease in fetal body weights ( p<0.05) with no change in brain weights when compared to the sham operated controls (SHAM). In addition, IUGR caused a ∼45% increase in fetal brain Glut 1 (55 kDa) with no change in Glut 3 (50 kDa) protein concentrations. This fetal brain Glut 1 change persisted, though marginal, through postnatal suckling stages of development (1d–21d), with no concomitant change in brain Glut 3 levels at day 1. In contrast, in the absence of a change in fetal skeletal muscle Glut 1 levels (48 kDa), a 70% increase was observed in the 1d IUGR with no concomitant change in either fetal or postnatal Glut 4 levels (45 kDa). The change in skeletal muscle Glut 1 levels normalized by d7 of age. We conclude that IUGR with hypoglycemia led to a compensatory increase in brain and skeletal muscle Glut 1 concentrations with a change in the brain preceding that of the skeletal muscle. Since Glut 1 is the isoform of proliferating cells, fetal brain weight changes were not as pronounced as the decline in somatic weight. The increase in Glut 1 may be protective against glucose deprivation in proliferating fetal brain cells and postnatal skeletal myocytes which exhibit `catch-up growth', thereby preserving the specialized function mediated by Glut 3 and Glut 4 towards maintaining the intracellular glucose milieu.

Heme oxygenase activity and acute and chronic ethanol exposure in the hippocampus, frontal cerebral cortex, and cerebellum of the near-term fetal guinea pig

Heme oxygenase (HO) catalyzes the oxidation of heme to produce carbon monoxide, which is considered to be a novel neuronal messenger in the brain and may play a role in neuronal development. The objective of this study was to determine the effects of in vitro, acute in vivo, and chronic in vivo ethanol exposure on HO activity in the hippocampus, frontal cerebral cortex, and cerebellum of the near-term fetal guinea pig. HO activity was determined using a gas chromatographic method to quantitate CO formation in the microsomal fraction of the homogenate of each selected brain region, incubated with saturating concentrations of heme, NADPH, and O 2. Fetal body, brain, hippocampal, and cerebellar weights were recorded. In vitro ethanol exposure (25–100 mM) did not affect hippocampal, cerebral cortical, or cerebellar HO activity of the fetal guinea pig at gestational day (GD) 62 (term, about GD 68). Acute maternal oral administration of 4 g ethanol/kg maternal body weight at GD 62 did not affect HO activity in these three fetal brain areas compared with control fetuses (maternal administration of isocaloric sucrose or water). For chronic daily maternal oral administration of 4 g ethanol/kg maternal body weight throughout gestation, fetal body, brain, hippocampal, and cerebellar weights were decreased at GD 62 compared with isocaloric-sucrose/pair-fed and water treatment control groups. Furthermore, isocaloric-sucrose/pair-feeding treatment decreased fetal body and brain weights compared with water treatment. Chronic in vivo ethanol exposure did not alter HO activity in the near-term fetal hippocampus, frontal cerebral cortex, or cerebellum. This is the first study of the effect of ethanol exposure on HO activity in the developing brain of any species. The data demonstrate, for ethanol CNS teratogenesis in the guinea pig manifesting as fetal brain growth restriction, there is no associated change in HO activity in the hippocampus, frontal cerebral cortex, or cerebellum.

A murine model of prenatal cocaine exposure: Effects on the mother and the fetus

To develop and characterize a murine model for investigating the long-term effects of prenatal cocaine exposure, the present study established the route of drug administration and the doses to be used for pregnant C57BL/6 mice. Comparison of the effects of a high dose of cocaine (60 mg/kg) when gavaged or injected subcutaneously (SC) established patterns of pathology characteristic of administration route but no dominating logic for selecting one over the other route for prenatal studies; however, because of the fourfold greater brain levels, with no evidence of greater pathology, the SC route was selected. When injected daily during gestation days 12–18, the period of prenatal development of dopamine systems, cocaine at doses producing plasma concentrations consistent with its stimulatory effects reduced food ingestion and weight gains during pregnancy and fetal body and brain weights at term. The extent of these reductions was comparable to reports on babies exposed to cocaine prenatally. Furthermore, the present study suggests that maternal undernutrition is not a likely mediator of these perinatal effects and that differences in the amount of cocaine exposure may cause the contrasting effects of maternal cocaine noted in the human literature.

Ethanol-induced changes in insulin-like growth factors and IGF gene expression in the fetal brain.

Brain growth retardation is a major feature of the fetal alcohol syndrome (FAS). Insulin-like growth factors (IGF-I and IGF-II) have been shown to exert significant metabolic and growth-promoting effects. Previously, we showed that circulating levels of IGF-I as well as hepatic gene expression of both IGFs were decreased in newborn offspring of rats fed ethanol during pregnancy. This study investigated the effects of maternal ethanol ingestion on fetal rat brain growth and on levels of IGF-I and IGF-II, as well as their mRNAs, in fetal brain. IGF-binding protein (IGFBP) levels also were determined. Rats were fed 5% w/v ethanol in a liquid diet during gestation (EF group). Weight-matched animals were pair-fed equicaloric control diet (PF group) or were fed ad libitum (AF group). The mean fetal brain weight of EF offspring was 13% and 16% lower (P < 0.01) than that of PF and AF offspring, respectively. Body weight of EF pups was decreased to a greater extent, resulting in higher brain to body weight ratios in EF pups than in either control group (P < 0.05). IGF-I levels in EF pups decreased by 33% and 41% compared with the corresponding PF and AF values (P < 0.01). IGF-I mRNA levels decreased by 27% and 40% compared with PF and AF values, respectively. A positive correlation was observed between brain IGF-I level and brain weight (r = 0.561, P < 0.01). IGF-II levels were not affected despite a 50% decrease in IGF-II expression. In PF animals, the fetal brain IGF-I and IGF-II mRNA levels were reduced by 28% and 21%, apparently in response to undernutrition. IGF-binding proteins levels were low in the EF group but not statistically significant compared with control values. The diminished fetal brain concentration of IGF-I and decreased gene expression of IGFs may play a role in brain growth retardation associated with FAS.

Effect of Chronic Maternal Ethanol Administration on Nitric Oxide Synthase Activity in the Hippocampus of the Mature Fetal Guinea Pig

Nitric oxide is a novel messenger that is involved in neuronal cell-cell communication and seems to play a neurotrophic role in normal brain development. Chronic prenatal ethanol exposure can produce central nervous system (CNS) teratogenesis, in which one of the target sites is the hippocampus. The main objective of our study was to test the following hypothesis: chronic maternal administration of an ethanol dosage regimen that produces CNS teratogenesis decreases nitric oxide synthase (NOS) activity in the fetal hippocampus. The ontogeny of NOS activity in the hippocampus of the developing guinea pig was further elucidated at two prenatal and two postnatal ages. The effects of chronic maternal oral administration of 4 g of ethanol/kg maternal body weight/day, isocaloric sucrose and pair feeding, or water [given as two equally divided doses 2 hr apart from gestational day (GD) 2 to GD 61] on body, brain, and hippocampal weights and hippocampal NOS activity were determined in the mature fetal guinea pig at GD 62 (term, about GD 68). NOS activity in the 25,000 x g supernatant fraction of hippocampal homogenate was measured using an optimized radiometric assay, based on the oxidation of L-[14C]arginine to L-[14C]citrulline. For the chronic ethanol regimen, the maternal blood ethanol concentration at 1 hr after the second divided dose on GD 57 was 157 +/- 45 mg/dl. Chronic maternal administration of ethanol decreased fetal body, brain, and hippocampal weights, compared with the isocaloric-sucrose/pair-fed and water treatment groups. The rate of L-[14C]citrulline formation and NOS activity in the fetal hippocampus were decreased in the ethanol treatment group, compared with the isocaloric-sucrose/ pair-fed and water treatment groups. There was no difference in the rate of L-[14C]citrulline formation, NOS activity, and fetal hippocampal and body weights between the isocaloric-sucrose/pair-fed and water treatment groups; however, fetal brain weight was decreased in the isocaloric-sucrose group, compared with the water group. Data of this study support the research hypothesis by demonstrating that chronic maternal administration of ethanol decreases fetal hippocampal NOS activity that is correlated with restricted growth of this brain region.

Persistent Alterations in Regional Brain Glial Fibrillary Acidic Protein and Synaptophysin Levels Following Pre- and Postnatal Polychlorinated Biphenyl Exposure

Pregnant Wistar WU rats were exposed to 0, 5, and 25 mg of the commercial polychlorinated biphenyl (PCB) mixture Aroclor 1254 per kilogram of body weight on Days 10 to 16 of gestation. Pregnant rats were sacrificed on Gestation Day 20 to observe effects on fetal body and brain weights. Male and female offspring were sacrificed on Postnatal Days 21 and 90 (PND21 and PND90, respectively) and examined for treatment-related effects on neurochemical parameters. The concentrations of the neuronal and glial cell markers, synaptophysin and glial fibrillary acidic protein (GFAP), were measured in diverse brain regions from the offspring using immunochemical techniques. The level of calcineurin (a calmodulin-regulated protein phosphatase) activity was measured in cerebellar homogenates. In addition, ethoxyresorufinO-deethylase (EROD) activity was determined in hepatic microsomes as a measure of a well-characterized response to PCB exposure in experimental animals. The major alterations of GFAP levels following maternal PCB treatment were significant increases in the lateral olfactory tract (LOT) and the cerebellum (CB) and significant decreases in the brain stem (BS) of the offspring on PND21 and 90. Synaptophysin levels were significantly decreased relative to controls in the LOT, prefrontal cortex, and striatum of the offspring on PND90. In the BS, synaptophysin levels were significantly decreased relative to controls in male and female weanlings on PND21 and males on PND90; however, significant increases were observed in the BS of females on PND90. No effect of maternal PCB treatment was observed on levels of GFAP and synaptophysin in the dorsal hippocampus on PND21 and 90. Due to analytical restrictions statistical comparisons of GFAP levels were limited to examining the effect of maternal PCB treatment per brain region per sex per time point. Calcineurin activity was decreased in the female CB on PND21, but a significant increase in activity was observed in the female CB on PND90. No effect of maternal PCB treatment was observed on the cerebellar calcineurin activity in male offspring on PND21 and 90. EROD activity was highly induced in maternal microsomes from both PCB treatment groups, but only slightly induced in fetal hepatic microsomes. On PND21 weanling hepatic microsomal EROD activity was highly induced following gestational and lactational PCB exposure; however, on PND90 EROD activity was unaffected by maternal PCB treatment in male offspring and significantly decreased in female offspring. The results of the present study indicate that gestational and lactational exposure to the commercial PCB mixture results in long-term alterations in a neuronal and glial cell markers in specific brain regions of rats. These marker proteins may be useful for determining the strucure–activity relationships in PCB-induced developmental neurotoxicity.

Embryofetal Effects of Neuroelectric Therapy (Net)

Neuroelectric therapy (NET) has been used for the treatment of symptoms of withdrawal from the use of substances for the past 22 years. The objective of the present study was to analyze possible effects of NET on rat pregnancy using parameters equivalent to those employed in human NET. The rats were divided into four equal groups, one a control group, and the other three given NET at the pulse frequencies used in treatment of the most commonly abused drugs. After impregnation, the rats were given NET transcranially for 1 h daily throughout the pregnancy. An NET pulse frequency-related increase in the incidence of early pregnancy loss and decrease in fetal body and brain weights were found. No external or internal congenital anomalies occurred in the control or in any of the treatment groups, either macroscopically or microscopically.

Effect of chronic maternal ethanol administration on glutamate and N-methyl- d-aspartate binding sites in the hippocampus of the near-term fetal guinea pig

The objective of this study was to determine the effect of chronic maternal administration of ethanol on hippocampal l-glutamate (glutamate) and N-methyl- d-aspartate (NMDA) binding sites in the near-term fetal guinea pig. Starting on gestational day (GD) 2, pregnant guinea pigs received one of the following oral treatments up to and including GD 62 (term, about GD 68): 4 g ethanol · kg maternal body weight −1 · day −1; isocaloric sucrose and pair-feeding; or water. Maternal blood ethanol concentration was determined at 1 h after the daily ethanol dose on GD 59. Fetuses were studied at GD 63 (mature, near-term fetus). Fetal body weight and brain weight were determined. The density ( B max) and affinity ( K d) of the glutamate and NMDA binding sites in the fetal hippocampus were measured using a radioligand membrane binding assay; saturation analysis was conducted on hippocampal synaptic membrane preparation (HSMP). Maternal blood ethanol concentration on GD 59 was 269 ± 111 (SD) mg/dl (59 ± 24 mM). There was no maternal or embryonic fetal lethality in any of the three treatment groups, and ethanol treatment did not affect maternal body weight gain compared with sucrose or water treatment. Fetal brain weight, but not body weight, was decreased in the ethanol treatment group compared with the sucrose and water treatment groups. The B max values of the glutamate and NMDA binding sites were decreased in the ethanol treatment group compared with the sucrose and water treatment groups; there was no difference in the K d values of the glutamate and NMDA binding sites among the three treatment groups. The data demonstrate that, in the guinea pig, chronic maternal administration of a binge-type ethanol regimen throughout gestation restricts brain growth and decreases the density of glutamate and NMDA binding sites in the hippocampus, as manifested in the mature fetus.

Effects of chronic ethanol consumption on gestation and lactation in rats.

Chronic consumption of ethanol during pregnancy and lactation may lead to abnormalities in the fetus or infant. A group of female Wistar rats was submitted to ethanol treatment over a period of a month. A pair-fed control group received sucrose solution isocaloric to ethanol and the control group received water "ad libitum." Afterward, the females were mated with males over a period of 20 days. At birth, each litter was maximized to eight pups and the remaining ones were decapitated to remove the fetal blood and brains. No significant difference was observed in fetal body and brain weight at birth. During lactation the ethanol and pair-fed groups gained less weight than the control group. After weaning, their weight became similar. Fetal blood glucose levels were decreased in the ethanol-treated group. One hundred percent of the pair-fed and control females delivered live fetuses at term and all survived; only 40% of the females in the ethanol group delivered, and one pup did not survive. Chronic ethanol treatment pointed to a possible reduction in the fertility. It seems likely that the change in body weight of ethanol-fed dams was caused by undernutrition.

Prenatal growth of the human cerebral cortex: brainprint analysis.

To construct a series of flat maps (brainprints) that document the prenatal growth of human cerebral cortex and help identify sulcal landmarks for division of cortical regions of interest (ROIs) on mapped surfaces, the authors photographed and traced histologic whole-brain slices of 25 normal human fetal brains aged 18-42 weeks gestation. Brainprints of both cerebral hemispheres from each fetus were constructed with semiautomatic brain-mapping software, and each map was divided into five ROIs based on sulcal landmarks: frontal, parietal, insular, occipital, and temporal cortices. Surface areas of cerebral hemispheres and the five ROIs were estimated. Corrected for histologic shrinkage, brainprint estimates of human fetal cortical surface area were approximately twice those of previous estimates. Cortical lobe proportions at 18 weeks appeared to be unchanged to term. Surface area estimates correlated with fetal age, brain weight, and brain volume. This collection of cortical maps may guide future quantitative analyses of cerebral hemispheric growth in premature and term infants who undergo magnetic resonance imaging, which may, in turn, help predict neurobehavioral outcomes of early cortical damage.

Restriction of Maternal Dietary Carbohydrate Decreases Fetal Brain Indoles and Glycogen in Rats

In spite of evidence that dietary carbohydrate can increase brain tryptophan and 5-hydroxytryptamine in adult rats, the possible influence of maternal dietary carbohydrate on fetal brain indoles has received little attention. We studied the effect of graded levels (0, 4, 12 and 60%) of maternal dietary fructose or glucose fed throughout pregnancy on fetal brain glycogen and indoles. The diets were isoenergetic and met the NRC energy requirements for pregnant rats. The results demonstrated that low maternal dietary carbohydrate, with adequate energy intake, reduced fetal brain weight and concentrations of glycogen, tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. There were no significant differences between glucose and fructose feeding at any dietary carbohydrate level for any fetal brain measurements, showing that it was the level and not the type of dietary carbohydrate that was important. Significant correlations between fetal brain 5-hydroxytryptamine and brain glycogen, and between fetal brain 5-hydroxytryptamine and brain weight, suggested that lowered brain 5-hydroxytryptamine was only one symptom of disrupted brain development in fetuses of dams fed low levels of carbohydrate. The results show that dietary carbohydrate restriction during pregnancy can have adverse effects on fetal brain development, glycogen levels, and neurotransmitter synthesis even when maternal dietary protein and energy intake are adequate.

Effects of Maternal Bilateral Adrenalectomy and Betamethasone Administration on Renal Rat Encephalic Development

The present study examined the effects of maternal bilateral adrenalectomy and betamethasone treatment on fetal encephalic development, in terms of fetal body weight, brain weight, DNA, protein and lipid content and morphological development. Both influenced the developmental time patterns of fetal brain and cerebellum. Fetuses of adrenalectomized rats had decreased body weights, whereas brain weight was not affected. Maternal adrenalectomy produces in fetal brain a decreased number of cells and increased cell size, while betamethasone treatment of adrenalectomized rats increased cell number, which was not different from control values; cell size remained lower than in control fetuses. Lipid content was increased in the fetuses of betamethasone-treated rats. In terms of morphological development, laminated structures (hippocampus and brain and cerebellar cortex) were the ones most affected.

Influence of sire, sex of fetus and type of pregnancy on conceptus development

Estrus was synchronized in 93 crossbred cows 3 to 7 yr old which were then superovulated with 10 mg FSH-P and bred artificially to either a Jersey or Charolais bull. Females pregnant to the Jersey sire were slaughtered at 95, 180 or 250 d of gestation; low pregnancy rate from the Charolais sire resulted in enough dams for slaughter and valid comparisons at 95 d only. Conceptus tissue and organ weights and dam carcass weights and measurements were collected at slaughter. At 95 d of gestation, sire differences were not significant; type of pregnancy (single vs multiple) had significant effects on placentome and membrane weight; fetus sex had highly significant effects on fetus weight and crown-rump length. Fetal brain and heart weights showed little effect of sire, fetus sex or type of pregnancy, indicating these early differentiating tissues are highly competitive for available nutrients for growth. Fetal data at 180 and 250 d of gestation showed highly significant effects of gestation stage on placentome, membrane and fetus weights, crown-rump and metatarsal lengths, and liver, kidney, heart and total brain weights. Type of pregnancy had greater effects on the conceptus traits than did fetus sex at these stages. Nonorthogonal analyses of data from the Jersey-sired pregnancies indicated growth of fetuses in multiple pregnancies was suppressed, and the reduction in fetus weight became more pronounced as gestation progressed. Correlations among conceptus traits and dam carcass data showed different relationships within single and multiple pregnancies. We suggest that the genetic contribution for fetal growth has a positive effect on fetal size throughout gestation while the importance of metabolite availability may change during gestation depending on the genetic growth potential of the fetus and on whether the pregnancy is single or multiple. We speculate that these fetus-dam relationships involve systems controlling fetus growth that arise from the fetus genetic growth potential interacting with positive and negative dam effects that are linked or related to the carcass skeletal-fat-muscle endpoints studied.

Effect of low dose of 70 kVp X-rays on the intrauterine development of mice

Pregnant Swiss albino mice were exposed to low doses of X-rays (approximately 9 mGy) in the range used for diagnostic exposure, on day 3.5 of gestation (preimplantation period), day 6.5 (early organogenesis period) or day 11.5 (late organogenesis period). The fetuses were examined on the 18th day of gestation. Exposure at 3.5 days post coitus (d.p.c.) resulted in a significant increase in prenatal mortality, and an increased incidence of retarded fetuses was observed after exposure at 3.5 and 6.5 d.p.c. The major effect of exposure at 11.5 d.p.c. was a significant decrease in the fetal head size and brain weight.

Effect of Ambient Temperature and Running Wheel Activity on the Outcome of Pregnancy in CD‐1 Mice

The effect of ambient temperature and running activity on fetal outcome was studied in CD-1 mice. Pregnant mice were allowed to be active in a running wheel at various ambient temperatures (26, 30, 32, 34, or 36 degrees C) for 100 min a day. The dams were killed near term, and various maternal and fetal measures made. Mean deep body temperature (measured using radio-telethermometers implanted in the abdomen) of pregnant dams was raised to 39.5 degrees C while running at an ambient temperature of 36 degrees C. Bred mice, pregnant or not, continued to increase their running activity, but pregnant mice exercised less from mid-pregnancy on. Running up to 1 km/hr had no effect on maternal weight gain, number of implantations, number of live fetuses, fetal body weight, and fetal relative brain weight. However, increasing ambient temperature was effective in decreasing maternal weight gain and fetal body weight and increasing fetal relative brain weight. Even though body temperature can be increased significantly by increasing either running rate or ambient temperature, the body temperature increase caused by running appears to have no significant influence on the outcome of pregnancy. At levels in this study, body temperature per se does not appear to be the variable on which to predict fetal effects. This is because only body temperature raised by higher ambient temperature, and not body temperature raised by increased running, was shown to effect a fetal change.

Maternal alcohol ingestion inhibits fetal glucose uptake and growth

The distribution of maternally-derived glucose was determined in selected tissues of fetuses from ethanol-fed (EF) rats and from pair-fed (PF) and ad lib-fed (AF) controls. Maternal ethanol ingestion resulted in reduced fetal brain and liver weights and lower liver and lung glycogen levels compared to those of the PF or AF control groups. In addition, experimental fetuses exhibited reduced uptake of maternally-derived [ 3H] 2-deoxy-D-glucose (2-DG) by placenta and fetal brain. Fetal body, liver, lung, and brain weights correlated with fetal plasma 3H activity and with the fetal:maternal plasma 3H ratio, an indicator of the rate of placental glucose transfer. Brain weight correlated with 2-DG content per gram tissue weight. These observations suggest that reduced nutrient availability due to impaired placental transfer plays a role in the intrauterine growth retardation associated with maternal ethanol ingestion.

A SURVEY OF MATERNAL COPPER STATUS AND FETAL TISSUE COPPER CONCENTRATIONS IN SASKATCHEWAN BOVINE

Copper (Cu) status of cattle raised in different soil zones of Saskatchewan was examined with emphasis on the relation between liver Cu concentration in pregnant cows, stage of pregnancy and fetal liver Cu status. Whole fetuses and livers from adult animals were obtained during routine slaughter operation at a local packing plant. Twenty percent of steers, 54% of pregnant cows, 52% of heifers and 77% of nonpregnant cows had liver Cu levels less than 25 mg kg−1 dry matter (DM). Hypocuprosis was most marked in cattle originating from northern regions of Saskatchewan. Fetal liver Cu concentration depended on the dam liver Cu concentration and on stage of pregnancy and could be represented as: Fetal liver Cu concentration (mg kg−1 DM) = 217.5 + 0.023 [(age of fetus (days) × dam liver Cu concentraiton (mg kg−1 DM)]. During gestation the level of Cu progressively increased in the fetal liver and decreased in maternal liver. Liver Cu levels of fetuses from dams with liver Cu greater than 25 mg kg−1 DM were higher (P &lt; 0.05) than those in fetuses from dams with liver Cu levels lower than 25 mg kg−1 DM. Dam liver Cu status did not influence fetal liver, kidney, heart and brain weights or the Cu concentration of fetal kidney, heart or brain. The magnitude of hypocuprosis in cattle in Saskatchewan is extensive and emphasizes the importance of adequate Cu nutrition in pregnant cattle with respect to maintaining acceptable fetal Cu status. Key words: Copper deficiency, Saskatchewan, soil zones, cattle, pregnancy, fetus