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Biomedical subjects

Michael G Ross

Publications and source records attributed to Michael G Ross.

At least 37 records · Page 2Linked to original sources
PubMed2005

Permanent reduction in heart and kidney organ growth in offspring of undernourished rat dams.

OBJECTIVE: Maternal undernutrition affects fetal growth and development. We investigated whether maternal food restriction during pregnancy and/or lactation permanently alters organ growth among adult offspring. STUDY DESIGN: From 10 days to term gestation and through 21 days lactation, control pregnant rats received ad libitum food, whereas study rats were 50% food restricted. Cross-fostering techniques were used to examine the effects of food restriction during pregnancy and/or lactation periods. Organs were dissected and weighed (percentage of body weight) at ages 3 weeks and 9 months. RESULTS: Food restriction during pregnancy produced growth-restricted newborns that exhibited catch-up growth that resulted in markedly heavier adult offspring, although with relatively decreased weights of heart, kidney, lung, and brain as compared with controls. Conversely, food restriction during pregnancy/lactation or lactation alone resulted in adult offspring with similar body weights as controls, but with relatively decreased growth of heart and kidney. Males exhibited relatively smaller livers, whereas the females showed relatively smaller adrenal glands. CONCLUSION: Sex-dependent, selective, and permanent changes in relative growth of heart and kidney may increase risk of adult diseases.

Animals↗
PubMed2005

Gastric emptying cycles in the human fetus.

OBJECTIVE: Fetal swallowing contributes greatly to amniotic fluid homeostasis and fetal somatic development. Despite the absorption and recirculation of significant volumes of amniotic fluid, little is known about the rates of fetal gastric emptying or gastrointestinal absorption. We sought to determine the patterns of human fetal gastric emptying cycles across gestation. STUDY DESIGN: The gastric emptying cycle of 80 normal human fetuses at 12 to 39 weeks of gestation was studied. Real-time ultrasound examination of the fetal stomach (defined as the largest gastric area inclusive of the pylorus) was recorded continuously for a minimum of 1 hour (60-112 minutes). Images were replayed with measurements of gastric size every minute. The gastric area ratio was defined as the ratio of the fetal gastric area divided by the area of the fetal abdominal transverse section. The changes in gastric area ratio of all subjects were analyzed with the discrete Fourier transform method. The calculable maximum cycle was 60 or 112 minutes, and the minimum cycle was 2 minutes. The highest and second highest peaks of all power spectrum were recorded, and each cycle was converted from frequency of each peak. RESULTS: The gastric emptying cycles of the highest peak before 24 weeks of gestation were scattered between 30 and 100 minutes with low power. At 32 to 35 weeks of gestation, cycles were focused at approximately 40 minutes with increased power. At term, the cycles increased to >80 minutes. The gastric emptying cycles of the second highest peak were constant at 20 minutes, with stronger power after 24 weeks of gestation. CONCLUSION: Fetal gastric emptying cycles normalize during the early third trimester. The near-term evidence of delayed emptying may contribute to newborn infant feeding satiation.

Adult↗
PubMed2005

Mechanisms of meconium passage: cholinergic stimulation of electromechanical coordination in the fetal colon.

OBJECTIVE: Fetal gastrointestinal function develops in utero, with evidence of enhanced motility near-term. Although colonic passage of meconium in utero may be associated with fetal maturation or stress, little is known of the mechanisms potentiating motility. We assessed the effect of bethanechol, a cholinergic prokinetic agent, on colonic muscle muscular contractile and electromyogram (EMG) activity in the near-term ovine fetus. METHODS: Near-term (130 days, n = 8) singleton ovine fetuses were chronically prepared with vascular catheters and three sets of miniature strain gauges and bipolar EMGs on the serosal surface of the transverse colon, left colic flexure, and distal colon. Following a 60-minute control period, fetuses received intravenous bethanechol (60 microg/kg, Low-Beth; 120 microg/kg, High-Beth) at 60 and 180 minutes. Colonic activity was recorded digitally and analyzed for short-duration (2<SHORT<15 seconds) and long-duration (15<LONG<120 seconds) strain gauge and EMG contractions. Data were expressed as means +/- SEM and analyzed using one-way analysis of variance (ANOVA) and paired t test. RESULTS: During the control period, there was significantly greater SHORT versus LONG strain gauge contractions in all segments (P <.05). As compared to control values, Low-Beth and High-Beth significantly increased SHORT strain gauge contractions in the transverse colon (160 +/- 13 to 201 +/- 36 and 307 +/- 74 spikes/30 min, respectively, P <.05), although not in left colic flexure or distal colon. Bethanecol did not affect LONG strain gauge contractions. SHORT-EMG and LONG-EMG spike bursts did not change in response to bethanecol (280 +/- 20, 59 +/- 2 spikes/30 min, respectively). CONCLUSION: Cholinergic stimulation of fetal sheep colonic activity at 0.9 gestation occurs in the transverse colon, but not the more distal left colic flexure or distal colon. The increased strain gauge, but not EMG activity, suggests that cholinergic stimulation improves electromechanical coordination in the fetal colon. We speculate that cholinergic-induced delivery of gastrointestinal contents to the distal colon evokes local contractile/expulsive mechanisms resulting in meconium passage.

Animals↗
PubMed2005

Placental and fetal membrane Nephrin and Neph1 gene expression: response to inflammation.

OBJECTIVE: Fetal and amniotic fluid (AF) proteins (eg, alpha fetoprotein [AFP]) are measurable in the maternal circulation. Elevated maternal serum AFP levels indicate a risk for fetal anomalies or for obstetrical complications that are often associated with inflammation (eg, preterm labor). However, little is known of the mechanism of protein exchange between the fetus, AF, and maternal circulation. Nephrin and Neph1 are cell membrane proteins that restrict glomerular protein filtration and which are differentially expressed with renal inflammation. We sought to investigate whether nephrin and Neph1 were expressed in placenta and fetal membranes, and whether inflammation modified the expression. METHODS: Pregnant rats at 18 days' gestation were injected with lipopolysacchride (LPS) or control saline intraperitoneally (IP) and killed at 1, 6, and 12 hours after injection. Placenta and fetal membranes were obtained and real-time polymerase chain reaction (PCR) performed for determination of nephrin and Neph1 levels. RESULTS: Nephrin and Neph1 were expressed in both placenta and fetal membranes. Following maternal LPS administration, nephrin mRNA significantly increased in the membranes (0.22 +/- 0.02 to 0.51 +/- 0.050, P <.05), while Neph1 expression significantly declined in the placenta (0.19 +/- 0.05 to 0.10 +/- 0.01, P <.05). CONCLUSION: Fetal membranes and placenta of the rat express mRNA for the protein barriers nephrin and Neph 1, suggesting a role in the regulation of protein transfer from the fetus to mother. Under basal conditions, AF AFP transfer across fetal membranes may account for maternal serum AFP levels, whereas gestational inflammatory conditions (eg, preterm labor, threatened abortion) may augment AFP transfer across the placenta.

Animals↗
PubMed2005

Gender specificity of programmed plasma hypertonicity and hemoconcentration in adult offspring of water-restricted rat dams.

OBJECTIVE: We studied the impact of maternal water-restriction during rat pregnancy on newborn plasma composition, and determined the persistence of plasma composition alterations in adult offspring. METHODS: Maternal dams were water-restricted from 10 days of pregnancy until term (21 days) and throughout lactation to increase plasma sodium levels by approximately 6 mEq/L. At 21 days of age, offspring were weaned, and subsequently maintained on ad libitum food and water until 12 weeks of age. Daily water and food intake was monitored. Blood samples and organs were collected from 1-day- and 12-week-old offspring. Hematocrit, plasma osmolality, sodium, and arginine vasopressin (AVP) levels were analyzed. Because water-restriction led to concomitant reduction in maternal food intake (ie, dehydration anorexia), henceforth these dams and their offspring are referred to as "water-deprived/food-reduced" rats. RESULTS: Water-deprived/food-reduced dams had significantly increased plasma sodium levels, reduced food intake, and lower body weight gain during pregnancy and lactation as compared to control dams. One-day-old newborns of water-deprived/food-reduced dams weighed 17% less and had increased plasma sodium levels, osmolality, and hematocrit. At 12 weeks of age, males exhibited 11% and females 19% reduction in body weight from controls. Notably, male offspring of water-deprived/food-reduced dams showed significantly elevated plasma sodium levels, osmolality, and hematocrit. Additionally, males demonstrated reduced adrenal growth and decreased water intake. Conversely, the female offspring had similar plasma osmolality with decreased sodium levels, though a persistently elevated hematocrit. No differences were evident in plasma AVP levels. CONCLUSIONS: Maternal water deprivation/food reduction is associated with increased newborn plasma osmolality and sodium levels and long-term physiologic changes in the offspring. The gender-specificity of programmed hyperosmolality, though not hemoconcentration, implicates differing pathways/mechanisms for these phenotypic alterations. The contributions of pregnancy hypertonicity versus nutrient restriction in the mechanism for programmed offspring phenotype remain to be elucidated.

Animals↗
PubMed2005

N-methyl-D-aspartate glutamate receptor mediates spontaneous and angiotensin II-stimulated ovine fetal swallowing.

BACKGROUND: In adult rats, N-methyl-D-aspartate (NMDA) receptors have been implicated in the central control of body fluid homeostasis, as intracerebroventricular (ICV) injection of NMDA receptor antagonists suppresses stimulated drinking behavior. Fetal swallowing occurs at a significantly higher rate as compared to adult drinking, contributing to amniotic fluid volume regulation and fetal gastrointestinal development. The aim of present study was to determine the role of central NMDA receptors in the modulation of fetal swallowing activity. METHODS: Eight time-dated pregnant ewes and fetuses were chronically prepared with fetal vascular and ICV catheters, electrocorticogram (ECoG), and esophageal electromyogram electrodes and studied at 130 +/- 1 days' gestation. Following an initial 2-hour baseline period (time 2 h), the NMDA receptor antagonist, dizocipline (1 mg), was injected ICV. At time 4 h, the dose of dizocipline was repeated, together with angiotensin II (AngII, 6.4 microg). Fetal swallowing was monitored for 2 hours after each injection. Four of these fetuses also received an identical control study (on an alternate day) in which dizocipline was replaced with artificial cerebrospinal fluid (aCSF). RESULTS: ICV dizocipline injection nearly abolished spontaneous fetal swallowing activities (0.6 +/- 0.1 to 0.2 +/- 0.1 swallows/min; P < .001). ICV AngII in the presence of dizocipline did not demonstrate a dipsogenic effect on fetal swallowing (0.1 +/- 0.1; P < .001). In the control study, ICV injection of aCSF did not change fetal swallowing activity (1.0 +/- 0.1 swallows/min), while ICV AngII resulted in a significant increase in fetal swallowing (2.0 +/- 0.1 swallows/min; P < .001). CONCLUSIONS: This study demonstrates that central NMDA-glutamate receptor-mediated activity contributes to the high rate of spontaneous and AngII-stimulated fetal swallowing. We speculate that reduced NMDA receptor expression within the forebrain dipsogenic neurons may account for observed differences in drinking activities between the fetus/neonate and the adult.

Angiotensin II↗
PubMed2005

Ontogeny of gastric emptying patterns in the human fetus.

OBJECTIVE: Fetal swallowing and gastric emptying contribute importantly to amniotic fluid (AF) homeostasis and fetal gastrointestinal development. We speculated that fetal gastric emptying must be functional early in gestation to prevent rapid increases in AF. We sought to determine the human fetal ontogenic pattern of gastric emptying. STUDY DESIGN: Gastric emptying of eighty normal fetuses at 12-39 weeks was studied. Real-time ultrasound of the fetal stomach was continuously recorded for 1 hour. The gastric area ratio (GAR) was defined as the gastric area divided by the abdominal transverse area. The delta GAR was defined as the change between the maximum and the minimum gastric area ratiox100 (expressed as percent). A change of the fetal gastric area more than the 10th percentile of the delta GAR at 36-39 weeks was used to define gastric emptying. RESULTS: The 10th, 50th and 90th percentile of delta GAR at 36-39 weeks' was 5.2, 6.5 and 8.7%, respectively. Fetal gastric emptying was detected as early as 12 5/7 weeks of gestation. The proportion of fetuses demonstrating gastric emptying (>10th percentile delta GAR) increased with gestational age: 4/33 (12.1%) 12-23 weeks, 3/9 (33.3%) at 24-27 weeks, 8/11 (72.7%) at 28-31 weeks, 12/14 (85.7%) at 32-35 weeks, and 11/13 (84.6%) at 36-39 weeks. CONCLUSIONS: Fetal gastric emptying occurs by the beginning of the second trimester, contributing to AF regulation. The increased frequency of gastric emptying in late gestation is likely secondary to increased swallowing, altered fetal behavioral state or endogenous production of gastrointestinal motility factors.

Cross-Sectional Studies↗
PubMed2005

Persistent sucrose stimulation of ovine fetal ingestion: lack of adaptation responses.

OBJECTIVE: Sweet taste responsiveness is reduced in adult rats and humans following continued oral sucrose. We have previously demonstrated that sublingual sucrose stimulates near term ovine fetal swallowing, suggesting intact taste responsiveness. We sought to determine if prolonged oral sucrose infusion to the near term ovine fetus will evoke adaptation, as manifested by reduced swallowing stimulation. METHODS: Time-dated pregnant ewes and fetuses (n = 4) were chronically prepared with fetal vascular and sublingual catheters, and electrocorticogram and esophageal electromyogram electrodes and studied at 129 +/- 1 d gestation. Following an initial 2 h basal period, sucrose (2.5%) was infused sublingually (0.25 ml/min) to the fetus for 8 h. Fetal swallowing activity, blood pressure and heart rate were continuously recorded while maternal and fetal arterial blood samples were taken at timed intervals. RESULTS: During the basal period, fetal swallowing averaged 0.9 +/- 0.1 swallows/min. Fetal swallowing increased significantly following sublingual 2.5% sucrose infusion and remained significantly elevated at 2, 4, 6 and 8 h after initiation of sucrose infusion (1.3 +/- 0.1, 1.2 +/- 0.1, 1.3 +/- 0.1, 1.3 +/- 0.1 swallows/min; p < 0.001). There were no significant changes in fetal cardiovascular or arterial blood parameters. CONCLUSIONS: Although oral sucrose significantly stimulates near term ovine fetal ingestive behavior, sweet taste adaptation or habituation does not occur, in contrast to that observed in adult animals and human. The lack of taste adaptation in the fetus/newborn may facilitate increased neonatal food intake and accelerated growth.

Adaptation, Physiological↗
PubMed2005

Meconium passage in utero: mechanisms, consequences, and management.

Meconium passage in newborn infants is a developmentally programmed event normally occurring within the first 24 to 48 hours after birth. Intrauterine meconium passage in near-term or term fetuses has been associated with fetomaternal stress factors and/or infection, whereas meconium passage in postterm pregnancies has been attributed to gastrointestinal maturation. Despite these clinical impressions, little information is available on the mechanism(s) underlying the normal meconium passage that occurs immediately after birth or during the intrauterine period of fetal development. Birth itself is a stressful process and it is possible that fetal stress-mediated biochemical events may regulate the meconium passage occurring either during labor or after birth. Aspiration of meconium during intrauterine life may result in or contribute to meconium aspiration syndrome (MAS), representing a continued leading cause of perinatal death. This article reviews aspects of meconium passage in utero, its consequences, and management.

Adult↗
PubMed2005

Maternal steroid enhancement of fetal rabbit gastrointestinal motility.

AIM: The purpose of the present study was to determine the potential maturational effects of maternal dexamethasone administration on fetal upper gastrointestinal motility. METHODS: Nineteen pregnant rabbits were randomized into two groups (DEX and CONT) and studied on either day 24, 27 or 30 of pregnancy (term 31 days). The DEX group received intramuscular dexamethasone (DEX) 2 days before study and the controls received saline. Under ultrasound guidance, a needle was percutaneously inserted into each fetal stomach and fluorescein, labeled with color-coded microspheres, was injected. Two hours later, the length of fluorescein travel throughout the small intestine was measured. The percent motility was calculated by dividing the length of fluorescein travel by the total fetal small intestinal length x 100%. RESULTS: All maternal and fetal rabbits survived. On day 24 the length of fluorescein travel and the percent motility of the DEX group were significantly longer than controls. There were no differences on either day 27 or 30. Fetal growth was significantly suppressed by a single course of DEX at all gestational ages. CONCLUSIONS: Fetal rabbit gastrointestinal motility is significantly increased after prenatal steroids are given early in the last trimester (day 24 of a 31-day gestation). Although beneficial in end-organ maturation, the timing of prenatal steroid administration is crucial to minimize its potential detrimental effects on fetal somatic growth.

Animals↗
PubMed2005

Gestational programming: population survival effects of drought and famine during pregnancy.

The process whereby a stimulus or stress at a critical or sensitive period of development has long-term effects is termed "programming." Studies in humans and animals convincingly demonstrate that environmental perturbations in utero may permanently change organ structure and metabolism and/or alter homeostatic regulatory mechanisms among the offspring. These programmed changes may be the origins of adult diseases, including cardiovascular disease, obesity, and diabetes. Throughout evolution and development, humans and animals have been exposed to two common environmental stresses, drought and famine. Notably, drought-induced water deprivation is associated with dehydration anorexia and thus a concomitant potential nutrient stress. Our laboratory has performed studies among pregnant rat and sheep in which we simulate drought conditions via maternal dehydration and famine conditions via nutrient restriction. Maternal dehydration results in low-birth-weight offspring, which demonstrate gender-specific plasma hypernatremia and hypertonicity and arterial hypertension. Gestational nutrient restriction also resulted in low-birth-weight offspring. If permitted rapid catch-up growth by nutrient availability, these offspring demonstrate evidence of increased body weight and body fat, and leptin resistance as adults. Conversely, if the catch-up growth is delayed by nutrition restriction, the offspring exhibit normal body weight, body fat, and plasma leptin levels as adults. These studies indicate that osmoregulatory and cardiovascular homeostasis and phenotypic predisposition to obesity may be programmed in utero. Importantly, these results suggest that programming effects may be either potentiated or prevented by interventions during the neonatal period.

Animals↗
PubMed2004

Central angiotensin II AT1 receptors mediate fetal swallowing and pressor responses in the near-term ovine fetus.

Swallowed volumes in the fetus are greater than adult values (per body weight) and serve to regulate amniotic fluid volume. Central ANG II stimulates swallowing, and nonspecific ANG II receptor antagonists inhibit both spontaneous and ANG II-stimulated swallowing. In the adult rat, AT1 receptors mediate both stimulated drinking and pressor activities, while the role of AT2 receptors is controversial. As fetal brain contains increased ANG II receptors compared with the adult brain, we sought to investigate the role of both AT1 and AT2 receptors in mediating fetal swallowing and pressor activities. Five pregnant ewes with singleton fetuses (130 +/- 1 days) were prepared with fetal vascular and lateral ventricle (LV) catheters and electrocorticogram and esophageal electromyogram electrodes and received three studies over 5 days. On day 1 (ANG II), following a 2-h basal period, 1 ml artificial cerebrospinal fluid (aCSF) was injected in the LV. At time 4 h, ANG II (6.4 microg) was injected in the LV, and the fetus was monitored for a final 2 h. On day 3, AT1 receptor blocker (losartan 0.5 mg) was administered at 2 h, and ANG II plus losartan was administered at 4 h. On day 5, AT2 receptor blocker (PD-123319; 0.8 mg was administered at 2 h and ANG II plus PD-123319 at 4 h. In the ANG II study, LV injection of ANG II significantly increased fetal swallowing (0.9 +/- 0.1 to 1.4 +/- 0.1 swallows/min; P < 0.05). In the losartan study, basal fetal swallowing significantly decreased in response to blockade of AT1 receptors (0.9 +/- 0.1 to 0.4 +/- 0.1 swallows/min; P < 0.05), while central injection of ANG II in the presence of AT1 receptor antagonism did not increase fetal swallowing (0.6 +/- 0.1 swallows/min). In the PD-123319 study, basal fetal swallowing did not change in response to blockade of AT2 receptor (0.9 +/- 0.1 swallows/min), while central injection of ANG II in the presence of AT2 blockade significantly increased fetal swallowing (1.5 +/- 0.1 swallows/min; P < 0.05). ANG II caused significant pressor responses in the control and PD-123319 studies but no pressor response in the presence of AT1 blockade. These data demonstrate that in the near-term ovine fetus, AT1 receptor but not AT2 receptors accessible via CSF contribute to dipsogenic and pressor responses.

Angiotensin II↗
PubMed2004

Modeling a hydropic recipient twin in twin-twin transfusion syndrome.

We developed a mathematical model of twin-twin transfusion syndrome (TTTS) that includes a hydropic recipient twin, adding interstitial and intracellular fluid compartments, fetal congestive cardiac failure, and the dynamics of renin-angiotensin system (RAS) mediators to our previous TTTS model. Ten differential equations for each twin, coupled by the net fetofetal transfusion of blood and blood components, i.e., colloids, osmoles, and RAS mediators, describe the development of fetal arterial and venous blood volumes, blood osmolality and colloid osmotic pressure (COP), interstitial fluid volume and COP, intracellular fluid volume, amniotic fluid volume and osmolality, and RAS mediator concentration. We included varying placental anastomoses, placental sharing, and amnionicity. The 20 differential equations were solved numerically from 0 to 40 wk with a 0.6-s time step. Consistent with clinical experience, model predictions are as follows. Unidirectional arteriovenous anastomoses and arteriovenous anastomoses inadequately compensated by oppositely directed anastomoses cause severe TTTS that includes a hydropic recipient. Adequately compensated arteriovenous anastomoses simulated TTTS without hydrops. The probability that oppositely directed anastomoses prevent onset of a hydropic recipient after TTTS onset, i.e., the largest interval between onset of TTTS and onset of hydrops in the recipient, was best for a venovenous anastomosis, closely followed by an arterioarterial and finally an oppositely directed arteriovenous anastomosis. Hydropic recipients have decreased amniotic fluid volume. Unequal placental sharing and amnionicity modify hydrops onset. In conclusion, our model simulates a sequence of events that results in a hydropic recipient twin in severe TTTS. The model may allow an assessment of the efficacy of current therapeutic interventions for TTTS cases that include a hydropic recipient twin.

Adult↗
PubMed2004

Prenatal programming of hypernatremia and hypertension in neonatal lambs.

Maternal water restriction and the accompanying dehydration-induced anorexia may induce long-term physiological changes in offspring. We determined the impact of prenatal hypertonicity (Pre-Dehy) on offspring cardiovascular and osmoregulatory function. Pre-Dehy lambs were exposed to in utero hypernatremia (8- to 10-meq increase; 110-150 days of gestation) induced by maternal water restriction. Control lambs were born to ewes provided ad libitum water and food throughout gestation. After delivery, all ewes were provided ad libitum water and all newborns were allowed ad libitum nursing. Lambs were prepared with vascular and bladder catheters at 15 +/- 2 days of age and studied at 21 +/- 2 days. After a 2-h basal period, lambs received an infusion of hypotonic (0.075 M) NaCl (0.15 ml.kg(-1).h(-1) iv) for 2 h. Lamb arterial blood pressure was monitored, and blood samples were obtained before, during, and after infusion. During the neonatal basal period, Pre-Dehy lambs had significantly increased plasma osmolality (302 +/- 1 vs. 294 +/- 1 mosmol/kgH(2)O, P < 0.01), sodium levels (144 +/- 1 vs. 140 +/- 1 meq/l, P < 0.01), hematocrit (28 +/- 1% vs. 25 +/- 1%, P < 0.05), and mean arterial blood pressure (79 +/- 2 vs. 68 +/- 1 mmHg, P < 0.001) compared with control lambs. Despite the infusion of hypotonic saline, Pre-Dehy lambs maintained relative hypertonicity, hypernatremia, and hypertension. However, plasma arginine vasopressin, glomerular filtration rate, and urinary osmolar and sodium excretion and clearance (per kg body wt) were similar in the groups. Offspring of prenatally water-restricted ewes exhibit hypernatremia, hypertonicity, and hypertension, which persist despite hypotonic saline infusion. In utero hypertonicity and perhaps maternal nutrient stress may program offspring osmoregulation and systemic arterial hypertension.

Animals↗
PubMed2004

Programmed obesity in intrauterine growth-restricted newborns: modulation by newborn nutrition.

The degree of nutrient enhancement during the newborn period may modulate programming of appetite-regulating hormones, body composition, and propensity to adult obesity in intrauterine growth-restricted (IUGR) newborns. Pregnant rats received, from day 10 to term gestation and throughout lactation, ad libitum food (AdLib) or 50% food restriction (FR) to produce IUGR newborns. AdLib vs. FR offspring were studied at day 1, and, to create two distinct groups of newborn catch-up growth (immediate, delayed) among the IUGR newborns, cross-fostering techniques were employed. The four groups of pups at 3 wk were IUGR immediate catch-up growth (FR/AdLib), IUGR delayed catch-up growth (FR/FR), control (AdLib/AdLib), and lactation FR control (AdLib/FR). From 3 wk to 9 mo, all offspring had AdLib rat chow. Maternal FR during pregnancy resulted in IUGR pups (6.0 +/- 0.3 vs. 7.1 +/- 0.3 g, P < 0.01) with decreased leptin (0.66 +/- 0.03 vs. 1.63 +/- 0.12 ng/ml, P < 0.001) and increased ghrelin (0.43 +/- 0.03 vs. 0.26 +/- 0.02 ng/ml, P < 0.001). Maternal FR during lactation (FR/FR) further impaired IUGR offspring growth at 3 wk. However, by 9 mo, these pups attained normal body weight, percent body fat, and plasma leptin levels. Conversely, IUGR offspring nursed by AdLib dams (FR/AdLib) exhibited rapid catch-up growth at 3 wk and continued accelerated growth, resulting in increased weight, percent body fat, and plasma leptin levels. Thus the degree of newborn nutrient enhancement and timing of IUGR newborn catch-up growth may determine the programming of orexigenic hormones and offspring obesity.

Animals↗
PubMed2004

Haemodynamic resistance model of monochorionic twin pregnancies complicated by acardiac twinning.

An acardiac twin is a severely malformed monochorionic twin fetus that lacks most organs, particularly a heart. It grows during pregnancy, because it is perfused by its developmentally normal co-twin (called the pump twin) via a set of placental arterioarterial and venovenous anastomoses. The pump twin dies intrauterine or neonatally in about 50% of the cases due to congestive heart failure, polyhydramnios and prematurity. Because the pathophysiology of this pregnancy is currently incompletely understood, we modified our previous haemodynamic model of monochorionic twins connected by placental vascular anastomoses to include the analysis of acardiac twin pregnancies. We incorporated the fetoplacental circulation as a resistance circuit and used the fetal umbilical flow that perfuses the body to define fetal growth, rather than the placental flow as done previously. Using this modified model, we predicted that the pump twin has excess blood volume and increased mean arterial blood pressure compared to those in the acardiac twin. Placental perfusion of the acardiac twin is significantly reduced compared to normal, as a consequence of an increased venous pressure, possibly implying reduced acardiac placental growth. In conclusion, the haemodynamic analysis may contribute to an increased knowledge of the pathophysiologic consequences of an acardiac body mass for the pump twin.

Biophysics↗