Search PubMed⌕ Search

Biomedical subjects

J E Harding

Publications and source records attributed to J E Harding.

At least 91 records · Page 5Linked to original sources
PubMed1993

Fetal nutrition and cardiovascular disease in adult life.

Babies who are small at birth or during infancy have increased rates of cardiovascular disease and non-insulin-dependent diabetes as adults. Some of these babies have low birthweights, some are small in relation to the size of their placentas, some are thin at birth, and some are short at birth and fail to gain weight in infancy. This paper shows how fetal undernutrition at different stages of gestation can be linked to these patterns of early growth. The fetuses' adaptations to undernutrition are associated with changes in the concentrations of fetal and placental hormones. Persisting changes in the levels of hormone secretion, and in the sensitivity of tissues to them, may link fetal undernutrition with abnormal structure, function, and disease in adult life.

Adult↗
PubMed1993

A colorimetric assay for amino nitrogen in small volumes of blood: reaction with beta-naphthoquinone sulfonate.

An assay has been developed for the colorimetric estimation of total amino acids in small volumes (100 microliters) of whole blood. The procedure utilizes the reaction of amino nitrogen with beta-naphthoquinone sulfonate. It represents a substantial improvement on previously published methods by decreasing reagent volumes and accurately specifying and maintaining pH conditions for the reaction itself (9.2-9.4) and for removal of excess reagent prior to measurement of the resulting complex (2.2-2.4). Ammonia is the only compound shown to significantly interfere with the assay but this is not a problem at physiological concentrations.

Amino Acids↗
PubMed1993

Adverse effects of neonatal transport between level III centres.

The effect of neonatal transport between level III intensive care nurseries was studied by comparing the outcome of 40 infants inborn at a regional level III centre but transported to other level III nurseries for intensive care, with 80 matched inborn controls. Transport appeared to affect respiratory status adversely but transiently. However, transported infants grew less well than control infants (32% were below 3rd centile for weight at 36 weeks vs 15% of controls), were more likely to suffer periventricular haemorrhage (40 vs 21% of controls) and had a worse neurodevelopmental outcome (70% normal at follow up vs 83% of controls). It can be concluded that for infants inborn at the National Women's Hospital, Auckland, transport to another level III centre for intensive care is associated with an increased risk of adverse outcome.

Female↗
PubMed1993

Pericardial effusion complicating a percutaneous central venous line in a neonate.

A premature infant developed pericardial effusion four days after the insertion of a 25-gauge silastic percutaneous central venous catheter. The effusion contained parenteral nutrition fluid and resolved rapidly after withdrawal of the catheter. Pericardial effusion is a potential complication of percutaneous, as well as surgically placed, central venous catheters.

Catheterization, Central Venous↗
PubMed1993

Glucose but not a mixed amino acid infusion regulates plasma insulin-like growth factor-I concentrations in fetal sheep.

The influence of fetal glucose and amino acid supply on the regulation of fetal plasma IGF-I levels was investigated in fetuses from starved ewes. Paired maternal and fetal blood samples were taken during an initial 2-d control period, after 48 h of maternal starvation, during a 24-h fetal infusion of glucose (n = 6) or an amino acid mixture (Synthamin 17, n = 5) with continued starvation, and after 48 h of maternal refeeding. After 48 h of starvation, maternal and fetal plasma IGF-I, insulin, and blood glucose fell significantly in both groups compared with control values (IGF-I for glucose group: maternal, -18.53 +/- 6.60; fetal, -5.23 +/- 1.81 nmol/L; amino acid group: maternal, -18.2 +/- 6.97, fetal, -5.12 +/- 1.61 nmol/L; both p < 0.05). Fetal glucose but not mixed amino acid infusion raised fetal plasma IGF-I, insulin, and blood glucose to near control values (glucose group fetal IGF-I, -1.77 +/- 1.98; amino acid group, -5.93 +/- 2.22 nmol/L; both p < 0.05). Maternal plasma IGF-I remained depressed during glucose infusion (-16.33 +/- 8.32 nmol/L), but continued to fall in the amino acid group (-21.41 +/- 8.20 nmol/L, p < 0.05). After 48 h of maternal refeeding, all values had returned to near control values for both groups (glucose group IGF-I: maternal, -5.2 +/- 3.86; fetal, 0.01 +/- 2.2; nmol/L; amino acid group: maternal, -11.66 +/- 3.2; fetal, -0.70 +/- 2.61 nmol/L). We conclude that in the ovine fetus glucose may have a more important role than amino acids in the regulation of fetal plasma IGF-I.

Amino Acids↗
PubMed1992

Effects of beta-hydroxybutyrate infusion on hind limb metabolism in fetal sheep.

OBJECTIVES: This study investigated the effects of high ketone levels on fetal carcass metabolism. Specifically, we aimed to determine whether beta-hydroxybutyrate was taken up by fetal muscle and whether lactate production by the fetal hind limb contributed to the raised circulating lactate levels seen in high ketone states. STUDY DESIGN: Hind limb metabolism was studied in 10 chronically catheterized fetal sheep. Substrate/oxygen quotients were measured before and after 2 hour infusions of beta-hydroxybutyrate and compared with the Wilcoxon signed-rank test. RESULTS: beta-Hydroxybutyrate was taken up by hind limb tissues in large amounts (butyrate/oxygen quotient = 1.02 +/- 0.40). Lactate was produced by the hind limb (lactate/oxygen quotient = -0.96 +/- 0.52) in amounts almost equivalent to glucose uptake (glucose/oxygen quotient = 1.32 +/- 0.29). Hind limb oxygen consumption increased 35% and fetal arterial oxygen content fell 16%. CONCLUSION: beta-Hydroxybutyrate may be consumed by the fetal carcass in amounts sufficient to entirely substitute for glucose. Glucose may then be released as lactate for metabolism elsewhere. Ketones may be important fetal substrates during maternal starvation.

3-Hydroxybutyric Acid↗
PubMed1992

The nutritional regulation of circulating placental lactogen in fetal sheep.

Maternal and fetal plasma ovine placental lactogen (oPL), insulin, and IGF-I levels were measured in response to the starvation and refeeding of pregnant sheep on two defined planes of nutrition. Chronically catheterized pregnant ewes were placed on either a high plane (n = 5) or low plane (n = 5) of nutrition at least 1 wk before the experiment. At 125 to 135 d gestation, the ewes were starved for 72 h and then an i.v. infusion of 10% glucose was administered over 4 h, followed by refeeding at the designated nutritional plane. Plasma oPL levels of fetuses whose mothers had been on a high plane of nutrition were significantly higher during starvation (p less than 0.05) than those of fetuses whose mothers had been on a low plane (high + 0.54 +/- 0.17 and low -0.02 +/- 0.17 nmol/L from mean control levels). Intravenous glucose infusion to the ewes at the end of starvation caused a marked rise in fetal plasma oPL levels in both groups (increments of 2.61 +/- 1.4 nmol/L in the high group and 2.81 +/- 1.16 nmol/L in the low group). Maternal oPL levels did not differ significantly between the two nutritional groups during starvation and did not change during glucose infusion. Fetal and maternal plasma IGF-I levels both fell during starvation. Maternal IGF-I levels fell faster in the high group (-17.9 +/- 4.5 at 24 h versus -4.7 +/- 7.2 nmol/L in the low group), but the groups were not different at the end of starvation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗
PubMed1992

Ontogenic differences in the nutritional regulation of circulating IGF binding proteins in sheep plasma.

Well-fed castrated male sheep (N = 3) and 125 days gestation pregnant ewes (N = 6) with chronically catheterized fetuses were fasted for 72 h. Insulin-like growth factor-binding protein (IGFBP) levels in fed and starved fetal, maternal and castrated male sheep plasma were measured using ligand blot analysis. IGFBPs in adult and fetal sheep differed in distribution both before and after 72 h starvation. IGFBP-3 was the major postnatal binding protein, while in the fetus IGFBP-2, IGFBP-3 and the circulating IGF type 2 receptor fragment each contributed 25-30% of total IGF binding capacity. After starvation, total IGF binding capacity and IGFBP-3 fell in plasma of maternal and castrated male sheep (p less than 0.05). Total IGF binding capacity rose with starvation in fetal plasma (p less than 0.05) as a result of an increase in IGFBP-1 (p less than 0.01) and IGFBP-2 (p less than 0.05). The different nutritional control of the IGFBPs in the fetus and the adult may reflect ontogenic differences in the regulation and function of circulating IGFs and their binding proteins.

Aging↗
PubMed1991

beta-Hydroxybutyrate is an alternative substrate for the fetal sheep brain.

Brain uptake of substrates other than glucose has been demonstrated in vivo in postnatal but not fetal life. In this study, brain uptake of potential alternative substrates beta-hydroxybutyrate and lactate was studied during 2 h substrate infusions in 10 chronically-catheterised fetal sheep at 135-141 days gestation. beta-hydroxybutyrate appeared to be taken up by the brain of 5 fetuses with spontaneously low arterial blood glucose concentrations, and produced by the brains of the 5 with higher glucose concentrations. Brain butyrate/oxygen quotients at the end of the infusions were directly related to fetal arterial blood glucose concentrations (r2 = 0.72, P less than 0.01. Brain butyrate/oxygen quotients were not related to the arterial beta-hydroxybutyrate concentrations at the beginning or end of the infusions. No brain uptake of lactate was demonstrated. This study suggests for the first time that the fetal brain in vivo may take up substrates other than glucose. The near term fetal sheep brain appears to take up beta-hydroxybutyrate only when arterial butyrate concentrations are high and glucose is low.

3-Hydroxybutyric Acid↗
PubMed1990

Effect of lactate and beta-hydroxybutyrate infusions on brain metabolism in the fetal sheep.

Brain uptake of substrates other than glucose has been demonstrated in neonatal but not fetal animals in vivo. This study was undertaken to investigate the ability of the fetal sheep brain to use potential alternative substrates when they were provided in increased amounts. Brain substrate uptake was measured in chronically catheterised fetal sheep during 2-h infusions of neutralised lactate (n = 12) or beta-hydroxybutyrate (n = 12). Despite large increases in fetal arterial lactate and beta-hydroxybutyrate during the respective infusions, no significant uptake of either substrate was demonstrated. However during both types of infusion, the brain arterio-venous difference for glucose decreased 30% (P less than 0.05). Since the brain arterio-venous difference for oxygen was unchanged, and blood flow to the cerebral hemispheres (measured in 11 studies) was also unchanged, the infusions appeared to cause a true decrease in brain glucose uptake. This decrease paralleled the rise in lactate concentration during lactate infusions, and the rise in lactate and butyrate concentrations during the butyrate infusions. Both substrates have metabolic actions that may inhibit brain glucose uptake. We speculate that the deleterious effects of high lactate and ketone states in the perinatal period may in part be due to inhibition of brain glucose uptake.

3-Hydroxybutyric Acid↗
PubMed1989

Views of mothers and midwives participating in the Bristol randomized, controlled trial of active management of the third stage of labor.

Mothers and midwives who had participated in the Bristol randomized controlled trial of active versus physiologic management of the Third Stage of Labor were asked for their views. One hundred ninety-one mothers (11% of the total randomized) and 49 midwives completed self-administered questionnaires. Both mothers and midwives commented adversely about the length of the third stage under physiologic management. In general, their views were in accord with the conclusions of the main trial (based on clinical data, including maternal blood loss, length of third stage, need for therapeutic oxytocic agents, and specified neonatal morbidity) in favor of continuing with the current practice of active management.

Attitude of Health Personnel↗
PubMed1988

The Bristol third stage trial: active versus physiological management of third stage of labour.

OBJECTIVE: To compare the effects on fetal and maternal morbidity of routine active management of third stage of labour and expectant (physiological) management, in particular to determine whether active management reduced incidence of postpartum haemorrhage. DESIGN: Randomised trial of active versus physiological management. Women entered trial on admission to labour ward with allocation revealed just before vaginal delivery. Five months into trial high rate of postpartum haemorrhage in physiological group (16.5% v 3.8%) prompted modification of protocol to exclude more women and allow those allocated to physiological group who needed some active management to be switched to fully active management. Sample size of 3900 was planned, but even after protocol modification a planned interim analysis after first 1500 deliveries showed continuing high postpartum haemorrhage rate in physiological group and study was stopped. SETTING: Maternity hospital. PARTICIPANTS: Of 4709 women delivered from 1 January 1986 to 31 January 1987, 1695 were admitted to trial and allocated randomly to physiological (849) or active (846) management. Reasons for exclusion were: refusal, antepartum haemorrhage, cardiac disease, breech presentation, multiple pregnancy, intrauterine death, and, after May 1986, ritodrine given two hours before delivery, anticoagulant treatment, and any condition needing a particular management of third stage. INTERVENTIONS: All but six women allocated to active management actually received it, having prophylactic oxytocic, cord clamping before placental delivery, and cord traction; whereas just under half those allocated to physiological management achieved it. A fifth of physiological group received prophylactic oxytocic, two fifths underwent cord traction and just over half clamping of the cord before placental delivery. ENDPOINT: Reduction in incidence of postpartum haemorrhage from 7.5% under physiological management to 5.0% under active management. MEASUREMENTS AND MAIN RESULTS: Incidence of postpartum haemorrhage was 5.9% in active management group and 17.9% in physiological group (odds ratio 3.13; 95% confidence interval 2.3 to 4.2), a contrast reflected in other indices of blood loss. In physiological group third stage was longer (median 15 min v 5 min) and more women needed therapeutic oxytocics (29.7% v 6.4%). Apgar scores at one and five minutes and incidence of neonatal respiratory problems were not significantly different between groups. Babies in physiological group weighed mean of 85 g more than those in active group. When women allocated to and receiving active management (840) were compared with those who actually received physiological management (403) active management still produced lower rate of postpartum haemorrhage (odds ratio 2.4;95% CI1.6 to 3.7). CONCLUSIONS: Policy of active management practised in this trial reduces incidence of postpartum haemorrhage, shortens third stage, and results in reduced neonatal packed cell volume.

Breast Feeding↗
PubMed1988

Neonatal transport: the Waikato experience.

The experience of the Waikato newborn transport service is reviewed from its inception in September 1980 until December 1986. The service has carried out 599 transports of which 311 were emergency retrievals. Total numbers of transports have increased each year although the demand for emergency retrievals has levelled off. The characteristics of babies requiring emergency retrieval have not changed. One-third of deaths occurred before retrieval could be effected, and 10% of retrieved babies subsequently died. Avoidable deaths seemed uncommon in the latter group. The neonatal transport service is an important part of regionalised perinatal care in the Waikato.

Hospital Planning↗
PubMed1988

Studies on the growth of the fetal sheep. Effects of surgical reduction in placental size, or experimental manipulation of uterine blood flow on plasma sulphation promoting activity and on the concentration of insulin-like growth factors I and II.

The effect of long- and short-term manipulations of uterine blood flow on fetal plasma levels of IGF-I and -II have been studied in sheep at days 125-139 of pregnancy and compared with those in near term rats and guinea pig. The primary objective is to show that both long- and short-term reduction of uterine blood flow is associated with increase in the fetal plasma concentration of IGF-II while that of IGF-I falls. In the pregnant sheep long-term depression of utero-placental blood flow was caused by surgical reduction in placental mass (carunclectomy) prior to conception. This reduced fetal weight to 2.42 +/- 0.49 kg (SD) compared with 3.41 +/- 0.46 in controls; the respective values for uterine blood flow being 1694 +/- 558 and 913 +/- 324 ml/min respectively. This was associated with a fall in fetal plasma IGF-I concentration from 22.6 +/- 3.4 ng/ml to 14.9 +/- 1.31 ng/ml and a rise in IGF-II from 1952 +/- 284 ng/ml to 3360 +/- 914 ng/ml respectively. Similar changes in the plasma concentrations of IGF peptides were observed in fetal rats and guinea pigs in response to uterine artery ligation. Short-term reduction (60 min) of the uterine blood flow was caused either by compression of the common uterine artery to depress flow from 1491 +/- 375 to 648 +/- 216 ml/min or through intraarterial infusion of adrenaline at 35 ug/min to lower flow from 1628 +/- 339 to 1195 +/- 128 ml/min. Such falls in uterine blood flow had no significant effect on fetal plasma IGF-I levels but increased IGF-II levels by 30 to 60%.

Animals↗
PubMed1987

First year mortality and hospital morbidity after newborn intensive care.

First year mortality and hospital morbidity were studied in 4678 surviving infants liveborn at National Women's Hospital during 1980, of whom 1113 had been admitted to the neonatal intensive care unit. Of children born there, but never admitted to the neonatal unit, 8.3% were hospitalised in their first year for a mean of 6.7 days per admission or 0.8 days per child. Hospitalisation rates were increased in neonatal unit survivors, ranging from 11.6% in normal birthweight to 15.5% in very low birthweight survivors. The hospital admissions were, on average, longer: 11 days per admission or 2.1 days per infant of low birthweight (LBW, under 2500g), and 21 days per admission or 4.8 days per infant of very low birthweight (VLBW, under 1500g). The longer averages reflected long hospital stays by only a few children. Admissions were largely for respiratory infections: no VLBW survivor was admitted for developmental delay, failure to thrive or non-accidental injury. Neonatal unit survivors had no increase in first year mortality compared with other Auckland children, and none died a cot death. Deaths in normal birthweight survivors were due to congenital abnormalities. No VLBW survivor died after discharge from National Women's Hospital. Children surviving neonatal unit care in Auckland in 1980 appeared to have less continuing first year morbidity and mortality than has been reported elsewhere.

Child, Hospitalized↗
PubMed1987

Metabolism of glucose by fetus and placenta of sheep. The effects of normal fluctuations in uterine blood flow.

The metabolism by the fetus and placenta of [2-3H, U-14C]glucose infused into fetal sheep has been studied. Uptake of glucose from the fetus by the placenta and transfer to the ewe, as well as placental metabolism of glucose to fructose and lactate have been quantified. About two-thirds of the glucose removed from the fetal circulation was taken up by placenta. Less than 15% of this passed back into the maternal circulation, the remainder was converted, at roughly equivalent rates, into lactate and fructose, most of which was transferred back to the fetus. It seems likely that little of this glucose is oxidised by the placenta. This data indicates that there are substrate cycles between the placenta and fetus, one possible function of which is to limit fetal glucose loss back to the mother; lactate and fructose have limited placental permeability. At uterine blood flow rates in the middle of the normal range net glucose uptake by the placenta from the maternal circulation was about 7-fold higher than that from the fetus. About 20% of this was transported to the fetus, 50% was oxidised and much of the remainder converted to lactate and transferred back to the ewe. Labelling patterns in fructose and lactate make it unlikely that this placental pool of glucose mixes freely with that derived from uptake from the fetus. Net movement of glucose across the placenta is markedly influenced by fluctuations in uterine blood flow over the normal range of 500-3000 ml/min. At low flow rates there is net output of glucose from the fetus to the placenta, and in some instances from the placenta to the ewe, i.e. there is evidence of net utero-placental production of glucose to the ewe separate from output by the fetus. There is a close linear relationship between uterine glucose supply (maternal arterial concentration x uterine blood flow) and net balance across the placenta. As uterine supply of glucose falls there is increased uptake by the placenta of glucose from the fetal circulation and corresponding enhanced recycling of fructose and lactate to the fetus. This production of fructose and lactate by the placenta may function to reduce glucose loss from the fetus to the ewe. Hence at high rates of placental uptake of glucose from the fetus placental production of lactate and particularly fructose may approach saturation and allow significant backflow of glucose from the fetus to the ewe. Under these conditions glucose uptake may in part sustain placental oxygen consumption.

Animals↗