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Biomedical subjects

A L Fowden

Publications and source records attributed to A L Fowden.

At least 91 records · Page 5Linked to original sources
PubMed1995

Maturational effects of cortisol on the exocrine abomasum and pancreas in fetal sheep.

The role of cortisol in the prenatal development of digestive enzymes in the abomasum (prochymosin and pepsinogen) and pancreas (amylase, trypsin, chymotrypsin) has been investigated in the fetal lamb during late gestation. The abomasum and pancreas were collected from 22 unoperated control fetuses (99-145 days gestation; term, 145 +/- 2 days), from seven pairs of twins infused with either saline or cortisol for five days preceding delivery at 127-133 days, and from four 139-143-day-old fetuses adrenalectomized at 120-123 days. Developmental increases (2-8-fold) occurred in protease concentrations in the fetal abomasum and in amylase and chymotrypsin contents in the fetal pancreas. These increases paralleled the normal prepartum rise in fetal plasma cortisol. In addition, the enzyme values were significantly higher in cortisol-infused than in saline-infused fetuses (with the exception of pancreatic amylase) and were significantly lower in adrenalectomized fetuses than in control fetuses at term. The pH of abomasal fluid remained neutral (pH 6.8-8.0) during late gestation and was not affected by cortisol treatment or adrenalectomy. The results suggest that cortisol stimulates the development of the exocrine abomasum and pancreas in fetal sheep and may, thereby, increase the digestive capacity in neonatal lambs. Compared with the pig, another long-gestation species, the sheep has an early development of gastric pepsinogen but a late development of gastric acidity and pancreatic protease activities.

Abomasum↗
PubMed1995

Fetal and maternal plasma lipids in chronically catheterized mares in late gestation: effects of different nutritional states.

The effects of different nutritional states on plasma lipid concentrations have been examined in pregnant mares and their fetuses. Maternal and fetal arterial catheters were inserted into 12 pony mares between 244-303 days' gestation (term 320-360 days) and observations made from 5 days following the insertion of catheters. After recovery from surgery maternal and fetal arterial samples were withdrawn from 7 mares with normal feeding patterns (Group IA), from four of these mares at the end of a 30 h fast and 3 h later following refeeding (Group IB) and six mares who failed to re-establish normal feeding patterns (Group II). The fatty acid concentrations and composition of the plasma free fatty acid (FFA), triacylglycerol and phospholipid fractions were analysed. Maternal FFA, triacylglycerol and phospholipid concentrations were significantly raised in the fasted (Group IB) and under-fed (Group II) mares. Fetal concentrations of FFA and phospholipid increased significantly in the group of under-fed (Group II) mares but not in the fasted (Group IB) mares. In the fetal plasma the proportions of polyunsaturated fatty acids derived from essential fatty acids in the FFA and phospholipid fractions were much higher than those in the mare. In the fasted (IB) and under-fed (II) groups the relative amounts of the polyunsaturated fatty acids in each fraction remained unchanged (P > 0.05). These results show a short fast or prolonged undernutrition result in raised maternal plasma lipid concentrations which in turn can effect the total amount of lipid in the fetal circulation. However any increases in polyunsaturated fatty acids in the fetus (e.g. in Group II) are unlikely to come from the maternal circulation; likely sources of these fatty acids are the placenta or fetal tissues.

Animals↗
PubMed1995

Immunohistochemical localisation of steroidogenic enzymes and phenylethanolamine-N-methyl-transferase (PNMT) in the adrenal gland of the fetal and newborn foal.

An increase in fetal adrenal cortisol output signals the onset of parturition in many animal species but, in the fetal horse, plasma concentrations of cortisol remain low for much of late pregnancy, with a rise occurring only very close to the time of birth (term 320-360 days). Immunohistochemistry was used to determine the localisation and changes in distribution of key steroidogenic enzymes for cortisol production; P450scc, P450C17 and 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) in adrenal tissue from fetal and newborn horses and these findings were correlated with the appearance of immunoreactive (IR)-phenylethanolamine-N-methyl-transferase (PNMT), a cortisol-dependent enzyme. Five micron sections of adrenal tissue from fetuses at Day 100-156 (n = 5), Day 244-295 (n = 8), greater than Day 300 (n = 4) and from newborn foals (n = 6), were stained using specific antibodies and the avidin-biotin-peroxidase technique. All 3 steroidogenic enzymes were present by Day 150, but in less than 20% of the cortical cells. By late gestation the steroidogenic enzymes were present in approximately 30% of the cells, but the distribution varied. P450SCC and P450C17 predominated in cortical cells proximal to the medulla; 3 beta HSD was present throughout the cortex, but more in the zona fasciculata. In foals after birth, IR-3 beta HSD and IR-P450SCC had increased substantially throughout the adrenal cortex, and IR-P450C17 was present in most cells of the presumptive zonae fasciculata and reticularis. IR-PMNT was localised to nuclei of scattered medullary cells at the medullary-cortical interface by Day 150.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxysteroid Dehydrogenases↗
PubMed1995

Localisation of 15-hydroxy prostaglandin dehydrogenase (PGDH) and steroidogenic enzymes in the equine placenta.

15-hydroxy prostaglandin dehydrogenase (PGDH) is the critical enzyme that determines metabolism of primary prostaglandins. Its expression is determined in part by steroid hormones, particularly progesterone, formed from delta(5) steroids through 3beta-hydroxysteroid dehydrogenase (3beta-HSD) activity. To assess whether the regulation of PGDH might occur in a paracrine, autocrine or intracrine fashion, we used immunohistochemistry (IHC) to determine the localisation of key steroidogenic enzymes in the equine placenta and compared these patterns to the distribution of immunoreactive (IR-) PGDH. Placental tissue was obtained from pony or Thoroughbred mares at about Days 150, 250-280 and >300 of pregnancy (term 320 to 360 days; n=5-8 each group). IR-PGDH, 3beta-HSD, cholesterol side chain cleavage enzyme (P450(scc)) and 17-hydroxylase/lyase (P450(C17)) were localised using specific antibodies and the avidin-biotin peroxidase technique and visualised using diaminobenzidine as substrate. IR-P450(scc) was present in trophoblast cells, but not in maternal tissues of the microcotyledons. In contrast, at Days 150 and 280, IR-PGDH was present in maternal epithelial and interstitial cells in the microcotyledons, but was not detected in trophoblast epithelium, chorioallantois or endometrial glands. After Day 300, IR-PGDH was present in the maternal epithelium and interstitial cells of the placenta and it was also present in trophoblast cells in some specimens.

3-Hydroxysteroid Dehydrogenases↗
PubMed1995

Vaginal birth versus elective caesarean section: effects on gastric function in the neonate.

Plasma gastrin concentration increases in late gestation and reaches a peak at birth or shortly after birth in many species ('neonatal hypergastrinaemia'). We investigated the hypothesis that gastrin and gastric acid secretion in the neonate is influenced by the final rise in plasma cortisol associated with spontaneous (vaginal) birth. Caesarean-delivered (CD, n = 28) or vaginally delivered (VD, n = 24) premature or full-term piglets (97-115 days gestation) were killed immediately after birth (using pentobarbitone). Compared with newborn CD pigs, the newborn VD pigs had significantly higher (P < 0.05) concentrations of cortisol (669 +/- 60 versus 223 +/- 2 nM) and gastrin (57 +/- 4 versus 33 +/- 1 pM) in plasma, and significantly lower gastric fluid pH (3.3 +/- 0.2 versus 4.7 +/- 0.3), amidated (bioactive) gastrin in the antrum (550 +/- 77 versus 1220 +/- 29 pmol g-1) and glycine-extended (precursor) gastrin in the antrum (81 +/- 10 versus 143 +/- 5 pmol g-1). There were significant linear correlations between log plasma cortisol values and plasma gastrin (r = 0.40, P < 0.05) or gastric fluid pH (r = -0.51, P < 0.05) in newborn pigs. The effects of cortisol in the immediate postnatal period were investigated in forty-one CD pigs born at 111-112 days gestation and treated with saline, metyrapone (an inhibitor of cortisol synthesis) or adrenocorticotrophic hormone (ACTH) from 0 to 7 days after birth. At 7 days, plasma gastrin in ACTH-treated pigs (elevated plasma cortisol) was significantly lower than in saline-treated pigs, but not different from that in metyrapone-treated pigs (low plasma cortisol). No treatment effects were observed postnatally for antral gastrin and fundic cobalamin-binding protein concentrations. These results suggest that in the intrapartum period the high circulating cortisol levels stimulate the normal rise in gastrin and acid secretion associated with spontaneous vaginal delivery in the piglet, whereas postnatally, cortisol is unlikely to play an important role in the subsequent development of gastrin and acid secretion.

Adrenal Glands↗
PubMed1995

Haemodynamic responses to an angiotensin II receptor antagonist (GR 117289) in maternal and fetal sheep.

An AT1-specific angiotensin II receptor antagonist (GR117289; 1 mg/kg I.V. bolus) was administered daily to ten chronically catheterized, normotensive ewes during late pregnancy (from 126 +/- 1 days) until parturition (139 +/- 1 days); five control animals received an equivalent volume of vehicle solution. Following drug administration, mean maternal blood pressure decreased from 87 +/- 1 mmHg to a minimum of 79 +/- 1 mmHg at 0.5 h (P < 0.05; n = 10) and remained low for 4-6 h without any concomitant change in fetal blood pressure or maternal and fetal heart rates. In animals fitted with flow probes, uterine blood flow decreased from 443 +/- 21 to 363 +/- 27 ml/min at 0.5 h post-drug (P < 0.05; n = 6); this change was positively correlated with the reduction in maternal blood pressure. The mean decrements in uterine and umbilical blood flows measured by steady-state infusion of tritiated water were -611 +/- 171 ml/min at 4-6 h (P < 0.05; n = 5) and -71 +/- 19 ml/min at 0.5-1 h (P < 0.05; n = 5), respectively. Significant reductions (P < 0.05; n = 10) in fetal arterial oxygen tension (-1.6 +/- 0.4 mmHg), saturation (-6.6 +/- 1.6%) and content (-0.3 +/- 0.1 mumol/ml) were evident at 0.5 h post-drug and were maintained for 6-12 h. Umbilical oxygen delivery decreased at 0.5-1 h following drug administration (P < 0.01; n = 5), but was unaccompanied by any significant change in fetal oxygen consumption. Chronic decreases in daily fetal pH and blood oxygen content occurred in GR117289-treated ewes. There were no significant differences in gestational length or neonatal outcome between vehicle- and GR117289-treated groups of ewes with single fetuses.

Angiotensin Receptor Antagonists↗
PubMed1995

The glucogenic capacity of the fetal pig: developmental regulation by cortisol.

In the present study, the ontogenic changes in gluconeogenic enzyme activities and in hepatic glycogen and beta-adrenergic receptor levels were investigated in fetal pigs from 70 days of gestation until delivery at term (114 +/- 2 days). The values were compared with those observed in fetuses infused subcutaneously with cortisol for 6 days beginning at 82-84 or 92-94 days of gestation. Tissue glucose-6-phosphatase (G6Pase) activity increased with increasing gestational age in the liver, kidney and duodenum of control fetal pigs. At birth, there was a further increase in G6Pase activity in the liver but not in the kidney or duodenum. In the kidney, there was a similar gestational increase in phosphoenolpyruvate carboxykinase (PEPCK) activity. These changes in enzyme activities closely paralleled the prepartum increase in fetal plasma cortisol and were accompanied by increases in hepatic glycogen content and beta-adrenergic receptor density. At 98-100 days, there were significant increases in G6Pase activity in the liver, kidney and duodenum of the cortisol-infused fetuses, whereas at 88-90 days only renal G6Pase was significantly elevated by cortisol infusion. Cortisol infusion also increased hepatic beta-receptor density at 88-90 days and hepatic glycogen content at both gestational ages. There were no changes in hepatic PEPCK, hepatic or renal fructose diphosphatase and aspartate amino transferase activities during cortisol infusion or with increasing gestational age. When the data from all the piglets were combined, irrespective of age or treatment, there were significant positive correlations between log plasma cortisol and G6Pase activity in the liver, kidney and duodenum. Similar positive correlations were observed between hepatic beta-adrenoceptor density and log plasma cortisol and between the latter values and the hepatic glycogen content. These findings show that cortisol induces tissue G6Pase activity in the fetal pig and suggest that the prepartum rise in endogenous cortisol may be responsible for the increase in fetal glucogenic capacity observed towards term in this as in other species.

Animals↗
PubMed1995

Sympathoadrenal and other endocrine and metabolic responses to hypoglycaemia in the fetal foal during late gestation.

In the present study, ten insulin challenge tests were carried out on nine chronically catheterized fetal foals between 253 and 314 days gestation (term > 320 days). Changes in fetal plasma concentrations of glucose, catecholamines, cortisol, ACTH, free fatty acid (FFA) and lactate were measured before and after a bolus dose of insulin (0.5-2.0 u/kg I.V.). Fetal blood gases, pH, haemoglobin levels and heart rate were measured throughout the 2-3h experimental period. The fetuses fell into two distinct groups on the basis of proximity to delivery and basal plasma cortisol and catecholamine levels. Those within 2-10 days of delivery after 300 days (group 2, number of experiments (n) = 4) had plasma cortisol and noradrenaline concentrations which were significantly higher (P < 0.05) than the corresponding values in fetuses sampled earlier in gestation or at least 2 weeks before foaling (group 1, n = 6). Although insulin administration resulted in a 50% fall in plasma glucose in all animals, group 2 showed significantly greater increases in plasma noradrenaline than group 1. In neither group were there detectable changes in plasma adrenaline. In group 2, increases in plasma cortisol were seen following insulin, whereas no cortisol changes were observed in group 1, despite rises in plasma ACTH. Insulin administration also led to acidosis and increases in heart rate and plasma lactate and FFA levels in all fetuses studied. However, only group 2 became consistently hypoxic during the insulin challenge. No significant changes in plasma glucose or any of the other parameters were observed in the fetuses after saline administration (n = 5). These findings suggest that hypoglycaemia activates the sympathoadrenal system in the fetal foal from 75% of gestation but has relatively little effect on the fetal pituitary-adrenocortical axis until much closer to term.

Adrenal Glands↗
PubMed1995

Glucose and oxygen metabolism in the fetal foal during late gestation.

With the use of [U-14C]glucose tracer methodology, the rates of umbilical uptake, utilization, oxidation, and production of glucose were determined in nine chronically catheterized fetal foals in the fed state between 268 and 325 days of gestation (term approximately 335 days). At the same time, the rates of umbilical O2 and lactate uptake were measured in all nine fetuses by Fick principle. The mean fetal rates of umbilical glucose uptake, glucose utilization, and CO2 production from glucose carbon were 36.9 +/- 2.5, 36.4 +/- 1.7, and 117.7 +/- 17.4 mumol.min-1.kg fetal body wt-1, respectively (n = 9). Endogenous glucose production was therefore negligible in the fetal foal in the fed state. Production of CO2 from glucose carbon accounted for 40.9 +/- 6.5% of the umbilical O2 uptake, which averaged 292 +/- 15 mumol.min-1.kg-1 (n = 9). No significant changes in fetal glucose or O2 metabolism were observed with increasing gestational age. The rates of umbilical glucose uptake, glucose utilization, and CO2 production from glucose carbon (P < 0.01), but not the rate of umbilical O2 uptake (P > 0.05), were positively correlated with the fetal blood glucose level. There was a significant umbilical lactate uptake in the fetuses older than 290 days (12.3 +/- 4.1 mumol.min-1.kg-1, n = 5, P < 0.05) but not in the younger animals (6.2 +/- 9.6 mumol.min-1.kg-1, n = 4, P > 0.05). Hence, glucose is used for both oxidative and nonoxidative metabolism in utero and is a major, although not the sole, oxidative substrate in the fetal foal during late gestation.

Animals↗
PubMed1995

The prenatal development and glucocorticoid control of brush-border hydrolases in the pig small intestine.

The development of brush-border enzymes and the possible regulatory role of cortisol were investigated in the small intestine of the fetal and neonatal pig. With the sows under pentobarbitone anesthesia, osmotic minipumps containing either saline or cortisol were inserted s.c. into 25 fetuses from 10 pregnant sows (82-96 d gestation). Six d later, the infused fetuses were removed by cesarean section and samples of the proximal, middle, and distal intestine taken for analysis. Samples were also obtained from 48 piglets that did not undergo an operation (controls) and that were removed at intervals from 82 d gestation until term (114 +/- 2 d). In the proximal and middle intestine, the mean levels of lactase-phlorizin hydrolase (EC 3.2.1.23-62), maltaseglucoamylase (EC 3.2.1.20), aminopeptidase N (EC 3.4.11.2), and aminopeptidase A (EC 3.4.11.7) increased during the last 10-15 d before term, correlated positively with log10 plasma cortisol values, and were higher in cortisol-infused than in saline-infused fetuses (p < 0.05). Activity of sucrase-isomaltase (EC 3.2.1.48-10) was low in fetal pigs, and this enzyme and dipeptidyl peptidase IV (EC 3.4.14.5) were not significantly affected by fetal age or exogenous cortisol. Maltase (EC 3.2.1.48-10 and EC 3.2.1.20) activity was significantly decreased in the middle and distal intestine of cortisol-infused fetuses. The results suggest that the prepartum rise in endogenous cortisol secretion stimulates the prenatal expression of certain brush-border enzymes in the pig small intestine at this critical time. However, the effects of cortisol on the developing intestine were highly idiosyncratic for particular enzymes and intestinal regions.

Aminopeptidases↗
PubMed1994

Release of lipid from the equine placenta during in vitro incubation.

An in vitro incubation technique was used to examine release of lipids from the equine placenta. Placental tissue was obtained at term (n = 5, term = 320-365 days) and earlier in gestation (n = 8, mean = 266 days). Term placentae were incubated at two temperatures, 4 degrees C (control) and 37 degrees C for 2 h. Pre-term placentae were incubated at 37 degrees C with two different concentrations of fatty acid in the medium. Tissues and media were analysed for their lipid concentrations. Term and pre-term placentae released free fatty acid (FFA) and phospholipid into the incubation medium during incubation at 37 degrees C. Long chain polyunsaturated fatty acids derived from the essential fatty acids were released into the media. The fatty acid profiles of the lipids released during incubation more closely resembled those of fetal plasma than maternal plasma lipids as measured in previous studies. These data are consistent with the view that the equine placenta is a source of both FFA and phospholipid for the fetus and that the placenta may provide long chain polyunsaturated fatty acids for the fetal foal.

Animals↗
PubMed1994

Nutritional regulation of uteroplacental prostaglandin production and metabolism in pregnant ewes and mares during late gestation.

Prostaglandins (PGs) are produced by a variety of uteroplacental tissues during pregnancy and are released into the fetal fluid sacs and both the uterine and umbilical circulations. Uterine PG output increases towards term and is enhanced by maternal undernutrition in pregnant ewes and mares. In both species, withdrawal of food but not water for 30-48 h increases uterine venous PG levels and the uterine venous arterial concentration differences in PGE and 13, 14, dihydro-15-keto-prostaglandin F2 alpha (PGFM), the stable metabolite of PGF2 alpha. The increments in uterine V-A concentration differences in PGE and PGFM increase towards term and are associated with raised plasma PG levels in the fetal circulation. The PG changes observed during fasting are closely related to the fall in plasma glucose and the rise in plasma FFA in peripheral plasma. When normal metabolite levels are restored either by refeeding or glucose infusion, there is a rapid fall in PG levels with a narrowing of the uterine V-A concentration differences in the ewe and mare. When the data from all the animals are combined, there is an inverse correlation between uterine glucose uptake and PGFM output in both the pregnant ewe and mare. The availability of glucose and FFA to the gravid uterus therefore has an important role in controlling uteroplacental PG production and metabolism in late gestation although the specific steps in biochemical pathways regulated by these metabolites remain unclear. In the ewe, fasting increases uterine contractility and leads to early delivery of viable lambs in animals close to term (> 95% gestation), whereas in the mare it causes premature delivery of non-viable foals in most animals in late gestation (> 80% gestation). Nutritionally induced changes in uteroplacental PG production and metabolism therefore have important consequences for the outcome of pregnancy and may have a pivotal role in the induction of labour both before and at normal term.

Animal Nutritional Physiological Phenomena↗
PubMed1994

Developmental regulation of the porcine exocrine pancreas by glucocorticoids.

The possible role of cortisol in development of the exocrine pancreas was investigated. In the first study, fetal pigs were removed from the uterus by caesarean section (pentobarbitone anesthesia) and the pancreas collected from 51 69 to 109-day-old fetuses (term = 114 +/- 2 days). Of these, 15 88 to 90-day-old fetuses had been infused subcutaneously for 6 days with either saline, adrenocorticotropic hormone or cortisol (osmotic mini-pumps implanted at 82-84 days). The pancreas was also removed from eight newborn pigs. Quantitative enzyme analysis showed that amylase and trypsin activities per milligram pancreatic protein increased toward term, correlated positively with fetal plasma cortisol (p < 0.01) and were stimulated by cortisol infusion (p < 0.05). In the second study, pigs were delivered by caesarean section 2-3 days before term (to circumvent the neonatal cortisol surge) and injected intramuscularly with saline (n = 11), metyrapone (an inhibitor of cortisol synthesis, n = 12), adrenocorticotropic hormone (n = 14) or cortisol acetate (n = 6) during the postnatal period. At 6-7 days of age, adrenocorticotropic hormone- and cortisol acetate-treated pigs had higher concentrations of amylase and trypsin in pancreas than metyrapone-treated pigs. The values in saline-injected pigs were intermediate. By gel electrophoresis and subsequent incubation with enzyme substrates, protease E, chymotrypsin C, and cathodic trypsin were first detected at 6-7 days of age, and the activities (semiquantitative densitometry) appeared lower in metyrapone-treated pigs than in pigs from other treatment groups. The results indicate that glucocorticoids stimulate the perinatal development of pancreatic enzymes in the pig.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1994

Secretion of acid, gastrin, and cobalamin-binding proteins by the fetal pig stomach: developmental regulation by cortisol.

The role of cortisol in the development of gastric function was investigated in the fetal pig. Pregnant sows (term = 114 +/- 2 days, n = 10) were anaesthetized (pentobarbitone) and osmotic minipumps containing either saline or cortisol inserted subcutaneously into fetuses at 82-84 (n = 11) or 91-96 (n = 14) days gestation. Six days later the infused pigs were removed by Caesarean section and the stomach and its contents collected for analysis. Samples were also obtained from unoperated (control) fetal pigs (n = 51) removed under anaesthesia at intervals from 70 days gestation until term. The concentrations of acid in gastric fluid, gastrin in plasma and antral tissue (bioactive as well as precursor forms), and cobalamin(CBL)-binding proteins in fundic tissue were low in control pigs until 100 days gestation. During the last 2 weeks before term, large increases occurred in gastric fluid acidity (from pH 6-7 to pH 3 at birth), plasma amidated gastrin (from 10 to 90 pM) and CBL-binding protein concentration (from 10 to 80 pmol (g fundus)-1). These changes occurred in parallel with a surge in plasma cortisol (from 20 to 200 ng ml-1). Immature fetuses infused with cortisol had significantly higher gastric acidity, plasma amidated gastrin, and concentration of CBL-binding proteins than the corresponding control fetuses (P < 0.05). Across age and treatment groups, significant correlations were found between log10 plasma cortisol values and the above parameters (r = 0.59-0.76, P < 0.01). The results suggest that endogenous cortisol secretion stimulates the secretion of gastric acid, gastrin and CBL-binding proteins in the prenatal period of the pig.

Animals↗
PubMed1994

Blood amino acids in the pregnant mare and fetus: the effects of maternal fasting and intrafetal insulin.

Blood amino acids were measured in twelve chronically catheterized mares and fetuses between 250 and 310 days gestation. The concentrations of the majority of individual amino acids were similar in maternal and fetal arterial blood and no gestational changes were detected. Only methionine, phosphoserine, 3-methyl-histidine and glutamine were consistently higher in the fetus than the mare, whilst certain other amino acids were higher in the maternal blood. Fasting the mares for 36 h led to significant falls in plasma glucose and rises in urea and maternal free fatty acids (FFA). Small but significant decreases in a few amino acids were seen in both fetus and mother, with an overall amino acid fall of 15% in the fetus and 13% in the mare. Virtually all amino acids had risen to basal values by 6 h after feeding. Intrafetal insulin (1 i.u./kg I.V.) as a bolus caused a more dramatic fall in fetal glucose than fasting, with no change in the mare. There were also rapid decreases in many amino acids by 30 min post-insulin and by 2 h all but five amino acids had fallen significantly. There was a drop in total fetal blood amino acids of 29%. These findings show that, in contrast to most other species studied, there is no overall feto-maternal gradient in blood amino acids in the mare, and that fasting leads to small falls in amino acid concentration, whereas intrafetal insulin induces a severe hypoglycaemia with dramatic decreases in almost all amino acids and no change in urea, suggesting a direct anabolic effect of insulin on fetal tissues.

Amino Acids↗
PubMed1994

Adrenocortical stimulation of stomach development in the prenatal pig.

Development of the porcine gastric proteases (chymosin, pepsin A, B and C) has been studied in the fetal pig in the last third of gestation (term 115 days). The possibility that the prepartum rise in circulating cortisol is involved in gastric maturation was investigated by infusing immature fetuses with cortisol (osmotic minipumps implanted at 82-90 days of gestation). Concentrations of prochymosin in fundic tissue and stomach contents increased before term, correlated positively with log10 plasma cortisol values (r = 0.68-0.76, p < 0.001), and were stimulated by cortisol infusion (p < 0.001). The pH of stomach contents decreased (from pH 7 to 3), correlated negatively with log10 plasma cortisol values (r = -0.69, p < 0.001), and was reduced by cortisol infusion (p < 0.05). Only trace amounts of pepsinogens could be detected in fetal pigs. By immunohistochemistry, it was shown that cortisol increased the number and distribution of prochymosin-containing cells in the fundic gland. Stimulating effects were also observed for the small populations of pepsinogen-reactive cells present in some of the fetal pigs. The results suggest that endogenous cortisol stimulates the rise in prochymosin synthesis and secretion together with increased gastric acidity in the prenatal period of the pig.

Adrenocorticotropic Hormone↗
PubMed1994

Prepartum adrenocortical maturation in the fetal foal: responses to ACTH.

The present study was carried out on 19 chronically catheterized mares and fetuses in late gestation (term > 320 days). In six animals which were monitored up to the time of delivery of a live foal, plasma and amniotic fluid cortisol concentrations remained low until 4-5 days before parturition when there was a rapid, significant rise (P < 0.05) which was not accompanied by any corresponding changes in maternal plasma cortisol. Circulating fetal ACTH concentrations became more variable close to delivery and ANOVA revealed no significant increases during this critical period, although a negative correlation between plasma ACTH and time to delivery was observed (P < 0.05). Tests on fetal adrenal responsiveness to exogenous ACTH1-24 were carried out on ten animals. Before 295 days of gestation no significant increases in fetal plasma cortisol above its basal level of 20-30 nmol/l could be elicited by ACTH, administered as a single i.v. injection (1-2 micrograms/kg). By 304 +/- 3 days (mean +/- S.E.M.) small but significant (P < 0.05) increments in plasma cortisol were detected after ACTH, while in the oldest group (313 +/- 2 days) significant (P < 0.01) 50-60% increments were seen throughout the test period (2 h). Only one fetus was tested within 3 days of delivery and here a fourfold rise in plasma cortisol was evoked by ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex↗