Effect of hypophysectomy on plasma catecholamines and enkephalins in fetal sheep

1993 ◽  
Vol 265 (2) ◽  
pp. E203-E209
Author(s):  
C. L. Coulter ◽  
I. R. Young ◽  
G. Simonetta ◽  
I. C. McMillen
Keyword(s):  
Gestational Age ◽  
Plasma Concentrations ◽  
Plasma Catecholamines ◽  
Plasma Norepinephrine ◽  
Plasma Epinephrine ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Hypoxic Conditions

The aim of this study was to determine the effect of fetal hypophysectomy on the plasma concentrations of catecholamines and enkephalins in the fetal sheep between 120 and 140 days gestation under basal and hypoxic conditions. During basal conditions, there was no difference in the plasma concentrations of norepinephrine and epinephrine between intact and hypophysectomized groups. Fetal plasma norepinephrine concentrations were significantly increased during hypoxia in intact fetal sheep (7.2 +/- 2.2 pmol/ml, -15 min; 20.2 +/- 7.7 pmol/ml, 30 min) between 130 and 140 days, but after fetal hypophysectomy there was no significant norepinephrine response to hypoxia at this gestational age (4.7 +/- 1.3 pmol/ml, -15 min; 8.8 +/- 2.8 pmol/ml, 30 min). In contrast, fetal plasma epinephrine concentrations were significantly increased during hypoxia in both the intact (1.5 +/- 0.5 pmol/ml, -15 min; 3.3 +/- 1.7 pmol/ml, 30 min) and hypophysectomized groups (1.8 +/- 0.6 pmol/ml, -15 min; 6.8 +/- 4.1 pmol/ml, 30 min) between 130 and 140 days. During basal conditions, plasma concentrations of free Met-Enk were significantly less in hypophysectomized fetal sheep (170.8 +/- 34.3 pg/ml; 120-140 days) than in intact fetal sheep (305.6 +/- 47.3 pg/ml). There were no differences, however, in the fetal plasma concentrations of total Met-Enk between the intact (18.0 +/- 1.9 ng/ml) and hypophysectomized (16.9 +/- 2.6 ng/ml) groups. During hypoxia, there were no changes in the fetal plasma concentrations of either free or total Met-Enk in the intact or hypophysectomized groups.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Coordinated changes in hepatic amino acid metabolism and endocrine signals support hepatic glucose production during fetal hypoglycemia

2015 ◽  
Vol 308 (4) ◽  
pp. E306-E314 ◽  
Author(s):  
Satya S. Houin ◽  
Paul J. Rozance ◽  
Laura D. Brown ◽  
William W. Hay ◽  
Randall B. Wilkening ◽  
...  
Keyword(s):  
Fetal Liver ◽  
Hepatic Glucose Production ◽  
Plasma Concentrations ◽  
Glucose Production ◽  
Late Gestation ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Hepatic Glucose ◽  
Molar Percent ◽  
Glucose Output

Reduced fetal glucose supply, induced experimentally or as a result of placental insufficiency, produces an early activation of fetal glucose production. The mechanisms and substrates used to fuel this increased glucose production rate remain unknown. We hypothesized that in response to hypoglycemia, induced experimentally with maternal insulin infusion, the fetal liver would increase uptake of lactate and amino acids (AA), which would combine with hormonal signals to support hepatic glucose production. To test this hypothesis, metabolic studies were done in six late gestation fetal sheep to measure hepatic glucose and substrate flux before (basal) and after [days (d)1 and 4] the start of hypoglycemia. Maternal and fetal glucose concentrations decreased by 50% on d1 and d4 ( P < 0.05). The liver transitioned from net glucose uptake (basal, 5.1 ± 1.5 μmol/min) to output by d4 (2.8 ± 1.4 μmol/min; P < 0.05 vs. basal). The [U-13C]glucose tracer molar percent excess ratio across the liver decreased over the same period (basal: 0.98 ± 0.01, vs. d4: 0.89 ± 0.01, P < 0.05). Total hepatic AA uptake, but not lactate or pyruvate uptake, increased by threefold on d1 ( P < 0.05) and remained elevated throughout the study. This AA uptake was driven largely by decreased glutamate output and increased glycine uptake. Fetal plasma concentrations of insulin were 50% lower, while cortisol and glucagon concentrations increased 56 and 86% during hypoglycemia ( P < 0.05 for basal vs. d4). Thus increased hepatic AA uptake, rather than pyruvate or lactate uptake, and decreased fetal plasma insulin and increased cortisol and glucagon concentrations occur simultaneously with increased fetal hepatic glucose output in response to fetal hypoglycemia.

Rebound increase in fetal breathing movements after 24-h prostaglandin E2 infusion in fetal sheep

1996 ◽  
Vol 80 (1) ◽  
pp. 166-175 ◽  
Author(s):  
S. A. Hollingworth ◽  
S. A. Jones ◽  
S. L. Adamson
Keyword(s):  
Prostaglandin E2 ◽  
Plasma Concentrations ◽  
Treated Group ◽  
High Plasma ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Pge2 Concentration ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Rebound Increase

We investigated the hypothesis that the precipitous decrease in prostaglandin E2 (PGE2), a potent inhibitor of fetal breathing, from high plasma concentrations during labor causes a rebound stimulation of breathing without newborn concentrations falling below prelabor fetal values. Fetal plasma PGE2 concentration was gradually increased from 384 +/- 82 (SE) pg/ml in 2-h steps [0 (baseline), 1.5, 3, and 6 micrograms/min] to labor levels (1,230 +/- 381 pg/ml at 6 micrograms/min) and then was maintained for 24 h (n = 9). PGE2 at 1.5 micrograms/min significantly decreased breathing incidence [from 42 +/- 4 (baseline) to 14 +/- 4%] and breath amplitude (from 2.1 +/- 0.5 to 1.5 +/- 0.2 arbitrary units) and increased breath-to-breath interval (from 1.16 +/- 0.07 to 1.56 +/- 0.06 s). No further dose-related changes were observed. During the first 2 h after PGE2 infusion was stopped, PGE2 concentration returned to basal (352 +/- 64 pg/ml) but breathing incidence and amplitude were significantly higher (74 +/- 8% and 2.4 +/- 0.3 arbitrary units, respectively) and breath-to-breath interval was significantly lower (0.95 +/- 0.10 s) than were basal levels. Changes arose within approximately 15 min and were maintained for at least 4 h. Breathing did not change significantly in the saline-treated group (n = 7). Results suggest that the rapid decrease in plasma PGE2 concentration at birth promotes the onset of breathing.

Effect of alteration of maternal plasma progesterone concentrations on fetal behavioural state during late gestation

1997 ◽  
Vol 152 (3) ◽  
pp. 379-386 ◽  
Author(s):  
M B Nicol ◽  
J J Hirst ◽  
D Walker ◽  
G D Thorburn
Keyword(s):  
Plasma Concentrations ◽  
Maternal Plasma ◽  
Late Gestation ◽  
Emg Activity ◽  
Fetal Sheep ◽  
Plasma Progesterone ◽  
Fetal Plasma ◽  
Progesterone Synthesis ◽  
Progesterone Metabolites ◽  
Vascular Catheters

Placental progesterone synthesis exposes the fetus to high levels of progesterone and progesterone metabolites during late gestation which may influence fetal behaviour. To determine the role of maternal progesterone synthesis in the control of fetal arousal state and fetal breathing movements (FBM), the effect of raising and lowering maternal progesterone concentrations was examined in chronically catheterised fetal sheep. Fetal and maternal vascular catheters, fetal tracheal and amniotic fluid catheters as well as electrodes for recording fetal electrocortical (ECoG), electro-ocular (EOG) and nuchal muscle electromyographic (EMG) activity were implanted between 118 and 122 days gestational age (GA). Progesterone, 100 mg, administered twice daily i.m. for 3 days (130–133 days GA) resulted in a marked elevation in maternal plasma progesterone concentrations (370 ± 121%, n=5, P<0·05), but had no effect on fetal plasma concentrations. Fetal EOG episodes and the duration of fetal behavioural arousal were significantly suppressed throughout the progesterone treatment period (74·4–81·1% and 58–65% respectively, P<0·05, n=5). Four ewes received Trilostane (25 mg i.v.), a 3β-hydroxysteroid dehydrogenase inhibitor, between 136 and 140 days GA. Maternal and fetal progesterone concentrations were significantly lowered by 60 min after treatment (19·8 ± 8·0% and 39·5 ± 24·3% respectively, P<0·05). The incidence of fetal EOG activity increased from a pretreatment level of 26·8 ± 1·5 min/h to 30·3 ± 2·8 min/h at 1–6 h and to 35·0 ± 1·7 min/h (P<0·05) during the 7–12 h after Trilostane treatment. The duration of FBM episodes was significantly higher at 1–6 h and 7–12 h after Trilostane treatment (19·5 ± 3·0 and 23·6 ± 5·5 min/h respectively, P<0·05) compared with pretreatment levels (11·2 ± 1·2 min/h). We conclude that increasing maternal progesterone levels suppresses fetal EOG activity and behavioural arousal, whereas reducing maternal progesterone synthesis leads to an elevation of EOG activity and FBM. Journal of Endocrinology (1997) 152, 379–386

scholarly journals Proopiomelanocortin Processing in the Anterior Pituitary of the Ovine Fetus after Lesion of the Hypothalamic Paraventricular Nucleus

Endocrinology ◽  
2005 ◽  
Vol 146 (6) ◽  
pp. 2665-2673 ◽  
Author(s):  
M. Elizabeth Bell ◽  
Thomas J. McDonald ◽  
Dean A. Myers
Keyword(s):  
Paraventricular Nucleus ◽  
Anterior Pituitary ◽  
Limit Of Detection ◽  
Plasma Concentrations ◽  
Hybridization Signal ◽  
Mrna Levels ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Ovine Fetus ◽  
Fetal Organs

Abstract The hypothalamic-pituitary-adrenocortical axis plays an essential role in the maturation of fetal organs and, in sheep, birth. Lesioning the paraventricular nucleus (PVN) in fetal sheep prevents adrenocortical maturation and parturition without altering plasma immunoreactive ACTH concentrations. The purpose of this study was to determine the effect of PVN lesion on anterior pituitary processing of proopiomelanocortin (POMC) to ACTH, plasma concentrations of ACTH and ACTH precursors (POMC; 22-kDa proACTH), and expression of subtilisin-like prohormone convertase 3 (SPC3) in corticotropes in fetal sheep. PVN lesion did not affect anterior pituitary POMC and 22-kDa proACTH levels, whereas ACTH was significantly affected. The ACTH precursor (POMC plus 22-kDa proACTH) to ACTH ratio in the anterior pituitary was significantly increased after PVN lesion. Post-PVN lesion, fetal plasma ACTH1–39, was below the limit of detection, whereas ACTH precursors (POMC plus 22-kDa proACTH) were not affected. In the inferior region of the anterior pituitary, 40–50% of corticotropes had detectable SPC3 hybridization signal, and PVN lesion did not change the extent of colocalization of POMC and SPC3, or SPC3 mRNA levels within corticotropes. Neither the percent of corticotropes in the superior region containing SPC3 hybridization (7–12%) or hybridization signal strength was altered in response to PVN lesion. In conclusion, the fetal PVN is necessary for sustaining adequate anterior pituitary processing of POMC to ACTH and ACTH release needed for maturing the adrenal cortex in the sheep fetus.

Arginine vasopressin responses to hypoxia and hypercapnia in late-gestation fetal sheep

1991 ◽  
Vol 260 (6) ◽  
pp. R1077-R1081 ◽  
Author(s):  
H. Raff ◽  
C. W. Kane ◽  
C. E. Wood
Keyword(s):  
Arginine Vasopressin ◽  
Late Gestation ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Hypoxic Conditions ◽  
Arterial Ph ◽  
Hypercapnic Hypoxia ◽  
Per Se ◽  
Peripheral Arterial

The purpose of this study was to determine the interaction of hypoxia and hypercapnia in the control of arginine vasopressin (AVP) secretion in fetal sheep and to determine the role of the peripheral arterial chemoreceptors in that response. We measured the plasma AVP response to hypercapnia and/or hypoxia in catheterized intact or sinoaortic-denervated fetal sheep between 123 and 144 days of gestation. Ewes were exposed to the following inspired gases: two successive 30-min periods of normocapnic normoxia, 30 min of normocapnic normoxia followed by 30 min of normocapnic hypoxia, two successive 30-min periods of hypercapnic normoxia, or 30 min of hypercapnic normoxia followed by 30 min of hypercapnic hypoxia (i.e., asphyxia). Hypercapnia per se had no significant effect on fetal plasma AVP. Normocapnic hypoxia per se resulted in a significant increase in fetal plasma AVP. Although hypercapnia resulted in a significant acidemia, the decrease in arterial pH was more marked under hypoxic conditions. Hypercapnia/acidemia augmented the AVP response to hypoxia. Fetal sinoaortic denervation did not significantly attenuate any of the AVP responses. We conclude that hypercapnia augments the fetal AVP response to hypoxia and that the AVP response to neither normocapnic nor hypercapnic hypoxia is dependent on afferent information carried in the carotid sinus or aortic nerves.

Are fetal adrenocorticotropic hormone and renin secretion suppressed by maternal cortisol secretion?

1988 ◽  
Vol 255 (3) ◽  
pp. R412-R417 ◽  
Author(s):  
C. E. Wood
Keyword(s):  
Plasma Cortisol ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Maternal Plasma ◽  
Renin Secretion ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Adrenal Secretion

Previous studies from this laboratory have demonstrated that intravenous infusions of hydrocortisone (cortisol) into fetal sheep at rates that produce plasma concentrations achieved during fetal stress inhibit fetal adrenocorticotropic hormone (ACTH) and renin secretion. The present study was designed to test for inhibition of fetal renin and ACTH after maternal adrenal secretion of cortisol. ACTH-(1-24) or saline infusion into 12 pregnant ewes (120-132 days gestation) at rates of 0, 1, 5, or 20 ng ACTH.kg-1.min-1 for 5 h produced dose-related increases in maternal plasma ACTH and cortisol concentrations and fetal plasma cortisol concentration. In the 20-ng.kg-1.min-1 group, increases in fetal plasma cortisol of 8.0 ng/ml (to 24.3 +/- 3.7 ng/ml) did not suppress basal fetal plasma renin activity. One hour after the end of the maternal vehicle or ACTH infusion, fetal ACTH secretion was stimulated by fetal intravenous infusion of sodium nitroprusside. In the 0-, 1-, and 5-ng.kg-1.min-1 groups, fetal ACTH responses to nitroprusside were suppressed in animals infused with ACTH. Together, these results indicate that the maternal adrenal secretion of cortisol inhibits stimulated secretion of ACTH but not renin in 120- to 132-day-gestation fetal sheep.

Fetal cardiovascular and endocrine responses to prolonged fetal hemorrhage

1986 ◽  
Vol 251 (2) ◽  
pp. R417-R424 ◽  
Author(s):  
R. A. Brace ◽  
C. Y. Cheung
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Moderate Volume ◽  
Circulating Levels ◽  
Initial Blood ◽  
Control Plasma

Twelve chronically catheterized fetal sheep averaging 131 +/- 1 (SE) days gestation (term = 145-150 days) were hemorrhaged an average of 30.8 +/- 1.8% of their initial blood volume over 2 h by removing blood at 10-min intervals. During the hemorrhage, fetal blood volume decreased by 14.3 +/- 1.4%, and arterial pressure (AP), venous pressure (VP), and heart rate (HR) did not change significantly, although fetal plasma renin activity (PRA), arginine vasopressin (AVP), and norepinephrine (NE) were elevated to 1.5-2.5 times their initial values (P less than 0.05). Circulating levels of PRA, AVP, and NE began to rise when 5-10, 10-15, and 20-30%, respectively, of the initial blood volume was removed. Three to five hours after the hemorrhage, blood volume had returned to normal, AP was reduced by an average of 6 mmHg, VP was unchanged, and HR was elevated by an average of 20 beat/min; PRA, AVP, and NE averaged two to three times control (P less than 0.05). Twenty-two hours after the hemorrhage, blood volume was 5.4 +/- 2.4% above control; AP and HR returned toward normal; VP was elevated by an average of 2 mmHg; PRA and NE levels remained elevated (P less than 0.05), but AVP was not different from control. Plasma concentrations of epinephrine, dopamine, and prolactin showed little change during or after the hemorrhage. Thus these studies indicate that the fetus rapidly returns its blood volume to normal after a substantial loss of blood. In addition, the fetal cardiovascular and endocrine responses to a prolonged fetal hemorrhage of moderate volume are substantially less than those that occur after rapid hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of lung liquid secretion by arginine vasopressin in fetal sheep

1990 ◽  
Vol 258 (1) ◽  
pp. R104-R111 ◽  
Author(s):  
M. J. Wallace ◽  
S. B. Hooper ◽  
R. Harding
Keyword(s):  
Gestational Age ◽  
Arginine Vasopressin ◽  
Plasma Cortisol ◽  
Fetal Lung ◽  
Inhibitory Effect ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Fetal Asphyxia ◽  
Lung Liquid ◽  
Secretion Rates

We have investigated the influence of gestational age on the inhibition of fetal lung liquid secretion by arginine vasopressin (AVP). In eight fetal sheep, lung liquid secretion rates were measured before and during infusion of AVP (300 mu.kg-1.h-1) at gestational ages between 110 and 148 days. During infusions, the concentration of AVP in fetal plasma increased from less than 8.7 +/- 0.2 pg/ml to 848.7 +/- 75.1 pg/ml. Fetal plasma epinephrine concentrations were not altered during AVP infusion. Infusions of AVP had no effect on fetal lung secretion before 135 days of gestation; they caused a 40.8% inhibition between 136 and 140 days, and at ages greater than 140 days induced an inhibition of 78.4%. In two ewes during labor, AVP infusion caused either a complete inhibition of secretion or reabsorption of lung liquid. The inhibitory effect of AVP increased in an exponential-like fashion with increasing gestational age and appeared to parallel the preparturient rise in fetal plasma cortisol concentrations. Our results indicate that AVP may be involved in the clearance of lung liquid at term and that AVP is unlikely to mediate the inhibitory effect of fetal asphyxia on lung liquid secretion, at least until after 135 days of gestation.

Temporal relationships among fetal urine flow, ANF, and AVP responses to hypertonic infusions

1990 ◽  
Vol 258 (2) ◽  
pp. R469-R475
Author(s):  
L. K. Miner ◽  
R. A. Brace ◽  
C. Y. Cheung
Keyword(s):  
Plasma Concentrations ◽  
Urine Flow ◽  
Initial Increase ◽  
Ang Ii ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Flow Response ◽  
Temporal Relationships ◽  
Fetal Urine

The fetal urine flow response to acute increases in osmolality may be mediated by changes in the plasma concentrations of atrial natriuretic factor (ANF), arginine vasopressin (AVP), and/or angiotensin II (ANG II). To explore this, hypertonic NaCl or mannitol was infused intravascularly over 10 min into chronically catheterized fetal sheep and their mothers simultaneously, followed by a 2-h maternal infusion at 1-2 ml/min to maintain the elevated osmolality. Fetal osmolality rose by 16 mosmol/kgH2O during 13% mannitol and 2.5% NaCl infusions and by 57 mosmol/kgH2O during 7% NaCl infusions. Large increases in fetal urine flow occurred in the three groups with peak flows (average of 304%, P less than 10(-6)) at 0-4 min after the end of the infusion. Flow declined to preinfusion values in all groups at 30-40 min. These changes in urine flow occurred in parallel with a rise (to 223%, P less than 10(-6)) and fall in plasma ANF concentrations. One hour after the infusions, urine flow declined to 50% of control concomitant with elevations in plasma AVP (to 414%, P less than 10(-6)), whereas plasma ANG II concentration did not change. Thus the initial increase in fetal urine flow in response to acute hypertonic infusions is temporally related to a rise in fetal plasma ANF, whereas the subsequent fall in urine flow is temporally related to a fall in plasma ANF and a simultaneous rise in AVP concentration. This suggests that ANF may contribute to the acute urine flow increase after hypertonic infusion, whereas AVP appears to be more important for the long-term regulation of fetal urine flow.

Inhibition of ACTH secretion blocks hypoxia-induced increase of adrenal cortical blood flow in fetal sheep

1995 ◽  
Vol 269 (3) ◽  
pp. E598-E604 ◽  
Author(s):  
A. M. Carter ◽  
J. Homan ◽  
M. Fraser ◽  
B. S. Richardson ◽  
J. R. Challis
Keyword(s):  
Blood Flow ◽  
Plasma Concentrations ◽  
Fetal Hypoxia ◽  
Control Groups ◽  
Plasma Acth ◽  
Fetal Sheep ◽  
Cortical Blood Flow ◽  
Blood Flows ◽  
Fetal Plasma

To examine the role of endogenous adrenocorticotropic hormone (ACTH) in adrenal blood flow responses to hypoxia, we studied unanesthetized ovine fetuses during an intravenous infusion of cortisol or vehicle. Fetal hypoxia was induced after 5 h of cortisol or vehicle infusion. Control fetuses were not made hypoxic. Blood flows were determined before and at three time points during the infusions. At 2 and 6 h of hypoxia, in vehicle-infused fetuses, fetal plasma concentrations of immunoreactive ACTH (irACTH) had risen from 9 +/- 3 (SE) pg/ml to 68 +/- 25 and 127 +/- 37 pg/ml, respectively. No significant change in fetal plasma irACTH occurred in the other groups. Adrenal cortical blood flow rose three- to fourfold during hypoxia in vehicle-infused fetuses but did not change from prehypoxia levels in cortisol-infused fetuses (P < 0.005). Medullary flow rose with hypoxemia, and this was not affected by concurrent cortisol infusion. Adrenal blood flows did not change in the control groups. Thus prior infusion of cortisol suppressed the rise in fetal plasma ACTH during hypoxia and selectively blocked the increase in adrenal cortical blood flow.

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