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)

Fetal cardiovascular, endocrine, and fluid responses to atrial natriuretic factor infusion

1989 ◽  
Vol 257 (3) ◽  
pp. R580-R587 ◽  
Author(s):  
R. A. Brace ◽  
L. A. Bayer ◽  
C. Y. Cheung
Keyword(s):  
Arterial Pressure ◽  
Blood Volume ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Urine Flow ◽  
Fetal Sheep ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

The purpose of this study was to determine the effects of atrial natriuretic factor (ANF) in the fetus and to explore the interactions among the fetal cardiovascular, endocrine, and fluid responses to ANF. In 12 chronically catheterized fetal sheep at 130 +/- 1 (SE) days gestation, ANF was infused intravenously for 30 min at 14-300 ng.min-1.kg-1. Fetal arterial plasma ANF concentration increased by 174 to 5,410 pg/ml from a preinfusion value of 163 +/- 13 pg/ml. The clearance of ANF from the circulation was 122 +/- 28 ml.min-1.kg-1 and the half-life was 0.46 +/- 0.07 min. When plasma ANF was greater than 2,000 pg/ml, fetal arterial pressure decreased, venous pressure increased transiently, and heart rate was unchanged. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) increased with high ANF concentrations, while norepinephrine concentrations were unaffected. Fetal blood volume decreased in all fetuses, and urine flow increased significantly but not in every fetus. Blood and urine osmolalities did not change. On terminating the infusion, venous pressure and urine flow decreased below control, while blood volume and arterial pressure remained reduced. Plasma AVP concentration increased further, and this was accompanied by an increase in urine osmolality. Thus the most consistent effect of ANF in the fetus was a reduction in blood volume, which was independent of urine flow changes. Other cardiovascular, endocrine, and fluid responses to ANF as well as interactions among them appeared to occur largely at supraphysiological concentrations and may be secondary to the changes in blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

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 blood volume restoration following rapid fetal hemorrhage

1990 ◽  
Vol 259 (2) ◽  
pp. H567-H573 ◽  
Author(s):  
R. A. Brace ◽  
C. Y. Cheung
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Plasma Renin ◽  
Late Gestation ◽  
Fetal Blood ◽  
Fetal Sheep ◽  
Hemorrhage Volume ◽  
Plasma Arginine ◽  
Time Required ◽  
Ovine Fetal

In a previous study, we found that ovine fetal blood volume returned to normal in 3 h after a slow hemorrhage of 31% over 2 h; volume was slightly elevated at 24-25 h. In the present study, we explored the time required for blood volume restoration in late gestation fetal sheep following a rapid hemorrhage over 10 min. The rate of hemorrhage was constant within each fetus but varied among fetuses from 13.5 to 32.2%. Two fetuses that were hemorrhaged 32% of their initial blood volume over 10 min underwent cardiovascular collapse during the hemorrhage. In 10 fetuses that were hemorrhaged 21.0 +/- 1.7% (SE) over 10 min, 6.5 h were required for blood volume to return to control. Fetal arterial pressure, venous pressure, and heart rate decreased during and immediately after the hemorrhage and returned to normal within 1 h. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) underwent large increases following the rapid hemorrhage. Volume restoration at 5-7 h posthemorrhage correlated negatively with PRA and norepinephrine (NE) concentration immediately after the hemorrhage. Three of the 10 fetuses died overnight, and in the remaining seven fetuses blood volume was 8.8 +/- 3.3% below control (P less than 0.01) at 24-25 h posthemorrhage. The fetuses were also hypoxic, acidotic, and had greatly elevated plasma AVP and NE concentrations at this time. We conclude that ovine fetuses are less able to survive a rapid hemorrhage compared with a slow hemorrhage of the same extent. In addition, fetal blood volume restoration is delayed after rapid hemorrhage, and the impaired restoration is to the detriment of the fetus.(ABSTRACT TRUNCATED AT 250 WORDS)

Norepinephrine effects on fetal cardiovascular and endocrine systems

1988 ◽  
Vol 254 (4) ◽  
pp. H734-H741 ◽  
Author(s):  
C. Y. Cheung ◽  
R. A. Brace
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Fold Increase ◽  
Dependent Manner ◽  
Vasoactive Hormones ◽  
Near Term ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Norepinephrine (NE) was infused intravenously into near-term chronically catheterized sheep fetuses for 30 min. Infusions of 0.39, 1.2, 3.9, 12, and 39 micrograms/min caused a 1- to 300-fold increase in plasma NE concentration. Fetal arterial pressure increased in a dose-dependent manner up to a maximum of 72 +/- 5% above basal levels at 6-7 min and gradually declined thereafter. Venous pressure increased during the four highest infusion rates to a maximum at 6-7 min followed by a return toward normal. Fetal blood volume underwent a rapid dose-dependent decrease by a maximum of 12 +/- 1% during 39-micrograms/min infusions of NE. Heart rate initially decreased by up to 40 beats/min during the 3.9-, 12-, and 39-micrograms/min infusions, returned to normal within 10 min, and increased to 50 beats/min above control by the end of the 30-min infusion. Plasma concentrations of arginine vasopressin, epinephrine, and plasma renin activity did not change during or after the four lowest infusion rates. Thus fetal vascular pressures and blood volume are altered in a dose-dependent manner over a broad range of plasma NE concentrations. In addition, NE does not appear to affect other circulating vasoactive hormones within its physiological range of concentrations.

Acidemia stimulates ACTH, vasopressin, and heart rate responses in fetal sheep

1989 ◽  
Vol 257 (2) ◽  
pp. R344-R349 ◽  
Author(s):  
C. E. Wood ◽  
H. G. Chen
Keyword(s):  
Heart Rate ◽  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Highly Correlated

Adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and renin responses to hemorrhage are highly correlated to the hemorrhage-induced decreases in arterial pH. The present study was designed to test the responses of these three systems to acute fetal acidemia, produced by intravenous infusion of H+. HCl was infused into chronically catheterized fetal sheep at rates of 0.02 (n = 5), 0.10 (n = 6), and 0.50 (n = 5) meq/min. Infusions at rates of 0.10 and 0.50 meq/min significantly decreased fetal arterial pH and increased arterial PCO2. Fetal heart rate and plasma concentrations of ACTH, cortisol, and AVP were significantly increased during infusion of HCl at 0.5 meq/min. Neither fetal plasma renin activity nor fetal arterial blood pressure was significantly altered by any of the infusions. The results of these experiments suggest that fetal ACTH, AVP, and heart rate are stimulated by decreases in arterial pH and/or increases in arterial PCO2. We speculate that these responses are chemoreceptor mediated, although we cannot distinguish the apparent relative roles of peripheral and central chemoreceptors on the basis of the present study.

Reflex control of fetal arterial pressure and hormonal responses to slow hemorrhage

1992 ◽  
Vol 262 (1) ◽  
pp. H225-H233 ◽  
Author(s):  
H. G. Chen ◽  
C. E. Wood
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Blood Gases ◽  
Plasma Renin ◽  
Late Gestation ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors ◽  
Fetal Plasma ◽  
Phenylephrine Infusion

Late-gestation fetal sheep respond to slow hemorrhage with increases in plasma concentrations of adrenocorticotropic hormone (ACTH), hydrocortisone, arginine vasopressin (AVP), and plasma renin activity (PRA) that correlate to the acidemia and hypercapnia also produced by hemorrhage. This study was designed to investigate the role of peripheral chemoreceptors in the mediation of these responses. Chronically catheterized fetal sheep were left intact or were subjected to bilateral section of cervical vagosympathetic trunks and carotid sinus nerves. At least 5 days after surgical preparation (between 121 and 138 days of gestation) fetuses were bled at a rate of 11 ml/10 min for 2 h. Denervated fetuses were studied with or without simultaneous infusion of phenylephrine. Denervation exaggerated the decrease in mean arterial pressure and arterial pH and the increase in arterial PCO2 during hemorrhage. Infusion of phenylephrine in the denervated fetuses prevented the decrease in blood pressure and reduced the magnitudes of changes in blood gases. Fetal plasma ACTH, hydrocortisone, and PRA responses to the hemorrhage were exaggerated in the denervated fetuses (not infused with phenylephrine) compared with the intact fetuses. Phenylephrine infusion attenuated the ACTH response and inhibited the AVP response but did not alter the PRA response. We conclude that the sectioned fibers are important for the maintenance of blood pressure and blood gases during hemorrhage and that the PRA, AVP, and ACTH responses to slow hemorrhage are not mediated by peripheral chemoreceptors.

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

Absence of fast negative feedback control of ACTH and renin in fetal and adult sheep

1986 ◽  
Vol 250 (3) ◽  
pp. R403-R410 ◽  
Author(s):  
C. E. Wood
Keyword(s):  
Negative Feedback ◽  
Feedback Inhibition ◽  
Plasma Renin ◽  
Renin Secretion ◽  
Fetal Sheep ◽  
Adult Sheep ◽  
Fetal Plasma ◽  
Negative Feedback Control ◽  
Time Courses ◽  
Vasodilator Drug

Fetal adrenocorticotropin (ACTH) and renin secretion are increased by a variety of stimuli and decreased by cortisol negative feedback inhibition. However, the time courses of these interactions are unknown. The present studies were designed to test for rapid feedback negative suppression of ACTH and renin secretion in fetal and adult sheep. In chronically catheterized fetal sheep, ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside, a vasodilator drug. Vehicle or cortisol, infused at rates of 1, 2, or 4 micrograms/min for 2 min before and during the infusion of nitroprusside did not significantly alter the fetal ACTH or renin responses to nitroprusside. In five nonpregnant ewes, chronically prepared with skin loops containing the carotid arteries, nitroprusside (20 micrograms X kg-1 X min-1) was infused beginning 2 min after infusion of vehicle or cortisol (3.5 or 7 micrograms X kg-1 X min-1). Cortisol infusion produced a rising plasma cortisol concentration similar to that after stress but did not alter the magnitude of the ACTH response to nitroprusside. The results indicate that cortisol-induced suppression of ACTH secretion does not occur rapidly in the fetal or adult sheep and that the cortisol-induced suppression of fetal plasma renin activity is a slow process.

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