Regional Blood Flow and the Endocrine Response to Sustained Hypoxemia in the Preterm Ovine Fetus

Richardson, Bryan; Korkola, Stephen; Asano, Hitoshi; Challis, John; Polk, Daniel H.; Fraser, Mhoyra

doi:10.1203/00006450-199608000-00024

Cited by 33 publications

(26 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effect may be the result of circulating catecholamines and local factors such as nitric oxide and adenosine released during the hypoxia period and the immediate posthypoxic period. Recently, a similar response was reported in the sheep fetus at 75% of gestation 1 h after an 8 h period of hypoxia (Richardson, Korkola, Asano, Challis, Polk & Fraser 1996), in that heart rate and carcass blood flow were increased compared with baseline. They did not find increased blood flow to the brain.…”

Section: Co Distribution After Reoxygenationmentioning

confidence: 55%

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Mulder

Golde

Prinzen

et al. 1998

The Journal of Physiology

View full text Add to dashboard Cite

The fetus develops cardiovascular adaptations to protect vital organs in situations such as hypoxia and asphyxia. These include bradycardia, increased systemic blood pressure and redistribution of the cardiac output. The extent to which they involve maternal or placenta influences is not known. The objective of the present work was to study the cardiac output distribution in response to hypoxia in the chick embryo, which is independent of the mother. Fertilized eggs were studied at three incubation times (10‐13 days, 14‐16 days and 17‐19 days of a normal incubation time of 21 days). Eggs were placed in a Plexiglass box in which the oxygen concentration could be changed. Eggs were opened at the air cell and a chorioallantoic vein was catheterized. Cardiac output distribution was measured with 15 μm fluorescent microspheres injected during normoxia, during the last minute of a 5 min period of hypoxia and after 5 min of subsequent reoxygenation. Hypoxia caused a redistribution of the cardiac output in favour of heart (+17 to +160 % of baseline) and brain (+21 to +57 % of baseline) at the expense of liver (‐3 to ‐65 % of baseline), yolk‐sac (‐46 to ‐77 % of baseline) and carcass (‐6 to ‐33 % of baseline). The magnitude of the changes in cardiac output distribution to the heart, brain, liver and carcass in response to hypoxia increased with advancing incubation time. The data demonstrate the development of a protective redistribution of the cardiac output in response to hypoxia in the chick embryo from day 10 of incubation.

show abstract

Section: Co Distribution After Reoxygenationmentioning

confidence: 55%

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Mulder

Golde

Prinzen

et al. 1998

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…Release of epinephrine (E) into the fetal circulation opposes vagal tone and returns FHR to basal levels (10). The fetal peripheral vasoconstriction is maintained by increased release of vasoactive agents into the fetal circulation, such as catecholamines, neuropeptide Y (NPY), and AVP (1,8,20,27,50,51,55,56,59).Although the cardiovascular responses to acute hypoxemia or asphyxia are known to change between mid and late gestation (7,30,33,34,64,65), no study has investigated developmental changes in cardiovascular responses to hy- …”

mentioning

confidence: 99%

mentioning

confidence: 99%

Development of the ovine fetal cardiovascular defense to hypoxemia towards full term

Fletcher¹,

Gardner²,

Edwards³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

. Development of the ovine fetal cardiovascular defense to hypoxemia towards full term. Am J Physiol Heart Circ Physiol 291: H3023-H3034, 2006. First published July 21, 2006 doi:10.1152/ajpheart.00504.2006.-We tested the hypothesis that fetal cardiovascular responses to hypoxemia change close to full term in relation to the prepartum increase in fetal basal cortisol and investigated, in vivo, the neural and endocrine mechanisms underlying these changes. Fetal heart rate and peripheral hemodynamic responses to 1 h of hypoxemia were studied in 25 chronically instrumented sheep within three narrow gestational age ranges: 125-130 (n ϭ 13), 135-140 (n ϭ 6), and Ͼ140 (n ϭ 6) days (full term ϳ145 days). Chemoreflex function and plasma concentrations of vasoconstrictor hormones were measured. Reductions in fetal arterial PO2 during hypoxemia were similar at all ages. At 125-130 days, hypoxemia elicited transient bradycardia, femoral vasoconstriction, and increases in plasma concentrations of catecholamines, neuropeptide Y (NPY), AVP, ACTH, and cortisol. Close to full term, in association with the prepartum increase in fetal basal cortisol, there was a developmental increase in the magnitude and persistence of fetal bradycardia and in the magnitude of the femoral constrictor response to hypoxemia. The mechanisms mediating these changes close to full term included increases in the gain of chemoreflex function and in the magnitudes of the fetal NPY and AVP responses to hypoxemia. Data combined irrespective of gestational age revealed significant correlations between fetal basal cortisol and fetal bradycardia, femoral resistance, chemoreflex function, and plasma AVP concentrations. The data show that the fetal cardiovascular defense to hypoxemia changes in pattern and magnitude just before full term because of alterations in the gain of the neural and endocrine mechanisms mediating them, in parallel with the prepartum increase in fetal basal cortisol.fetus; prepartum cortisol surge; glucocorticoid IN ALL MAMMALIAN SPECIES studied to date, fetal basal cortisol concentration increases immediately before full term (23). In the ovine fetus, this increase in plasma cortisol begins in the last 15 days of gestation, at ϳ130 days (full term ϳ145 days) (3, 43), and increases most dramatically within the last 5 days before delivery, between 140 and 145 days. The prepartum cortisol surge is known to be an important factor in the developmental maturation of fetal tissues and physiological systems in preparation for the transition to neonatal life (23). For example, the prepartum maturation of basal cardiovascular function in the fetus is influenced by cortisol. The developmental increase in ovine fetal mean arterial blood pressure (FBP) and fall in fetal heart rate (FHR) are prevented by fetal adrenalectomy and restored to normal by cortisol replacement (63). Similarly, the prepartum cortisol surge has been associated with developmental changes in the basal activity of many fetal endocrine vasoconstrictor mechanisms, such as the norad...

show abstract

“…Persistent hypoxemia produces a redistribution of fetal cardiac output, which in turn is thought to result in asymmetrical fetal growth patterns. Richardson et al (1996) reported that redistribution effects in response to a sustained hypoxic insult (8 h) were qualitatively similar for both preterm and nearterm ovine fetuses. To sustain this redistribution, peripheral vasoconstriction in the fetus must be essentially maintained by sustaining hormonal effects.…”

Section: Discussionmentioning

confidence: 99%

“…Relatively few studies (Akagi and Challis 1990b;Carter et al 1998;Iwamoto et al 1989;Matsuda et al 1992;Richardson et al 1996) have been conducted in fetal sheep or goats at such early stages of development. We investigated fetal responses to sustained hypoxemia with pO 2 values around 15 mmHg for a duration of 24 h. Continuous infusion of nitrogen through the maternal tracheal catheter allowed us to rapidly and accurately adjust fetal pO 2 to the desired level.…”

Section: Discussionmentioning

confidence: 99%

Stress Hormone Responses During 24-Hour Hypoxemia in Preterm Goat Fetus

Fujimori

Takanashi²,

Endo³

et al. 2008

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Fetal endocrinological responses to chronic hypoxemia are useful in elucidating the process of growth restriction at earlier stages of fetal development. The purpose of this study was to observe endocrinological responses to prolonged (24-h) non-acidemic hypoxemia in preterm goat fetuses. Fetal hormonal changes were examined in chronically instrumented goat fetuses at gestational day 96-102 (0.7 gestation) during continuous nitrogen infusion into the maternal trachea to create prolonged fetal hypoxemia. Plasma levels of arginine vasopressin (AVP), epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH) and cortisol were measured, along with fetal heart rate (FHR) and fetal blood pressure (FBP). Fetal arterial pO 2 declined significantly from 25.0 ± 1.0 mmHg at baseline to 15.3 ± 1.0 mmHg after 2 h of hypoxemia, then remained at this level. FHR increased significantly throughout the experiment, but FBP remained unchanged. AVP and ACTH levels rose significantly after 2 h of hypoxemia, and declined to the control values after 12 h. There was no significant increase in the epinephrine level during 24-hr hypoxemia. In contrast, norepinephrine significantly increased after 2 h of hypoxemia and remained at the elevated levels throughout the remainder of the experiment. Thus, preterm fetuses could respond to acute hypoxic stress by increasing the plasma levels of AVP, norepinephrine and ACTH. However, despite the rapid increase in ACTH, the level of cortisol in the fetal plasma was significantly elevated only after 18 h of hypoxemia. The chemoreceptors of preterm fetuses, which regulate the release of cortisol or epinephrine, may be less sensitive to hypoxic insults. goat fetus; hypoxia; arginine vasopressin; catecholamines; cortisol.Tohoku

show abstract

Regional Blood Flow and the Endocrine Response to Sustained Hypoxemia in the Preterm Ovine Fetus

Cited by 33 publications

References 14 publications

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Cardiac output distribution in response to hypoxia in the chick embryo in the second half of the incubation time

Development of the ovine fetal cardiovascular defense to hypoxemia towards full term

Stress Hormone Responses During 24-Hour Hypoxemia in Preterm Goat Fetus

Contact Info

Product

Resources

About