Fetal heart rate, arterial pressure, and blood volume responses to cortisol infusion

1987 ◽  
Vol 253 (6) ◽  
pp. R904-R909 ◽  
Author(s):  
C. E. Wood ◽  
C. Y. Cheung ◽  
R. A. Brace

The purpose of this study was to determine whether physiological amounts of cortisol affect the fetal cardiovascular system. Cortisol (4 micrograms/min) or the vehicle was infused intravenously for 5 h into six chronically catheterized sheep fetuses at 127-143 days gestation (term = 145-150 days). In the cortisol-infused animals, plasma cortisol concentration increased from 2.0 +/- 0.6 (SE) to 8.3 +/- 0.9 ng/ml. There was a concomitant decrease in fetal heart rate of 38 beats/min (P less than 1 X 10(-6)) and an increase in arterial pressure. Estimated blood volume decreased by 6% in the cortisol-infused fetuses compared with the vehicle-infused animals (P less than 1 X 10(-4]. In addition, plasma norepinephrine and epinephrine concentrations decreased to 70% of control at the end of the 5-h cortisol infusion, whereas plasma renin concentration decreased to 34% of control. The simultaneous increase in fetal arterial pressure and decrease in estimated blood volume suggest that fetal vascular resistance increased, whereas vascular compliance and/or nonstressed vascular volume decreased. However, this does not appear to be mediated by increases in circulating vasoconstrictor hormone concentrations or increased sympathetic tone. Thus the present study shows that physiological amounts of cortisol have significant effects on the fetal cardiovascular system but the mechanisms are unknown.

1973 ◽  
Vol 216 (1) ◽  
pp. 15-22 ◽  
Author(s):  
S. E. Cloeren ◽  
T. H. Lippert ◽  
R. Fridrich

1982 ◽  
Vol 243 (3) ◽  
pp. R433-R444 ◽  
Author(s):  
F. H. Lawler ◽  
R. A. Brace

We attempted to shed light on the characterization and control of fetal arterial pressure and fetal heart rate in the chronically catheterized fetal lamb. To do this we continuously recorded fetal and maternal arterial pressures and heart rates as well as amniotic fluid pressures using on-line computer techniques. The data were analyzed for histogram distributions, correlations and regressions, and for intrinsic rhythms within each variable. We found the following: 1) neither fetal nor maternal variables are normally distributed because of an exaggerated mode and frequent skewing to the right, 2) there was no correlation between fetal and maternal variables over time periods of 10 min to 24 h, 3) a positive correlation exists between fetal arterial pressure and fetal heart rate, 4) there were no major rhythms in the fetal or maternal variables or in amniotic fluid pressure with cycles between 10 min and 24 h. The data suggest that 1) fetal arterial pressure and heart rate are largely independent of the mother, 2) fetal and maternal variables are well controlled about a physiological set point, and 3) rhythms in fetal arterial pressure and heart rate are not significant under normal laboratory conditions.


2009 ◽  
Vol 296 (6) ◽  
pp. R1813-R1819 ◽  
Author(s):  
Charles E. Wood ◽  
Melanie Powers Fraites ◽  
Maureen Keller-Wood

Decreases in fetal blood pressure stimulate homeostatic stress responses that help return blood pressure to normal levels. Fetal hypothalamus-pituitary-adrenal (HPA) axis responses to hypotension are mediated by chemoreceptor and baroreceptor reflexes and ischemia of the fetal central nervous system. Indomethacin, a nonselective inhibitor of prostaglandin endoperoxide synthase (PGHS)-1 and -2, attenuates the HPA response to hypotension in the fetus. The present study was designed to test the hypothesis that selective inhibition of PGHS-2 also inhibits the HPA response to cerebral hypoperfusion. We studied 13 chronically catheterized fetal sheep (126–136 days gestation). Five fetal sheep were subjected to intracerebroventricular infusion of nimesulide (0.01 mg/day), a specific inhibitor of PGHS-2, and eight were treated with vehicle (DMSO in water) for 5 days. Each fetus was subjected to a 10-min period of brachiocephalic occlusion, which decreased carotid arterial pressure ∼75% and reflexively increased fetal plasma concentrations of ACTH, POMC, cortisol, and femoral arterial pressure, and decreased fetal heart rate. Nimesulide significantly inhibited the ACTH response to the BCO, while significantly augmenting the reflex cardiovascular response and altering fetal heart rate variability consistent with increased sympathetic nervous system activity. The results of this study demonstrate that the activity of PGHS-2 in the brain is a necessary component of the fetal HPA response to cerebral hypoperfusion in the late-gestation fetal sheep. These results are consistent with those of recent study, in which we demonstrated that the preparturient increase in fetal ACTH secretion depends upon PGHS-2 activity within the fetal brain.


Author(s):  
Joanne Haroutounian

Alullaby winds its way through the intimate confines of the nursery, as a restless baby is soothed to sleep. The rhythm and rocking chair synchronize a pulse as a mother sings softly to her child. The baby listens to the gentle flow of the melody, which drifts into a hum that vibrates against the sleeping child’s tiny head. A few short years later, Mom smiles as she looks in to her three-year-old’s room. Her daughter is nestled in the same rocking chair, singing a rather lopsided version of the same lullaby, gently stroking a rag doll wrapped in a frayed old baby blanket. Children listen before they are born. They are aware of their mother’s heartbeat and the different environmental sounds that filter into the cozy womb. They are surrounded by the low-pitched pulsating sounds of their mother’s cardiovascular system at work. Studies show that pregnant singers find their babies much quieter when they are singing. Instrumentalists report the opposite effect, with lots of internal activity when they are performing. Even before birth, a child recognizes the sound of a mother’s voice and responds to music or familiar sounds. Prenatal studies abound that can measure the movements and startle reflexes of these yet-to-be-born listeners. Loud, sudden noises (above 100 db) cause the fetal heart to beat faster and an immediate startle response. One experiment zapped 15 seconds of a Bach organ prelude (at 100 db) through headphones nestled close to a mother’s abdomen. Not surprisingly, the fetal heart rate accelerated within five seconds of this musical stimulation. Once a baby is born, the effects of these prenatal sounds still have an influence on behavior. Studies of newborns by Salk in the 1960s resulted in the popularity of crib devices that play the sound of an adult heartbeat to soothe babies to sleep. Other studies show the same soothing effect for seven-day-old neonates listening to taped sounds of intrauterine background noises. From birth, the mother’s voice is distinguished from other women’s voices and recognized more readily than the father’s voice—again stemming from prenatal listening experiences.


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