Effect of prolonged catecholamine infusion on heart rate, blood pressure, breathing, and growth in fetal sheep

1995 ◽  
Vol 73 (12) ◽  
pp. 1750-1758 ◽  
Author(s):  
A. D. Bocking ◽  
S. E. White ◽  
S. Kent ◽  
L. Fraher ◽  
V. K. M. Man ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Fetal Heart Rate ◽  
Fetal Heart ◽  
Tissue Growth ◽  
Uterine Blood Flow ◽  
Epinephrine Infusion ◽  
Fetal Sheep ◽  
Norepinephrine Infusion

Norepinephrine and epinephrine were infused into fetal sheep for 24 h to compare the effects on fetal heart rate, blood pressure, breathing movements, and tissue growth with those of prolonged reductions in uterine blood flow. Norepinephrine concentrations increased (p < 0.01) from 871 ± 71 to 6831 ± 1090 pg/mL (2 h) with norepinephrine infusion, and epinephrine concentrations increased from 310 ± 95 to 1424 ± 288 pg/mL (2 h) with epinephrine infusion. Fetal pH decreased (p < 0.01) from 7.37 ± 0.01 to 7.29 ± 0.02 at 0.5 h of the norepinephrine infusion and returned to control values by 2 h, whereas fetal lactate concentrations increased (p < 0.05) from 1.6 ± 0.2 to 4.6 ± 1.0 mmol/L at 2 h and remained elevated for 12 h. Lactate concentrations also increased with epinephrine infusion. Fetal heart rate increased (p < 0.05) from 176 ± 5 to 246 ± 6 and 220 ± 6 beats/min in the 1st h of norepinephrine and epinephrine infusions, respectively, with a subsequent decline. Fetal blood pressure increased (p < 0.05) from 43 ± 3 and 40 ± 2 to 53 ± 3 and 47 ± 2 mmHg (1 mmHg = 133.3 Pa) during the 1st h of norepinephrine and epinephrine infusions, respectively, remaining elevated for 24 h. Fetal body weights were not different between the groups of animals, although liver/body weight ratio was less (p < 0.05) in epinephrine-infused fetuses (0.030 ± 0.001) compared with vehicle-infused animals (0.036 ± 0.002). There was no change in DNA synthesis rate in any of the fetal organs, despite changes in organ-specific DNA and protein content. Our results indicate that the changes in fetal cardiovascular and behavioural function, as well as tissue growth, that occur with prolonged reductions in uterine blood flow are not mediated solely by elevated circulating catecholamine concentrations.Key words: fetal physiology, catecholamines, pregnancy.

scholarly journals Blockade of PGHS-2 inhibits the hypothalamus-pituitary-adrenal axis response to cerebral hypoperfusion in the sheep fetus

2009 ◽  
Vol 296 (6) ◽  
pp. R1813-R1819 ◽  
Author(s):  
Charles E. Wood ◽  
Melanie Powers Fraites ◽  
Maureen Keller-Wood
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Arterial Pressure ◽  
Fetal Heart Rate ◽  
Fetal Heart ◽  
Cerebral Hypoperfusion ◽  
Fetal Sheep ◽  
Intracerebroventricular Infusion ◽  
Hpa Response

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.

scholarly journals Acute reduction of uterine blood flow and fetal heart rate changes in pregnant sheep near term

1977 ◽  
Vol 5 (1) ◽  
pp. 39-55 ◽  
Author(s):  
Heinz-Dieter Junge ◽  
Wolfgang Künzel ◽  
Friedrich Karl Klöck
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Fetal Heart Rate ◽  
Fetal Heart ◽  
Uterine Blood Flow ◽  
Pregnant Sheep ◽  
Near Term

scholarly journals Peripheral chemoreflex control of fetal heart rate decelerations overwhelms the baroreflex during brief umbilical cord occlusions in fetal sheep

2020 ◽  
Vol 598 (20) ◽  
pp. 4523-4536 ◽  
Author(s):  
Christopher A. Lear ◽  
Michi Kasai ◽  
Lindsea C. Booth ◽  
Paul P. Drury ◽  
Joanne O. Davidson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Umbilical Cord ◽  
Fetal Heart Rate ◽  
Fetal Heart ◽  
Fetal Sheep ◽  
Peripheral Chemoreflex

scholarly journals Large Conductance Ca2+-Activated and Voltage-Activated K+ Channels Contribute to the Rise and Maintenance of Estrogen-Induced Uterine Vasodilation and Maintenance of Blood Pressure

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 6012-6020 ◽  
Author(s):  
Charles R. Rosenfeld ◽  
Timothy Roy
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Uterine Artery ◽  
K Channel ◽  
Uterine Blood Flow ◽  
K Channels ◽  
Channel Inhibition ◽  
Estradiol 17Β ◽  
Cgmp Synthesis

Abstract Uterine blood flow (UBF) increases greater than 4-fold 90 min after systemic estradiol-17β (E2β) in nonpregnant sheep and remains elevated longer than 6–8 h; mean arterial pressure (MAP) is unchanged. Large-conductance Ca+2-activated (BKCa) and voltage-activated (KV) K+ channels contribute to the acute rise in UBF; their role in maintaining UBF and MAP longer than 90 min is unknown. We examined this in five nonpregnant, ovariectomized ewes with uterine artery (UA) flow probes and catheters in a UA for infusion of K+ channel inhibitors and uterine vein to sample venous effluent. Animals received systemic E2β (1.0 μg/kg; control), E2β+UA tetraethylammonium (TEA; 0.4–0.8 mm, n = 4), and E2β+UA 4-aminopyridine (4-AP; 0.01–0.08 mm, n = 4) to block BKCa and KV, respectively, while monitoring MAP, heart rate, and UBF. Uterine cGMP synthesis was measured. Ninety minutes after E2β, UBF rose 4.5-fold, uterine vascular resistance (UVR) fell greater than 5-fold and MAP was unchanged [78 ± 0.8 (sem) vs. 77 ± 1.5 mm Hg] in control studies and before UA inhibition with TEA and 4-AP. Between 90 and 120min, UBF, UVR, and MAP were unchanged after E2β alone. E2β+TEA dose dependently decreased ipsilateral UBF and increased UVR (24 ± 8.9 and 38 ± 16%, respectively, at 0.8 mm; P &lt; 0.03); MAP was unchanged. Contralateral UBF/UVR were unaffected. E2β+4-AP also dose dependently decreased ipsilateral UBF and increased UVR (27 ± 5.3 and 76 ± 18%, respectively, at 0.08 mm; P &lt; 0.001); however, MAP rose 27 ± 6.9% (P ≤ 0.006). E2β increased uterine cGMP synthesis greater than 3.5-fold and was unaffected by local K+ channel inhibition. BKCa and KV contribute to the rise and maintenance of E2β-induced uterine vasodilation, which is partially cGMP dependent. Systemic vascular KV also contributes to maintaining MAP after systemic E2β.

TELEMETRY OF FETAL HEART RATE AND MATERNAL BLOOD PRESSURE FROM HOME

1990 ◽  
Vol 18 (s1) ◽  
pp. 25-25
Author(s):  
K.J. Dalton ◽  
P. Mooney ◽  
W. Cartwright ◽  
H. Swindells ◽  
S. Rushant
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Fetal Heart Rate ◽  
Fetal Heart ◽  
Maternal Blood ◽  
Maternal Blood Pressure
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