Peripheral chemoreflex activation and cardiac function during hypoxemia in near term fetal sheep without placental compromise

2021 ◽  
Author(s):  
Juulia Lantto ◽  
Tiina Erkinaro ◽  
Mervi Haapsamo ◽  
Heikki Huhta ◽  
Leena Alanne ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Carotid Artery ◽  
Arterial Oxygen ◽  
Sheep Model ◽  
Fetal Sheep ◽  
Descending Aorta ◽  
Arterial Blood ◽  
Near Term ◽  
Peripheral Chemoreflex

A drop in arterial oxygen content activates fetal chemoreflex including an increase in sympathetic activity leading to peripheral vasoconstriction and redistribution of blood flow to protect the brain, myocardium, and adrenal glands. By using a chronically instrumented fetal sheep model with intact placental circulation at near-term gestation, we investigated the relationship between peripheral chemoreflex activation induced by hypoxemia and central hemodynamics. 17 Åland landrace sheep fetuses at 115-128/145 gestational days were instrumented. Carotid artery was catheterised in 10 fetuses and descending aorta in 7 fetuses. After a 4-day recovery, baseline measurements of fetal arterial blood pressures, blood gas values, and fetal cardiovascular hemodynamics by pulsed Doppler ultrasonography were obtained under isoflurane-anesthesia. Comparable data to baseline was collected 10 (acute hypoxemia) and 60 minutes (prolonged hypoxemia) after maternal hypo-oxygenation to saturation level of 70-80% was achieved. During prolonged hypoxemia, pH and base excess (BE) were lower, and lactate levels higher in the descending aorta than in the carotid artery. During hypoxemia mean arterial blood pressure (MAP) in the descending aorta increased, while in the carotid artery MAP decreased. In addition, right pulmonary artery pulsatility index values increased, and the diastolic component in the aortic isthmus blood flow velocity waveform became more retrograde. Both fetal ventricular cardiac outputs were maintained even during prolonged hypoxemia when significant fetal metabolic acidemia developed. Fetal chemoreflex activation induced by hypoxemia decreased the perfusion pressure in the cerebral circulation. Fetal weight-indexed LVCO or AoI Net Flow-ratio did not correlate with a drop in carotid artery blood pressure.

Effects of l-Epinephrine and l-Norepinephrine on the Splanchnic Bed of Intact Dogs

1957 ◽  
Vol 189 (3) ◽  
pp. 576-579 ◽  
Author(s):  
E. Allbaugh Farrand ◽  
R. Larsen ◽  
Steven M. Horvath
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Splanchnic Blood Flow ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Metabolic Functions ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Change In Mean ◽  
Infusion Period

The changes in splanchnic blood flow and related metabolic functions which occurred as the result of the infusion of 0.1 µg/kg/min. of l-epinephrine and l-norepinephrine for 10 minutes were measured in anesthetized dogs. l-Epinephrine elicited a marked increase in estimated splanchnic blood flow and no change in mean arterial pressure. While a significantly increased mean arterial blood pressure was observed following the administration of l-norepinephrine, no change in estimated splanchnic blood flow occurred. Arterial oxygen content was increased significantly with both drugs. Utilization of oxygen by the splanchnic bed was not changed during the infusion of either drug but was increased during the postepinephrine infusion period.

Cerebrovascular effects of intravenous dopamine infusions in fetal sheep

2002 ◽  
Vol 92 (2) ◽  
pp. 717-724 ◽  
Author(s):  
Christine A. Gleason ◽  
Roderick Robinson ◽  
Andrew P. Harris ◽  
Dennis E. Mayock ◽  
Richard J. Traystman
Keyword(s):  
Blood Pressure ◽  
Sch 23390 ◽  
Adrenergic Blockade ◽  
Receptor Blockade ◽  
Fetal Sheep ◽  
Dopamine Infusion ◽  
Cerebral Vasoconstriction ◽  
Arterial Blood ◽  
Near Term ◽  
Few Data

Preterm infants are often treated with intravenous dopamine to increase mean arterial blood pressure (MAP). However, there are few data regarding cerebrovascular responses of developing animals to dopamine infusions. We studied eight near-term and eight preterm chronically catheterized unanesthetized fetal sheep. We measured cerebral blood flow and calculated cerebral vascular resistance (CVR) at baseline and during dopamine infusion at 2.5, 7.5, 25, and 75 μg · kg−1 · min−1. In preterm fetuses, MAP increased only at 75 μg · kg−1 · min−1 (25 ± 5%), whereas in near-term fetuses MAP increased at 25 μg · kg−1 · min−1 (28 ± 4%) and further at 75 μg · kg−1 · min−1 (51 ± 3%). Dopamine infusion was associated with cerebral vasoconstriction in both groups. At 25 μg · kg−1 · min−1, CVR increased 77 ± 51% in preterm fetuses and 41 ± 11% in near-term fetuses, and at 75 μg · kg−1 · min−1, CVR increased 80 ± 33% in preterm fetuses and 83 ± 21% in near-term fetuses. We tested these responses to dopamine in 11 additional near-term fetuses under α-adrenergic blockade (phenoxybenzamine, n = 5) and under dopaminergic D1-receptor blockade (SCH-23390, n = 6). Phenoxybenzamine completely blocked dopamine's pressor and cerebral vasoconstrictive effects, while D1-receptor blockade had no effect. Therefore, in unanesthetized developing fetuses, dopamine infusion is associated with cerebral vasoconstriction, which is likely an autoregulatory, α-adrenergic response to an increase in blood pressure.

Cardiovascular Hemodynamics Consequence to Crossed Circulation in the Dog

1958 ◽  
Vol 192 (2) ◽  
pp. 345-352 ◽  
Author(s):  
W. J. Roberson ◽  
Steven M. Horvath
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Carotid Artery ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Diastolic Pressure ◽  
Recovery Period ◽  
Arterial Blood ◽  
The Mean

Twelve experiments were conducted on anesthetized and paired dogs of similar weights subjected to unimpeded, unregulated crossed circulation. Shunts were made between the carotid arteries and external jugular veins and free flow allowed for 60 minutes or longer. Statistically significant changes occurred in the mean femoral arterial blood pressures, carotid shunt blood flow, heart rate, cardiac output, cardiac work, percentage of cardiac output flowing through the shunt and pulmonary systolic and diastolic pressures of one or both animals from their control values. The mean arterial blood pressure remained at control levels for several minutes and then dropped precipitously to hypotensive levels. The lowest mean pressures between 42 and 49 mm Hg occurred within the first 16.5 minutes of the open shunt phase with a gradual return toward control levels. The volume of blood flowing through the shunt was increased initially 250% above the control carotid blood flow, followed by a reduction in flow after 15 minutes; the volume flow at this moment was still double precross circulation levels. A secondary increase in the shunt blood flow occurred throughout the remainder of the open shunt phase. In general, the heart rates and peripheral vascular resistance were slightly elevated during the open shunt phase while cardiac output and work decreased below their control values. A marked and similar increase in the percentage of the cardiac output flowing through the carotid artery was observed in both animals. During the 60 minutes of the recovery period mean arterial blood pressure, cardiac output and work tended to return to control levels while the carotid artery blood flow and pulmonary systolic and diastolic pressure remained slightly below their control values.

Distribution of cardiac output in ovine pregnancy

1977 ◽  
Vol 232 (3) ◽  
pp. H231-H235 ◽  
Author(s):  
C. R. Rosenfeld
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mammary Gland ◽  
Maternal Weight ◽  
Blood Flows ◽  
Arterial Blood ◽  
Near Term ◽  
Distribution Of Cardiac Output

Cardiac output and organ blood flows were measured in 6 nonpregnant and 24 pregnant ewes from 38 to 141 days of gestation employing radionuclide-labeled microspheres. From the nonpregnant state to term increases in cardiac output, from 73.7 +/- 4.6 ml/min-kg of maternal weight to 148 +/- 2.4 ml/min-kg, and heart rate, from 88.5 +/- 10.3 to 106 +/- 4.6 beats/min, were noted, while mean arterial blood pressure was unchanged. Near term, the blood flows to the uterus and mammary gland represented approximately 18% of cardiac output. The blood flow to nonreproductive organs increased from 76.6 +/- 6.8 ml/min-kg of nonreproductive tissue in the nonpregnant state to 132 +/- 3.5 ml/min-kg at 130-140 days' gestation (P less than 0.01). No significant changes in renal blood flow were detected.

Fetal ACTH and blood pressure responses to thromboxane mimetic U-46619

1993 ◽  
Vol 265 (4) ◽  
pp. R858-R862 ◽  
Author(s):  
C. E. Wood ◽  
T. A. Cudd ◽  
C. Kane ◽  
K. Engelke
Keyword(s):  
Blood Pressure ◽  
Central Nervous System ◽  
Nervous System ◽  
Carotid Artery ◽  
Common Carotid Artery ◽  
Thromboxane A2 ◽  
Renin Secretion ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Carotid Arterial

This study was performed to test the hypothesis that thromboxane A2 stimulates increases in fetal adrenocorticotropic hormone (ACTH), vasopressin, or renin secretion and affects fetal cardiovascular function by an action on the fetal central nervous system. We infused a stable synthetic analogue of thromboxane A2, U-46619, into one common carotid artery or inferior vena cava or infused saline into one common carotid artery in chronically catheterized fetal sheep between 127 and 140 days gestation. We found that intracarotid but not intravenous infusions of U-46619 at a rate of 750 ng/min stimulated increases in fetal plasma ACTH concentration. Infusions of U-46619 at both sites increased fetal blood pressure; the infusion into the carotid arterial blood produced a more rapid increase in blood pressure and a significant decrease in central venous pressure. None of the infusions altered plasma vasopressin concentration or plasma renin activity, blood gases, hematocrit, or plasma cortisol concentration. We conclude that thromboxane A2 stimulates fetal ACTH, but not vasopressin or renin, secretion via an action within the area perfused by carotid arterial blood. Thromboxane A2 increases blood pressure via an action at the fetal central nervous system, as well as via a direct vasoconstrictor action in the systemic circulation.

Fetal cerebral and peripheral circulatory responses to hypoxia after nitric oxide synthase inhibition

2001 ◽  
Vol 281 (2) ◽  
pp. R381-R390 ◽  
Author(s):  
Andrew P. Harris ◽  
Sabah Helou ◽  
Christine A. Gleason ◽  
Richard J. Traystman ◽  
Raymond C. Koehler
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Treated Group ◽  
Arterial Oxygen ◽  
Control Group ◽  
Fetal Sheep ◽  
Arterial Oxygen Content ◽  
Arterial Blood ◽  
Nos Inhibitor ◽  
Oxide Synthase

The increase in cerebral blood flow (CBF) during hypoxia in fetal sheep at 0.6 gestation is less than the increase at 0.9 gestation when normalized for differences in baseline CBF and oxygen consumption. Nitric oxide (NO) synthase (NOS) catalytic activity increases threefold during this period of development. We tested the hypothesis that administration of the NOS inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) decreases the CBF response to systemic hypoxia selectively at 0.9 gestation. We also tested whether any peripheral vasoconstriction during hypoxia is potentiated byl-NAME at 0.9 gestation. Administration ofl-NAME increased arterial blood pressure and decreased microsphere-determined CBF during normoxia in fetal sheep at both 0.6 and 0.9 gestation. With subsequent reduction of arterial oxygen content by ∼50%, the percent increase in forebrain CBF in a control group (57 ± 11%; ± SE) and l-NAME-treated group (51 ± 6%) was similar at 0.6 gestation. Likewise, at 0.9 gestation, the increase in CBF was similar in control (90 ± 25%) andl-NAME (80 ± 28%) groups. At 0.9 gestation,l-NAME treatment attenuated the increase in coronary blood flow and increased gastrointestinal vascular resistance during hypoxia. We conclude that NO exerts a basal vasodilatory influence in brain as early as 0.6 gestation in fetal sheep but is not an important mechanism for hypoxic vasodilation in brain at either 0.6 or 0.9 gestation. Thus the developmental increase in NOS catalytic capacity does not appear to be responsible for developmental increases in the CBF response to hypoxia during this period. In contrast, NO modulates the vascular response to hypoxia in heart and gastrointestinal tract.

scholarly journals Interleukin-1 Blockade Attenuates White Matter Inflammation and Oligodendrocyte Loss After Progressive Systematic Lipopolysaccharide Exposure in Near-Term Fetal Sheep

2021 ◽  
Author(s):  
Sharmony B. Kelly ◽  
Vanesa Stojanovska ◽  
Valerie Zahra ◽  
Alison Moxham ◽  
Suzanne L Miller ◽  
...  
Keyword(s):  
White Matter ◽  
Carotid Artery ◽  
Interleukin 1 ◽  
Brain Maturation ◽  
Saline Control ◽  
Fetal Sheep ◽  
Eeg Activity ◽  
Arterial Blood ◽  
Near Term ◽  
Artery Perfusion

Abstract BackgroundIncreased systemic and tissue levels of interleukin(IL)-1β are associated with greater risk of impaired neurodevelopment after birth. In this study, we tested the hypothesis that systemic IL-1 receptor antagonist (Ra) administration can attenuate neuroinflammation and injury in near-term fetal sheep exposed to lipopolysaccharide (LPS). MethodsChronically instrumented near-term fetal sheep at 0.85 of gestation were randomly assigned to saline (control, n=9), LPS infusions (0 h=300 ng, 24 h=600 ng, 48 h=1200 ng, n=8) or LPS plus 3 infusions of IL-1Ra (13 mg/kg infused over 4 h) started 1 h after each LPS infusion (n=9). Sheep were euthanized 4 days after starting infusions for histology.ResultsLPS infusions were associated with electroencephalogram (EEG) suppression with transiently reduced mean arterial blood pressure, and increased carotid artery perfusion and fetal heart rate (P<0.05 vs. control). In the periventricular and intragyral white matter, LPS-exposure increased IL-1β immunoreactivity, apoptosis and microglial activation, and reduced astrocyte and total oligodendrocyte survival, but did not change myelin expression or numbers of neurons in the cortex and subcortical regions. IL-1Ra infusions reduced circulating cytokines and improved recovery of EEG activity and carotid artery perfusion. Histologically, IL-1Ra reduced microgliosis, IL-1β expression and apoptosis, and improved total oligodendrocyte survival.ConclusionIL-1Ra improved EEG activity and markedly attenuated systemic inflammation, microgliosis and oligodendrocyte loss, but did not improve survival of astrocytes after LPS-induced inflammation in near-term fetal sheep. Further studies of long term brain maturation are now needed.

Responses of fetal sheep to simulated no-decompression dives

1980 ◽  
Vol 48 (5) ◽  
pp. 776-780 ◽  
Author(s):  
M. K. Stock ◽  
E. H. Lanphier ◽  
D. F. Anderson ◽  
L. C. Anderson ◽  
T. M. Phernetton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Maternal Blood ◽  
Arterial System ◽  
Fetal Sheep ◽  
Monitoring Result ◽  
Placental Blood ◽  
Near Term ◽  
Placental Blood Flow ◽  
Maternal Blood Pressure

The effect of simulated standard no-decompression dives to 60 and 100 ft of seawater was tested in 12 near term sheep carrying 16 fetuses. In the immediate postdive period there were no significant changes in fetal blood pressure or fetal placental or renal blood flow, but the maternal blood pressure was elevated and the maternal placental blood flow was depressed. Six surgically prepared fetuses were dived to 100 ft. Five died within 20 min of ascent and the sixth suffered severe cardiac arrhythmia and hypotension. At autopsy all fetuses were observed to have massive bubbling in the arterial system and heart. Five fetuses were dived to 100 ft without surgery. Two were alive 3 h later and no bubbles were present at autopsy, and three were born alive at term. With the 60-ft dives, three fetuses were subjected to surgery and all suffered massive bubbling. Two fetuses were dived to 60 ft without surgery; one was alive after 3 h and the other was born alive at term. We conclude that surgery and monitoring result in the formation of postdive gas bubbles that would not otherwise appear.

scholarly journals Does Maturity Affect Cephalic Perfusion and T/QRS Ratio during Prolonged Umbilical Cord Occlusion in Fetal Sheep?

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Guido Wassink ◽  
Robert Galinsky ◽  
Paul P. Drury ◽  
Eleanor R. Gunn ◽  
Laura Bennet ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Metabolic Acidosis ◽  
Umbilical Cord ◽  
Fetal Sheep ◽  
Fetal Asphyxia ◽  
Arterial Blood ◽  
Rapid Fall ◽  
Severe Hypotension ◽  
Fetal Compromise

T/QRS ratio monitoring is used to help identify fetal asphyxia. However, immature animals have greater capacity to maintain blood pressure during severe asphyxia, raising the possibility that they may show an attenuated T/QRS increase during asphyxia. Chronically instrumented fetal sheep at 0.6 of gestation (0.6 GA;n= 12), 0.7 GA (n= 12), and 0.8 GA (n= 8) underwent complete umbilical cord occlusion for 30 min, 25 min, or 15 min, respectively. Cord occlusion was associated with progressive metabolic acidosis and initial hypertension followed by severe hypotension, with a more rapid fall in mean arterial blood pressure (MAP) and carotid blood flow (CaBF) with advancing gestation. T/QRS ratio rose after occlusion more rapidly at 0.8 GA than in immature fetuses, to a similar final peak at all ages, followed by a progressive fall that was slower at 0.8 GA than in the immature fetuses. The increase in T/QRS ratio correlated with initial hypertension at 0.8 GA (P<0.05,R2= 0.38), and conversely, its fall correlated closely with falling MAP in all gestational groups (P<0.01,R2= 0.67). In conclusion, elevation of the T/QRS ratio is an index of onset of severe asphyxia in the last third of gestation, but not of fetal compromise.

Renal sympathetic nerve activity during asphyxia in fetal sheep

2012 ◽  
Vol 303 (1) ◽  
pp. R30-R38 ◽  
Author(s):  
Lindsea C. Booth ◽  
Simon C. Malpas ◽  
Carolyn J. Barrett ◽  
Sarah-Jane Guild ◽  
Alistair J. Gunn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Fetal Sheep ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Near Term ◽  
Renal Sympathetic

The sympathetic nervous system (SNS) is an important mediator of fetal adaptation to life-threatening in utero challenges, such as asphyxia. Although the SNS is active well before term, SNS responses mature significantly over the last third of gestation, and its functional contribution to adaptation to asphyxia over this critical period of life remains unclear. Therefore, we examined the hypotheses that increased renal sympathetic nerve activity (RSNA) is the primary mediator of decreased renal vascular conductance (RVC) during complete umbilical cord occlusion in preterm fetal sheep (101 ± 1 days; term 147 days) and that near-term fetuses (119 ± 0 days) would have a more rapid initial vasomotor response, with a greater increase in RSNA. Causality of the relationship of RSNA and RVC was investigated using surgical (preterm) and chemical (near-term) denervation. All fetal sheep showed a significant increase in RSNA with occlusion, which was more sustained but not significantly greater near-term. The initial fall in RVC was more rapid in near-term than preterm fetal sheep and preceded the large increase in RSNA. These data suggest that although RSNA can increase as early as 0.7 gestation, it is not the primary determinant of RVC. This finding was supported by denervation studies. Interestingly, chemical denervation in near-term fetal sheep was associated with an initial fall in blood pressure, suggesting that by 0.8 gestation sympathetic innervation of nonrenal vascular beds is critical to maintain arterial blood pressure during the rapid initial adaptation to asphyxia.

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