scholarly journals Dopamine does not limit fetal cerebrovascular responses to hypoxia

2007 ◽  
Vol 102 (1) ◽  
pp. 130-134 ◽  
Author(s):  
Dennis E. Mayock ◽  
Rachel Bennett ◽  
Roderick D. Robinson ◽  
Christine A. Gleason
Keyword(s):  
Infusion Rate ◽  
Perfusion Pressure ◽  
High Dose ◽  
Fetal Hypoxia ◽  
Fetal Sheep ◽  
Dopamine Infusion ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Cerebral Vasodilatation ◽  
Near Term

Dopamine is used clinically to stabilize mean arterial blood pressure (MAP) in sick infants. One goal of this therapeutic intervention is to maintain adequate cerebral blood flow (CBF) and perfusion pressure. High-dose intravenous dopamine has been previously demonstrated to increase cerebrovascular resistance (CVR) in near-term fetal sheep. We hypothesized that this vascular response might limit cerebral vasodilatation during acute isocapnic hypoxia. We studied nine near-term chronically catheterized unanesthetized fetal sheep. Using radiolabeled microspheres to measure fetal CBF, we calculated CVR at baseline, during fetal hypoxia, and then with the addition of an intravenous dopamine infusion at 2.5, 7.5, and 25 μg·kg−1·min−1 while hypoxia continued. During acute isocapnic fetal hypoxia, CBF increased 73.0 ± 14.1% and CVR decreased 38.9 ± 4.9% from baseline. Dopamine infusion at 2.5 and 7.5 μg·kg−1·min−1, begun during hypoxia, did not alter CVR or MAP, but MAP increased when dopamine infusion was increased to 25 μg·kg−1·min−1. Dopamine did not alter CBF or affect the CBF response to hypoxia at any dose. However, CVR increased at a dopamine infusion rate of 25 μg·kg−1·min−1. This increase in CVR at the highest dopamine infusion rate is likely an autoregulatory response to the increase in MAP, similar to our previous findings. Therefore, in chronically catheterized unanesthetized near-term fetal sheep, dopamine does not alter the expected cerebrovascular responses to hypoxia.

Cerebrovascular autoregulation during fetal development in sheep

1994 ◽  
Vol 266 (3) ◽  
pp. H1069-H1074 ◽  
Author(s):  
S. Helou ◽  
R. C. Koehler ◽  
C. A. Gleason ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Perfusion Pressure ◽  
Fetal Brain ◽  
Blood Gases ◽  
Fetal Sheep ◽  
Cerebrovascular Autoregulation ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Near Term

There are scant data regarding the development of cerebrovascular autoregulation in fetuses. We tested the hypothesis that a decrease in cerebrovascular resistance (CVR) at reduced cerebral perfusion pressure (CPP) is absent in midgestation and near-term fetal sheep. Catheters were chronically implanted for microsphere determination of cerebral blood flow (CBF) in 9 fetuses at 92 days and in 10 fetuses at 132 days gestation (full term = 145 days). CPP was reduced by ventricular infusion of artificial cerebrospinal fluid. In 92-day fetuses, CPP was reduced stepwise from 35 to 25 and 18 mmHg and CBF decreased from 52 +/- 5 to 43 +/- 4 and 27 +/- 5 (SE) ml.min-1 x 100 g-1, respectively. Half of the immature fetuses showed some reduction in CVR at moderate reduction in CPP; however, there was no significant change in CVR in the group as a whole (from 0.72 +/- 0.06 to 0.61 +/- 0.04 and 0.89 +/- 0.20 mmHg.ml-1.min.100 g). In 132-day fetuses, CPP was reduced from 45 to 33 and 28 mmHg and CBF was unchanged (from 105 +/- 7 to 97 +/- 11 and 89 +/- 8 ml.min-1 x 100 g-1). CVR decreased from 0.45 +/- 0.05 to 0.41 +/- 0.08 and 0.33 +/- 0.03 mmHg.ml-1.min.100 g. There were no significant changes in arterial blood gases at reduced CPP in either age group. We conclude that cerebrovascular autoregulation at reduced CPP is not well developed at 92 days (0.63 gestation) in fetal sheep but that autoregulatory capacity is evident near term. We speculate that poor autoregulation may place the premature fetal brain at risk for injury.

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.

Fetal responses to acute fetal cocaine injection in sheep

1994 ◽  
Vol 267 (5) ◽  
pp. H1968-H1975 ◽  
Author(s):  
H. Iida ◽  
C. A. Gleason ◽  
T. P. O'Brien ◽  
R. J. Traystman
Keyword(s):  
Fetal Sheep ◽  
Blood Flows ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Cerebral O2 Consumption ◽  
O2 Extraction ◽  
Near Term ◽  
Group 2 ◽  
Arterial Po2 ◽  
Group 1

Maternal cocaine injection causes fetal hypoxemia, hypertension, and increased cerebral blood flow (CBF) in sheep. To test the hypothesis that increased fetal CBF is not due solely to fetal hypoxemia, we injected cocaine directly into a fetal vein. A single dose of cocaine [1 (group 1; n = 7) or 2 (group 2; n = 8) mg/kg i.v.] was administered to chronically catheterized, unanesthetized, near-term fetal sheep. Fetal CBF (microspheres), arterial blood pressure (BP), O2 content, and cerebral O2 consumption (CMRo2) were measured at baseline, 30 s, and 2, 5, and 15 min after fetal cocaine injection. Fetal CBF increased 27 +/- 9% (SE) at 5 min in group 1 and returned to baseline by 15 min, whereas fetal CBF increased 57 +/- 8% at 5 min and remained elevated at 15 min in group 2. Fetal BP increased at 30 min in both groups and remained increased at 2 min in group 1 and at 5 min in group 2. Cerebrovascular resistance increased at 30 s in both groups and then decreased at 5 min only in group 2. Fetal hypoxemia was observed in group 2 5 min after cocaine injection (arterial PO2 decreased 24 +/- 5%), whereas no hypoxemia was noted in group 1. CMRO2 was unchanged in group 1 but increased in group 2 at 5 min (41 +/- 10%) and was associated with an increase in cerebral O2 extraction. Increases in myocardial and adrenal blood flows and reductions in both small and large intestinal blood flows were noted at 5 min in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Ontogeny of renal response to specific dopamine DA1-receptor stimulation in sheep

1992 ◽  
Vol 263 (4) ◽  
pp. R868-R873 ◽  
Author(s):  
J. L. Segar ◽  
F. G. Smith ◽  
E. N. Guillery ◽  
P. A. Jose ◽  
J. E. Robillard
Keyword(s):  
Sch 23390 ◽  
Plasma Renin ◽  
Fractional Excretion ◽  
Receptor Activation ◽  
Urinary Flow ◽  
Fetal Sheep ◽  
Plasma Aldosterone Concentration ◽  
Arterial Blood ◽  
Fractional Excretion Of Sodium ◽  
Near Term

The present study was designed to characterize the developmental changes in the renal responses to dopamine DA1-receptor activation in chronically instrumented preterm (109-115 days) and near-term (130-140 days, full term 145 days) fetal sheep. Cumulative doses of the selective DA1-agonist fenoldopam increased mean arterial blood pressure (MABP) in both preterm (+16 +/- 3%) and near-term fetuses (+16 +/- 3%) but had no significant effect on renal blood flow velocity. Infusion of the DA1-antagonist SCH-23390 did not affect the increase in MABP, suggesting that the effect of fenoldopam on MABP was not directly related to activation of DA1-receptors. Fenoldopam infusion had no significant effects on renal function parameters in preterm fetuses. In near-term fetuses, however, fenoldopam increased urinary flow rate (82.6 +/- 20.9%, P < 0.003), glomerular filtration rate (GFR; 16.6 +/- 4.9%, P < 0.01), urinary sodium excretion (40.1 +/- 14.9%, P < 0.02), and fractional excretion of sodium (26.8 +/- 11.2%, P < 0.03). Infusion of the DA1-antagonist SCH-23390 blocked the fenoldopam-induced diuresis and natriuresis but had no significant effect on the rise in GFR. Fenoldopam infusion had no significant effects on plasma renin activity and plasma aldosterone concentration and on urinary prostaglandin (PG) excretion (PGE2, PGF2 alpha, and 6-keto-PGF1 alpha). Taken together, these results suggest that the renal effect of DA1-receptor activation is age dependent and that stimulation of DA1-receptor in near-term fetuses is associated with a diuresis and natriuresis that seem to be independent of renal hemodynamics and adrenal effects.

scholarly journals Dopamine infusion for postresuscitation blood pressure support after profound asphyxia in near-term fetal sheep

2012 ◽  
Vol 98 (3) ◽  
pp. 699-709 ◽  
Author(s):  
Paul P. Drury ◽  
Lindsea C. Booth ◽  
Laura Bennet ◽  
Joanne O. Davidson ◽  
Bert Wibbens ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pressure Support ◽  
Fetal Sheep ◽  
Dopamine Infusion ◽  
Near Term

Effect of intracisternal phentolamine on cerebral blood flow after subarachnoid injection of blood

1976 ◽  
Vol 44 (3) ◽  
pp. 353-358 ◽  
Author(s):  
Albert N. Martins ◽  
Norwyn Newby ◽  
Thomas F. Doyle ◽  
Arthur I. Kobrine ◽  
Archimedes Ramirez
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Subarachnoid Injection ◽  
Ischemic Encephalopathy ◽  
Hydrogen Clearance

✓ The hydrogen clearance method was used to measure total and focal cerebral blood flow (CBF) in the monkey before and for 5 hours after a simulated subarachnoid hemorrhage (SAH). Some monkeys also received 0.2 to 1.0 mg/kg phentolamine intracisternally 3 hours after SAH. Results show that SAH did not change cerebrovascular resistance, but as cerebral perfusion pressure decreased, CBF fell transiently. Phentolamine injected intracisternally 3 hours after SAH produced a significant fall in arterial blood pressure; cerebrovascular resistance did not change but CBF decreased significantly. These data indicate that intracisternal phentolamine cannot be considered potentially useful to treat ischemic encephalopathy after SAH.

scholarly journals Deleterious Effects of High Dose Connexin 43 Mimetic Peptide Infusion After Cerebral Ischaemia in Near-Term Fetal Sheep

2012 ◽  
Vol 13 (5) ◽  
pp. 6303-6319 ◽  
Author(s):  
Joanne O. Davidson ◽  
Colin R. Green ◽  
Louise F. B. Nicholson ◽  
Laura Bennet ◽  
Alistair J. Gunn
Keyword(s):  
Cerebral Ischaemia ◽  
Connexin 43 ◽  
High Dose ◽  
Fetal Sheep ◽  
Mimetic Peptide ◽  
Near Term

Adenosine mediates hypoxic release of arginine vasopressin in fetal sheep

1994 ◽  
Vol 266 (1) ◽  
pp. R215-R220 ◽  
Author(s):  
B. J. Koos ◽  
B. A. Mason ◽  
M. G. Ervin
Keyword(s):  
Arginine Vasopressin ◽  
Diastolic Pressure ◽  
Vena Cava ◽  
High Dose ◽  
Slight Reduction ◽  
Fetal Sheep ◽  
Vasopressin Release ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Po2

The effects of adenosine on plasma arginine vasopressin (AVP) concentrations were determined in chronically catheterized fetal sheep (> 0.8 term). Infusion of adenosine [0.35 +/- 0.01 (SE) mg.min-1.kg-1] into the inferior vena cava of six fetuses caused a transient fall in arterial PO2 (by approximately 3 Torr), a slight reduction in arterial pH, and a 5- to 6-mmHg decrease in diastolic pressure without significantly affecting systolic or mean arterial values. A lower rate of infusion (0.19 +/- 0.01 mg.min-1 x kg-1) in five fetuses had virtually no effect on arterial blood gases, pH, or arterial pressures. Both the low- and high-dose adenosine infusions significantly increased fetal plasma AVP concentrations (1.7 +/- 0.2 to 25 +/- 7 pg/ml and 1.6 +/- 0.1 to 54 +/- 8 pg/ml, respectively). Intravenous infusion of papaverine lowered fetal diastolic and mean arterial pressures by approximately 8 mmHg but had no significant effect on plasma levels of AVP. During an hour of isocapnic hypoxia (arterial PO2 12-13 Torr), fetal plasma AVP levels increased from 1.7 +/- 0.2 to 40 +/- 6 pg/ml. Intra-arterial infusion of the adenosine receptor antagonist 8-(p-sulfophenyl)-theophylline significantly blunted the hypoxia-induced rise in plasma AVP concentrations to a maximum mean level of 11 +/- 6 pg/ml. These results indicate that 1) adenosine causes a dose-dependent increase in plasma AVP concentrations and 2) a hypoxia-induced rise in fetal adenosine levels triggers vasopressin release.

Fetal acidosis and hypotension during repeated umbilical cord occlusions are associated with enhanced chemoreflex responses in near-term fetal sheep

2005 ◽  
Vol 99 (4) ◽  
pp. 1477-1482 ◽  
Author(s):  
Laura Bennet ◽  
Jenny A. Westgate ◽  
Yung-Chi (“Jack”) Liu ◽  
Guido Wassink ◽  
Alistair J. Gunn
Keyword(s):  
Umbilical Cord ◽  
Fetal Heart ◽  
Severe Hypoxia ◽  
Acid Base ◽  
Fetal Sheep ◽  
Arterial Blood ◽  
Acid Base Status ◽  
Near Term ◽  
Fetal Acidosis ◽  
Fetal Compromise

This study examined the hypothesis that repeated episodes of brief but severe hypoxia would not attenuate the chemoreflex-mediated rapid initial fall in fetal heart rate (FHR) and, further, that greater hypoxic stress, as shown by hypotension and metabolic acidosis, would be associated with an enhanced chemoreflex response. Chronically instrumented, near-term fetal sheep received 1 min total umbilical cord occlusion either every 5 min for 4 h (1:5 group; n = 8) or every 2.5 min (1:2.5 group; n = 8) until mean arterial blood pressure fell to <20 mmHg on two successive occlusions. Umbilical cord occlusion caused variable decelerations, with sustained hypertension in the 1:5 group and little change in acid-base status (pH 7.34 ± 0.03 after 4 h). In contrast, the 1:2.5 group showed progressive hypotension and metabolic acidemia (pH 6.92 ± 0.04 after the last occlusion). The 1:2.5 group showed a significant increase in the rate of initial fall in FHR during the occlusion series, which was greater than the 1:5 group in the last 30 min of the occlusion series (9.4 ± 1.4 vs. 3.5 ± 0.3 beats·min−1·s−1; P < 0.01), with a greater fall in FHR (71.9 ± 6.5 vs. 47.0 ± 8.7 beats/min; P < 0.05). In summary, this study demonstrated that repetitive laborlike cord occlusions, which led to severe fetal compromise, were associated with an increase in the slope and magnitude of the initial FHR deceleration. These findings support the concept of the chemoreflex as a central, robust component of fetal adaptation to severe hypoxia.

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