Acute anemic hypoxemia produces a transient depression in fetal respiratory activity

1987 ◽  
Vol 63 (5) ◽  
pp. 1942-1946 ◽  
Author(s):  
J. M. Bissonnette ◽  
A. R. Hohimer
Keyword(s):  
Metabolic Rate ◽  
Respiratory Activity ◽  
Fetal Sheep ◽  
Control Value ◽  
Cerebral Metabolic Rate ◽  
O2 Concentration ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Sheep Fetus

Isovolemic anemia was produced in 11 unanesthetized fetal sheep by withdrawal of blood and replacement with saline-dextran. Fetal hematocrit fell from 36 +/- 1 to 19 +/- 1% (SE). Fetal breathing movements, which were present during 34.4 +/- 5.5% of 3 h before the anemia, occurred 10.1 +/- 5.3, 14.8 +/- 4.4, and 27.1 +/- 6.7% in the 3 h following. The anemia caused a fall in arterial O2 concentration from 8.4 +/- 0.3 to 3.6 +/- 0.1 vol% and sagittal vein PO2 fell from 15.4 +/- 0.5 to 12.4 +/- 0.3 Torr. Cerebral metabolic rate during the period of anemia was 2.9 +/- 0.1 ml.100 g-1.min-1, which was unchanged from the control value of 3.0 +/- 0.2 ml.100 g-1.min-1. Sagittal vein PCO2 (54.2 +/- 1.4 Torr) remained constant after the fetus was made anemic. We conclude that respiratory activity in the sheep fetus is depressed by anemic hypoxemia but that the effect is transient.

Behavioral activity during prolonged hypoxemia in fetal sheep

1988 ◽  
Vol 65 (6) ◽  
pp. 2420-2426 ◽  
Author(s):  
A. D. Bocking ◽  
R. Gagnon ◽  
K. M. Milne ◽  
S. E. White
Keyword(s):  
Blood Flow ◽  
Eye Movements ◽  
Normal Incidence ◽  
Behavioral Activity ◽  
Uterine Blood Flow ◽  
Fetal Sheep ◽  
Pregnant Sheep ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Internal Iliac

Experiments were conducted in unanesthetized, chronically catheterized pregnant sheep to determine the fetal behavioral response to prolonged hypoxemia produced by restricting uterine blood flow. Uterine blood flow was reduced by adjusting a vascular occluder placed around the maternal common internal iliac artery to decrease fetal arterial O2 content from 6.1 +/- 0.3 to 4.1 +/- 0.3 ml/dl for 48 h. Associated with the decrease in fetal O2 content, there was a slight increase in fetal arterial PCO2 and decrease in pH, which were both transient. There was an initial inhibition of both fetal breathing movements and eye movements but no change in the pattern of electrocortical activity. After this initial inhibition there was a return to normal incidence of both fetal breathing movements and eye movements by 16 h of the prolonged hypoxemia. These studies indicate that the chronically catheterized sheep fetus is able to adapt behaviorally to a prolonged decrease in arterial O2 content secondary to the restriction of uterine blood flow.

Rebound increase in fetal breathing movements after 24-h prostaglandin E2 infusion in fetal sheep

1996 ◽  
Vol 80 (1) ◽  
pp. 166-175 ◽  
Author(s):  
S. A. Hollingworth ◽  
S. A. Jones ◽  
S. L. Adamson
Keyword(s):  
Prostaglandin E2 ◽  
Plasma Concentrations ◽  
Treated Group ◽  
High Plasma ◽  
Fetal Sheep ◽  
Fetal Plasma ◽  
Pge2 Concentration ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Rebound Increase

We investigated the hypothesis that the precipitous decrease in prostaglandin E2 (PGE2), a potent inhibitor of fetal breathing, from high plasma concentrations during labor causes a rebound stimulation of breathing without newborn concentrations falling below prelabor fetal values. Fetal plasma PGE2 concentration was gradually increased from 384 +/- 82 (SE) pg/ml in 2-h steps [0 (baseline), 1.5, 3, and 6 micrograms/min] to labor levels (1,230 +/- 381 pg/ml at 6 micrograms/min) and then was maintained for 24 h (n = 9). PGE2 at 1.5 micrograms/min significantly decreased breathing incidence [from 42 +/- 4 (baseline) to 14 +/- 4%] and breath amplitude (from 2.1 +/- 0.5 to 1.5 +/- 0.2 arbitrary units) and increased breath-to-breath interval (from 1.16 +/- 0.07 to 1.56 +/- 0.06 s). No further dose-related changes were observed. During the first 2 h after PGE2 infusion was stopped, PGE2 concentration returned to basal (352 +/- 64 pg/ml) but breathing incidence and amplitude were significantly higher (74 +/- 8% and 2.4 +/- 0.3 arbitrary units, respectively) and breath-to-breath interval was significantly lower (0.95 +/- 0.10 s) than were basal levels. Changes arose within approximately 15 min and were maintained for at least 4 h. Breathing did not change significantly in the saline-treated group (n = 7). Results suggest that the rapid decrease in plasma PGE2 concentration at birth promotes the onset of breathing.

Hormonal and biophysical responses to acute hypoxemia in fetal sheep at 0.7–0.8 gestation

1990 ◽  
Vol 68 (12) ◽  
pp. 1527-1532 ◽  
Author(s):  
Kozo Akagi ◽  
John R. G. Challis
Keyword(s):  
Eye Movements ◽  
Arginine Vasopressin ◽  
Adrenocorticotropic Hormone ◽  
Minimal Change ◽  
Fetal Sheep ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Biophysical Changes

We examined whether there was a minimal change in fetal arterial [Formula: see text] necessary to elicit alterations in plasma adrenocorticotropic hormone, arginine vasopressin, or cortisol or to affect the incidence of breathing movements or eye movements in fetal sheep at 106–117 days of gestation. Fetal sheep were exposed to two levels of hypoxemia, mild (4.1 mmHg [Formula: see text] drop) (1 mmHg = 133.32 Pa) and moderate (8.4 mmHg [Formula: see text] drop), for 1 h without acidemia. Hypoxemia was induced by altering the inspired percent oxygen of the mother. No significant hormonal and biophysical changes were observed in mild hypoxemia. In moderate hypoxemia, there were significant increases of fetal adrenocorticotropic hormone and arginine vasopressin and decreased incidence of fetal breathing movements. However, there were no significant changes in cortisol or eye movements. We conclude that a fetal arterial [Formula: see text] drop of between 4.1 and 8.4 mmHg is necessary to elicit responses to hypoxemia in fetal sheep at 106–117 days of gestation in adrenocorticotropic hormone, arginine vasopressin, and fetal breathing movements, but this degree of hypoxemia does not cause changes in cortisol or fetal eye movements.Key words: fetal sheep, hypoxemia, adrenocorticotropic hormone, arginine vasopressin, cortisol, fetal breathing movements, fetal eye movements.

Fetal breathing, sleep state, and cardiovascular responses to graded hypoxia in sheep

1987 ◽  
Vol 62 (3) ◽  
pp. 1033-1039 ◽  
Author(s):  
B. J. Koos ◽  
H. Sameshima ◽  
G. G. Power
Keyword(s):  
Low Voltage ◽  
Cardiovascular Responses ◽  
Severe Hypoxia ◽  
Sleep State ◽  
Fetal Sheep ◽  
Fetal Bradycardia ◽  
O2 Concentration ◽  
Fetal Breathing ◽  
The Mean ◽  
Mild Hypoxia

Graded isocapnic hypoxemia was produced in unanesthetized fetal sheep by varying the inspired O2 concentration (21, 12, 10.5, and 9%) of the ewe. This produced corresponding mean preductal arterial O2 tension (PaO2) values of 25.2 +/- 1.1 (control), 20.1 +/- 1.0 (mild hypoxia), 17.8 +/- 0.9 (moderate hypoxia), and 16.8 +/- 1.4 Torr (severe hypoxia). These were associated with mean arterial O2 contents (CaO2) of 7.18 +/- 0.44, 5.19 +/- 0.34, 4.24 +/- 0.33, and 3.27 +/- 0.20 ml/dl, respectively. The most severe hypoxia was associated with metabolic acidosis and fetal bradycardia. Hypoxia did not reduce significantly the incidence of low-voltage electrocortical activity. The incidence of breathing and rapid eye movements was not affected by mild hypoxia; however, the incidence of both was significantly reduced during moderate and severe hypoxia. It is concluded that 1) acute reductions in the mean PaO2 of 5.9 +/- 0.6 Torr and CaO2 of 2.00 +/- 0.23 ml/dl are critical in that greater reductions inhibit fetal eye and breathing activity and 2) hypoxia probably inhibits eye and breathing movements by altering sleep state.

Effects of intracisternal monoamines on breathing movements in fetal sheep

1993 ◽  
Vol 264 (6) ◽  
pp. R1139-R1149
Author(s):  
S. A. Joseph ◽  
D. W. Walker
Keyword(s):  
Cerebrospinal Fluid ◽  
High Voltage ◽  
Large Amplitude ◽  
Rapid Onset ◽  
In Utero ◽  
Fetal Sheep ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Intracisternal Injection

The effects of intracisternal administration of tyramine on fetal breathing movements (FBM), electrocortical (ECoG) and nuchal muscle activities, and cerebrospinal fluid (CSF) monoamine concentrations have been studied in unanesthetized fetal sheep (124-140 days gestation) in utero. In 18 trials (8 fetuses) infusion of 50 or 100 micrograms/kg tyramine increased the incidence of FBM from 32.2 +/- 2.0 to 79.4 +/- 4.7%/h (P < 0.05) and increased mean breath amplitude from 6.4 +/- 0.4 to 11.8 +/- 1.6 mmHg (P < 0.05). FBM incidence during high-voltage ECoG activity increased from 3.3 +/- 0.6 to 22.5 +/- 3.6%/h (P < 0.05). Tyramine infusion (100 micrograms/kg) significantly increased (P < 0.05) the CSF concentrations of dopamine from 129.5 +/- 26.2 to 10,222.4 +/- 1,103.6 pg/ml, of norepinephrine from 74.7 +/- 11.0 to 2,238.6 +/- 143.5 pg/ml, and of serotonin from 1,824.5 +/- 340.7 to 3,888.7 +/- 1,335.2 pg/ml. Intracisternal injection of dopamine or norepinephrine (10-20 micrograms) caused the rapid onset of large-amplitude FBM, which often continued throughout high-voltage ECoG activity. In contrast, serotonin (20-40 micrograms) caused cessation of FBM and change of the ECoG from low- to high-voltage activity. These results indicate that neuronal release of catecholamines in the CNS has excitatory effects on FBM.

Effects of prostaglandins on fetal breathing do not involve peripheral chemoreceptors

1987 ◽  
Vol 62 (1) ◽  
pp. 271-277 ◽  
Author(s):  
D. T. Murai ◽  
L. D. Wallen ◽  
C. C. Lee ◽  
R. I. Clyman ◽  
F. Mauray ◽  
...  
Keyword(s):  
Carotid Sinus ◽  
Vagus Nerves ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors ◽  
Respective Control ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Site Of Action ◽  
Pg E2 ◽  
Stimulation Of

In sheep, prostaglandin (PG) E2 inhibits fetal breathing movements and meclofenamate, a PG synthetase inhibitor, causes a marked stimulation of fetal breathing movements; the site of action of these agents is not known. To determine whether these effects are mediated through the peripheral chemoreceptors, we studied 13 fetal sheep at gestational ages of 127 to 138 days. Seven fetuses had bilateral section of the carotid sinus and vagus nerves (denervated); six had sham operations. Beginning at least 6 days after the operation, we infused PGE2 (0.6 microgram X kg-1 X min-1) into five denervated and five sham-operated fetuses and meclofenamate (0.4 mg X kg-1 X h-1) into six denervated and four sham-operated fetuses. Infusions averaged 20 h in duration. During preinfusion control periods, the incidence of fetal breathing movements (% of time) was lower in denervated than in sham-operated fetuses (18.9% vs. 31.5%; P less than 0.005). In both groups, the incidence of fetal breathing movements was decreased by PGE2 and was increased by meclofenamate; when expressed as absolute values, the magnitude of the changes with both agents was greater in sham-operated fetuses than denervated fetuses. However, the effects were similar in both groups when the changes were expressed as a percent of the respective control values. The incidence of fetal breathing movements (% of control) was decreased by PGE2 to 25.4% in denervated and to 28.2% in sham-operated fetuses and was increased by meclofenamate to 297.3% in denervated and to 304.0% in sham-operated fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of acute oligohydramnios on respiratory system of fetal sheep

1992 ◽  
Vol 73 (2) ◽  
pp. 610-617 ◽  
Author(s):  
R. D. Savich ◽  
F. A. Guerra ◽  
C. C. Lee ◽  
J. F. Padbury ◽  
J. A. Kitterman
Keyword(s):  
Amniotic Fluid ◽  
Production Rate ◽  
Respiratory System ◽  
Control Period ◽  
Volume Of Fluid ◽  
The Other ◽  
Fetal Sheep ◽  
Short Period ◽  
Fetal Breathing ◽  
Fetal Breathing Movements

Prolonged oligohydramnios, or a lack of amniotic fluid, is associated with pulmonary hypoplasia and subsequent perinatal morbidity, but it is unclear whether short-term or acute oligohydramnios has any effect on the fetal respiratory system. To investigate the acute effects of removal of amniotic fluid, we studied nine chronically catheterized fetal sheep at 122–127 days gestation. During a control period, we measured the volume of fluid in the fetal potential airways and air spaces (VL), production rate of that fluid, incidence and amplitude of fetal breathing movements, tracheal pressures, and fetal plasma concentrations of cortisol, epinephrine, and norepinephrine. We then drained the amniotic fluid for a short period of time [24–48 h, 30.0 +/- 4.0 (SE) h] and repeated the above measurements. The volume of fluid drained for the initial studies was 1,004 +/- 236 ml. Acute oligohydramnios decreased VL from 35.4 +/- 2.9 ml/kg during control to 22.0 +/- 1.6 after oligohydramnios (P less than 0.004). Acute oligohydramnios did not affect the fetal lung fluid production rate, fetal breathing movements, or any of the other measured variables. Seven repeat studies were performed in six of the fetuses after reaccumulation of the amniotic fluid at 130–138 days, and in four of these studies the lung volume also decreased, although the overall mean for the repeat studies was not significantly different (27.0 +/- 5.2 ml/kg for control vs. 25.5 +/- 5.5 ml/kg for oligohydramnios). Again, none of the other measured variables were altered by oligohydramnios in the repeat studies.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxic inhibition of breathing in fetal sheep: relationship to brain adenosine concentrations

1994 ◽  
Vol 77 (6) ◽  
pp. 2734-2739 ◽  
Author(s):  
B. J. Koos ◽  
B. A. Mason ◽  
O. Punla ◽  
A. M. Adinolfi
Keyword(s):  
Brain Stem ◽  
Fetal Brain ◽  
Normal Incidence ◽  
Halothane Anesthesia ◽  
Microdialysis Probe ◽  
Fetal Sheep ◽  
Arterial Ph ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Arterial Po2

Because hypoxic inhibition of fetal breathing may be caused by a rise in central adenosine levels, the effects of O2 deficiency on fetal brain adenosine concentrations were determined at levels of hypoxia that inhibited fetal breathing. Under halothane anesthesia, the brains of fetal sheep (0.8 term) were implanted with guide cannulas exteriorized through a Silastic rubber window in the uterus and flank of the ewe. At least 4 days after surgery, a microdialysis probe was inserted into a cannula with the membrane tip placed in the rostral brain stem. During 1 h of isocapnic hypoxia, mean fetal arterial PO2 was reduced from 24.0 +/- 0.9 Torr (control) to 13 +/- 0.6 Torr and arterial pH fell progressively from 7.354 +/- 0.007 to 7.273 +/- 0.023. Hypoxia decreased the incidence of fetal breathing movements from 33 +/- 5.2 to 5 +/- 2.2 min/h, with a normal incidence (29 +/- 3.5 min/h) during the hour after arterial PO2 returned to control values. Adenosine concentrations in microdialysis perfusate under control conditions averaged approximately 35 nM, increased up to 2.3-fold during the hour of O2 deficiency, and fell toward control values when normoxia was restored. We conclude that fetal brain adenosine levels are increased at levels of O2 deficiency that inhibit fetal breathing, which are results consistent with a role for adenosine in hypoxic inhibition of fetal breathing.

Increased oxygen consumption associated with breathing activity in fetal lambs

1983 ◽  
Vol 54 (3) ◽  
pp. 701-707 ◽  
Author(s):  
D. W. Rurak ◽  
N. C. Gruber
Keyword(s):  
Blood Flow ◽  
Large Amplitude ◽  
O2 Consumption ◽  
Blood Gas ◽  
Control Value ◽  
Umbilical Blood ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Umbilical Blood Flow ◽  
Low Amplitude

To examine the relationship between fetal O2 consumption and fetal breathing movements, we measured O2 consumption, umbilical blood flow, and cardiovascular and blood gas data before, during, and after fetal breathing movements in conscious chronically catheterized fetal lambs. During fetal breathing movements, O2 consumption increased by 30% from a control value of 7.7 +/- 0.7 (SE) ml X min-1 X kg-1. Umbilical blood flow was 210 +/- 21 ml X min-1 X kg-1 before fetal breathing movements; in 9 of 16 samples it increased by 52 +/- 12 ml X min-1 X kg-1, while in the other 7 it decreased by 23 +/- 9 ml X min-1 X kg-1. Umbilical arterial and venous O2 partial pressures and pH fell during fetal breathing movements, and the fall was greater when umbilical blood flow was decreased. Partial CO2 pressure rose in both vessels, and again the increase was greatest when umbilical blood flow fell during fetal breathing movements. Also associated with a fall in umbilical blood flow was the transition from low-amplitude irregular to large-amplitude regular fetal breathing movements. It is concluded that fetal breathing movements increase fetal O2 demands and are associated with a transient deterioration in fetal blood gas status, which is most severe during large-amplitude breathing movements.

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