Fetal cardiac bypass alters regional blood flows, arterial blood gases, and hemodynamics in sheep

1992 ◽  
Vol 263 (3) ◽  
pp. H919-H928 ◽  
Author(s):  
S. M. Bradley ◽  
F. L. Hanley ◽  
B. W. Duncan ◽  
R. W. Jennings ◽  
J. A. Jester ◽  
...  

Successful fetal cardiac bypass might allow prenatal correction of some congenital heart defects. However, previous studies have shown that fetal cardiac bypass may result in impaired fetal gas exchange after bypass. To investigate the etiology of this impairment, we determined whether fetal cardiac bypass causes a redistribution of fetal regional blood flows and, if so, whether a vasodilator (sodium nitroprusside) can prevent this redistribution. We also determined the effects of fetal cardiac bypass with and without nitroprusside on fetal arterial blood gases and hemodynamics. Eighteen fetal sheep were studied in utero under general anesthesia. Seven fetuses underwent bypass without nitroprusside, six underwent bypass with nitroprusside, and five were no-bypass controls. Blood flows were determined using radionuclide-labeled microspheres. After bypass without nitroprusside, placental blood flow decreased by 25–60%, whereas cardiac output increased by 15–25%. Flow to all other fetal organs increased or remained unchanged. Decreased placental blood flow after bypass was accompanied by a fall in PO2 and a rise in PCO2. Nitroprusside improved placental blood flow, cardiac output, and arterial blood gases after bypass. Thus fetal cardiac bypass causes a redistribution of regional blood flow away from the placenta and toward the other fetal organs. Nitroprusside partially prevents this redistribution. Methods of improving placental blood flow in the postbypass period may prove critical to the success of fetal cardiac bypass.

1992 ◽  
Vol 1 (1) ◽  
pp. 15-21
Author(s):  
B. A. Meyer ◽  
J. E. Dickinson ◽  
S. W. Walsh ◽  
V. M. Parisi

We hypothesized that foetal administration of SQ-29,548, a putative thromboxane receptor blocker, would prevent foeto–placental vasoconstriction produced by the thromboxane mimic U46619. Arterial blood gases, continuous monitoring of maternal and foetal heart rates and blood pressures were performed in chronically catheterized pregnant ewes. Foetal blood flows and vascular resistance were determined with radioactive microspheres. SQ-29,548 effectively blocked the expected vasoconstrictive effects of thromboxane. However, prolonged infusion of SQ-29,548 resulted in significant decreases in umbilical–placental blood flow and foetal mean arterial pressure. This was accompanied by a respiratory acidemia. Potential therapy for the vasoconstrictive disorders of pregnancy with SQ-29,548 awaits further investigation of its intrinsic vasoactive properties in the umbilical–placental vasculature.


1988 ◽  
Vol 65 (1) ◽  
pp. 165-172 ◽  
Author(s):  
C. M. Blatteis ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
T. A. Mashburn

To determine whether the reported absence of fever in full-term-pregnant ewes might be associated with shifts of regional blood flows from thermogenic tissues to placenta during this critical period, fevers were induced twice by injections of Escherichia coli lipopolysaccharide (LPS, 0.25 microgram/kg iv) into each of six Merino ewes from 8 to 1 days prepartum, and their regional blood flow distribution was measured with radioactive, 15-microns-diam microspheres before and during the rise in fever (when their rectal temperature had risen approximately 0.4 degree C). Unexpectedly, fever always developed, rising to heights not significantly different at any time before parturition [4-8 days prepartum = 0.81 +/- 0.23 degree C (SE); 1-3 days prepartum = 0.75 +/- 0.17 degree C) and similar to those in three wethers treated similarly (0.90 +/- 0.10 degree C). Generally, during rising fever, blood flow in the ewes shifted away from heat loss tissues (e.g., skin, nose) to heat production tissues (e.g., shivering muscle, fat) and cardiac output increased; blood flow through redistribution organs (e.g., splanchnic bed) decreased. The reverse occurred during defervescence. Utero-placental blood flow remained high in the febrile ewes. These regional blood flow distributions during febrigenesis and lysis are essentially the same as those during exposures to ambient cold and heat, respectively. Some differences in the responses of cardiac output and its redistribution, however, were apparent between wethers and pregnant ewes. We conclude that 1) the previously reported "absence of fever in the full-term-pregnant sheep" should not be regarded as a general phenomenon and 2) full-term-pregnant sheep support fever production without sacrificing placental blood flow.


1989 ◽  
Vol 256 (3) ◽  
pp. H613-H620 ◽  
Author(s):  
H. S. Iwamoto ◽  
T. Kaufman ◽  
L. C. Keil ◽  
A. M. Rudolph

A majority of previous studies of fetal responses to acute hypoxemia has focused on the response of the sheep fetus greater than 120 days of gestation when many regulatory systems have been established. To assess the response of younger, less well-developed fetuses, we exposed two groups of fetal sheep (I, 84-91 days; II, 97-99 days gestational age) to acute hypoxemia by giving the ewe a gas mixture containing 9% O2 to breathe. We decreased descending aortic PO2 in both groups of fetuses [I, 24 +/- 6 to 14 +/- 3 (SD) Torr; II, 23 +/- 3 to 12 +/- 4 Torr] by a degree similar to that achieved in previous studies of fetuses greater than 120 days of gestation. Mean arterial blood pressure (I, 31 +/- 6; II, 40 +/- 3 Torr) did not change significantly from control values, and heart rate (I, 224 +/- 27; II, 203 +/- 16 beats/min) increased significantly in group II fetuses with hypoxemia. In group I and II fetuses, as in older fetuses, cerebral, myocardial, and adrenal blood flows, measured by the microsphere technique, increased, and pulmonary blood flow decreased. These responses mature early and are likely local vascular responses to decreases in oxygen content. Combined ventricular output and umbilical-placental blood flow decreased significantly in both groups. Unlike the response of the fetus greater than 120 days, acute hypoxemia did not decrease blood flow to the musculoskeletal and cutaneous circulations (group I only), gastrointestinal, or renal circulations.(ABSTRACT TRUNCATED AT 250 WORDS)


1993 ◽  
Vol 265 (1) ◽  
pp. H9-H14
Author(s):  
C. A. Gleason ◽  
H. Iida ◽  
T. P. O'Brien ◽  
M. D. Jones ◽  
E. J. Cone ◽  
...  

Maternal cocaine abuse has been associated with neonatal neurological and neurobehavioral problems of unknown pathogenesis. We administered a single intravenous dose of cocaine (2 mg/kg) to 12 unanesthetized pregnant sheep; their fetuses had been catheterized in utero 2 days before the study. We measured fetal cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), mean arterial blood pressure (MAP), and blood gases before and 2, 5, 15, and 30 min after maternal cocaine injection. Fetal CBF increased by 37 +/- 33% (mean +/- SD) at 5 min and returned to baseline by 15 min. Regional brain blood flow changes paralleled CBF changes with the greatest increases occurring in cerebellum (54 +/- 43%) and brain stem (54 +/- 52%). Cerebral vascular resistance was decreased for cerebellum (22%) and brain stem (19%) but was unchanged for cerebral hemispheres and caudate. Increased CBF at 5 min was associated with a 20 +/- 9% increase in fetal MAP and a 38 +/- 13% decrease in fetal arterial O2 content. Fetal CMRO2 was unchanged. There was a decrease in fetal intestinal blood flow at 2 min, an increase in myocardial, adrenal, and renal blood flow at 5 min, and no change in placental blood flow. Maternal cocaine injection causes fetal hypoxemia, hypertension, and increased CBF. Possible mechanisms for cerebral vasodilation (in some areas) include hypoxemia, impaired autoregulatory response to increased blood pressure, and/or direct or indirect vascular effects of cocaine or its metabolites.


PEDIATRICS ◽  
1977 ◽  
Vol 59 (6) ◽  
pp. 858-864
Author(s):  
G. Gabriele ◽  
C. R. Rosenfeld ◽  
D. E. Fixler ◽  
J. M. Wheeler

Continuous airway pressure delivered by a head-box is an accepted means of treating clinical hyaline membrane disease. To investigate hemodynamic alterations resulting from its use, eight newborn lambs, 1 to 6 days of age, were studied at 6 and 11 mm Hg of positive pressure, while spontaneously breathing room air. Organ blood flows and cardiac output were measured with 25 µ-diameter radioactive microspheres. Heart rate, left ventricular pressure, and arterial blood gases did not change during the study. Jugular venous pressures increased from 6.4 mm Hg to 18.6 and 24.2 mm Hg at 6 and 11 mm Hg, respectively (P < .005). Cardiac output decreased approximately 20% at either intrachamber pressure setting. Renal blood flow fell 21% at 11 mm Hg. No significant changes in blood flow were found in the brain, gastrointestinal tract, spleen, heart, or liver when compared to control flows. Of particular interest was the finding of a 28% reduction in ocular blood flow at 6 mm Hg and 52% at 11 mm Hg. From these results, we conclude that substantial cardiovascular alterations may occur during the application of head-box continuous airway pressure breathing, including a significant reduction in ocular blood flow.


2015 ◽  
Vol 35 (5) ◽  
pp. 873-881 ◽  
Author(s):  
Christopher K Willie ◽  
David B MacLeod ◽  
Kurt J Smith ◽  
Nia C Lewis ◽  
Glen E Foster ◽  
...  

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO2 would affect cerebral metabolism more than hypoxia. PaO2 and PaCO2 were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO2-H+ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO2 reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.


1985 ◽  
Vol 249 (3) ◽  
pp. H485-H491 ◽  
Author(s):  
R. F. Tuma ◽  
G. L. Irion ◽  
U. S. Vasthare ◽  
L. A. Heinel

The purpose of this investigation was to characterize the changes in regional blood flow and central hemodynamic measures that occur in the rat as a result of the aging process. The isotope-labeled microsphere technique was used to measure cardiac output and regional blood flows in conscious and anesthetized adult (12 mo) and senescent (24 mo) Fischer 344 virgin female rats. No significant changes were observed in central hemodynamic measurements or regional blood flows in conscious rats with the exception of a 25% reduction in splenic blood flow. Pentobarbital anesthesia significantly reduced cardiac index and heart rate but elevated total peripheral resistance and mean arterial blood pressure. There was a decrease in blood flow to skeletal muscle, spleen, duodenum, stomach, and brain tissue samples and increased hepatic arterial blood flow in both age groups. The use of anesthesia caused a greater reduction in the cardiac index and brain blood flow in the senescent anesthetized rats than in the adult rats. Heart and kidney blood flows were decreased by anesthesia in the senescent rats but not in the adult rats. Skeletal muscle blood flow, however, was significantly greater in the senescent anesthetized rats than in the younger anesthetized animals. Although body weight and organ weights of the liver, spleen, kidneys, stomach, heart, and brain were significantly greater for the senescent rats, no differences could be demonstrated in tibial length or lean body mass.


1981 ◽  
Vol 240 (1) ◽  
pp. H45-H48 ◽  
Author(s):  
P. L. Toubas ◽  
N. H. Silverman ◽  
M. A. Heymann ◽  
A. M. Rudolph

The effects of acute hemorrhage were studied in two groups each with six fetal lambs (100-116 amd 128-147 days gestation) 3-4 days after we implanted catheters. Fetal blood pressures, heart rate, arterial blood gases and pH, and combined ventricular output and its distribution (radionuclide-labeled microsphere technique) were measured before and 5 min after removal of 15% of fetal-placental blood volume measured by 125I-albumin dilution. Because there were no differences in responses in the two age groups, the data were pooled. Fetal arterial mean pressure fell significantly (50.7 +/- 2.5 to 45.5 +/- 2.6 mmHg) as did heart rate (186 +/- 6 to 151 +/- 13 beats/min) and arterial blood pH (7.39 +/- 0.02 to 7.30 +/- 0.02); arterial blood carbon dioxide tension rose (39.7 +/- 29 to 44.1 +/- 4.4). Combined ventricular output fell from 610 +/- 58 to 448 +/- 45 ml . kg-1 . min-1 (P < 0.05). Blood flow to the umbilical-placental circulation, as well as to the fetal body, fell significantly. Blood flow to the kidneys, gastrointestinal tracts, and lungs also fell, but flow to other organs was maintained. Blood volume reduction in the fetus markedly influences blood gas exchange, because it results in a reduction of umbilical-placental blood flow associated with the fall in arterial pressure.


Resuscitation ◽  
1992 ◽  
Vol 23 (2) ◽  
pp. 101-111 ◽  
Author(s):  
Mark G. Angelos ◽  
Daniel J. DeBehnke ◽  
James E. Leasure

1984 ◽  
Vol 247 (3) ◽  
pp. R567-R574 ◽  
Author(s):  
D. F. Anderson ◽  
J. J. Faber

Inflatable occluders were placed on the distal aorta of 11 fetal lambs. After 1 wk of control measurements, fetal placental blood flow was reduced to about two-thirds of its control value for an average period of 2 wk. No allowance was made for fetal growth. During the period of flow restriction, fetal growth was 2%/day. Femoral arterial blood pressure was reduced from a control value of 41 to 27 mmHg (P less than 0.001). There was an insignificant increase in carotid arterial blood pressure from 48 to 50 mmHg. Placental resistance to flow did not decrease more than could be accounted for by the increase in gestational age in the course of the experiment. It is concluded that fetal placental blood flow is not under feedback control, since neither of the determinants of flow (i.e., driving pressure and resistance) responded to its chronic reduction.


Sign in / Sign up

Export Citation Format

Share Document