Effects of ovine maternal hyperglycemia on fetal regional blood flows and metabolism

1985 ◽  
Vol 249 (5) ◽  
pp. E454-E460 ◽  
Author(s):  
S. S. Crandell ◽  
D. J. Fisher ◽  
F. H. Morriss
Keyword(s):  
Blood Flow ◽  
Regional Distribution ◽  
Cardiovascular Responses ◽  
Late Gestation ◽  
Intravenous Glucose ◽  
Blood Flows ◽  
Umbilical Blood ◽  
Maternal Hyperglycemia ◽  
Regional Blood Flows ◽  
Placental Blood

Fetal combined ventricular output (CVO) and regional distribution of blood flow were measured in 12 ewes in late gestation by the radiolabeled microsphere method. Three sets of determinations were made in sequence beginning with a control study and repeating the measurements after the ewe had received intravenous glucose at 0.35 g X min-1 for 90 min and again after the ewe had received glucose at 0.85 g X min-1 for a second 90-min period. Maternal whole blood glucose concentrations were 2.98 +/- 0.18 (means +/- SE), 10.43 +/- 0.45, and 21.59 +/- 0.90 mM during the respective study periods. Fetal CVO did not change during maternal hyperglycemia; however, it was redistributed, with a decrease in umbilical blood flow to the placenta from 43.5% of CVO to 31.9 and 30.8%, respectively. The fetal carcass, heart, intestines, kidneys, liver, and adrenals each received increased percent CVO; these increases equaled the decrease in placental blood flow. Fetuses became hypoxemic and developed a mixed acidemia during induced maternal hyperglycemia, but oxygen delivery to the heart, brain, and kidneys was unchanged. These observations indicate that maternal hyperglycemia results in previously unsuspected fetal cardiovascular responses.

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 ◽  
...  
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Blood Flows ◽  
Arterial Blood ◽  
Cardiac Bypass ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Fetal Organs ◽  
Placental Blood Flow

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.

Transplacental clearance and blood flows of bovine gravid uterus at several stages of gestation

1987 ◽  
Vol 253 (5) ◽  
pp. R735-R739 ◽  
Author(s):  
L. P. Reynolds ◽  
C. L. Ferrell
Keyword(s):  
Blood Flow ◽  
Statistical Model ◽  
Deuterium Oxide ◽  
Gravid Uterus ◽  
Uterine Blood Flow ◽  
Blood Flows ◽  
Bovine Placenta ◽  
Umbilical Blood ◽  
Placental Blood ◽  
Umbilical Blood Flow

Rates of uterine and umbilical blood flows and transplacental clearance of deuterium oxide (D2O) were determined for cows on 137 +/- 1.0 (SE, n = 9), 180 +/- 0.5 (n = 8), 226 +/- 0.4 (n = 9), and 250 +/- 1.8 (n = 5) days of gestation. From days 137 to 250, rates increased 4.5-fold for uterine blood flow, 21-fold for umbilical blood flow, and 14-fold for clearance of D2O. Changes in rates of umbilical blood flow and D2O clearance paralleled increased rates of fetal growth and metabolism, which have previously been reported to occur during the last half of gestation. The regressions of D2O clearance on uterine and umbilical blood flows were significant (P less than 0.01) and explained 94-99% of the variation in placental clearance of D2O. Because the rate of D2O clearance was always less than that of uterine and umbilical blood flows, and because a relatively simple statistical model explained most of the variation in clearance, it was suggested that a concurrent or countercurrent arrangement of maternal and fetal placental microvasculatures is not adequate to explain clearance of highly diffusable substances across the bovine placenta. In addition, a placental exchange diagram of the data showed the existence of severe uneven distribution of maternal and fetal placental blood flows and/or significant shunting of maternal and fetal placental flows away from areas of exchange. Taken together, these data indicate that the placenta of the cow, like those of the sheep and goat, represents a relatively inefficient system of transplacental exchange.

Fever and regional blood flows in wethers and parturient ewes

1988 ◽  
Vol 65 (1) ◽  
pp. 165-172 ◽  
Author(s):  
C. M. Blatteis ◽  
J. R. Hales ◽  
A. A. Fawcett ◽  
T. A. Mashburn
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Full Term ◽  
Blood Flows ◽  
Pregnant Sheep ◽  
Regional Blood Flows ◽  
Placental Blood ◽  
Placental Blood Flow

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.

scholarly journals Cardiovascular adjustments to acute hypoxemia superimposed on chronic hypoxemia in lambs

1995 ◽  
Vol 268 (3) ◽  
pp. H974-H979
Author(s):  
M. Dalinghaus ◽  
J. W. Gratama ◽  
W. G. Zijlstra ◽  
J. R. Kuipers
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Supply ◽  
Pulmonary Stenosis ◽  
Arterial Oxygen Saturation ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Blood Flows ◽  
Regional Blood Flows ◽  
Chronic Hypoxemia

Cardiovascular responses to acute hypoxemia are in part mediated through adrenergic and chemoreceptor stimulation. In chronic hypoxemia the response to these stimuli may be blunted. Therefore, we determined whether the cardiovascular responses to acute hypoxemia superimposed on 3–4 wk of chronic hypoxemia were blunted in lambs with an experimental cardiac right-to-left shunt (combination of atrial septal defect and variable pulmonary stenosis). Cardiovascular variables and regional blood flows were determined during chronic hypoxemia and after acutely reducing the arterial oxygen saturation by increasing the cardiac right-to-left shunt. Arterial oxygen saturation decreased (65 +/- 7 to 40 +/- 7%, P < 0.001) and systemic blood flow increased (164 +/- 63 to 233 +/- 100 ml.min-1.kg-1, P < 0.01), maintaining systemic oxygen supply and oxygen uptake. Blood flow to the myocardium (P < 0.01), the adrenals (P < 0.05), and the brain (0.05 < P < 0.10) increased, and oxygen supply to these organs was maintained. Conversely, blood flow to the kidneys and the gastrointestinal tract was unaltered, so that oxygen supply to these organs was decreased. The responses to acute hypoxemia in chronically hypoxemic lambs were similar to those previously reported in normoxemic lambs. We conclude that the cardiovascular responses to acute hypoxemia in chronically hypoxemic lambs are not blunted.

An autoradiographic study of regional distribution of gastric mucosal blood flow

1988 ◽  
Vol 254 (4) ◽  
pp. G566-G574
Author(s):  
W. J. Angerson ◽  
J. G. Geraghty ◽  
D. C. Carter
Keyword(s):  
Blood Flow ◽  
Regional Distribution ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Autoradiographic Study ◽  
Acute Injury ◽  
Antral Mucosa ◽  
Blood Flows ◽  
Greater Curvature ◽  
Mucosal Folds

Iodo[14C]antipyrine autoradiography was used to measure gastric mucosal blood flow in anesthetized rats and to study regional distribution. Blood flows of 61 +/- 8 ml.100 g-1.min-1 (means +/- SE) in corpus and 84 +/- 9 ml.100 g-1.min-1 in antral mucosa compared well with previously reported measurements by hydrogen clearance. Blood flow in the crests of corpus mucosal folds was significantly higher than in the valleys between folds, indicating that the greater susceptibility of the former areas to acute injury, documented in several studies, is not associated with a perfusion defect in the resting stomach. Corpus mucosal blood flow was also higher in the side walls of the stomach than in the greater curvature region, and in distal than in proximal locations. No systematic regional variations within antral mucosa were demonstrated.

Lack of evidence for impaired preload or Bezold-Jarisch activation during brief umbilical cord occlusions in fetal sheep

2021 ◽  
Author(s):  
Christopher A. Lear ◽  
Laura Bennet ◽  
Benjamin S. A. Lear ◽  
Jenny A. Westgate ◽  
Alistair Jan Gunn
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Cardiovascular Responses ◽  
Diastolic Filling ◽  
Fetal Sheep ◽  
Blood Flows ◽  
Rapid Fall ◽  
Filling Time ◽  
Cervical Vagotomy ◽  
Femoral Blood

Impaired cardiac preload secondary to umbilical cord occlusion (UCO) has been hypothesized to contribute to intrapartum decelerations, brief falls in fetal heart rate (FHR), through the activation of the Bezold-Jarisch reflex. This cardioprotective reflex increases parasympathetic and inhibits sympathetic outflows triggering hypotension, bradycardia and peripheral vasodilation but its potential to contribute to intrapartum decelerations has never been systematically examined. In this study we performed bilateral cervical vagotomy to remove the afferent arm and the efferent parasympathetic arm of the Bezold-Jarisch reflex. 22 chronically instrumented fetal sheep at 0.85 of gestation received vagotomy (n=7) or sham-vagotomy (control, n=15), followed by three 1-min complete UCOs separated by 4-min reperfusion periods. UCOs in control fetuses were associated with a rapid fall in FHR and reduced femoral blood flow mediated by intense femoral vasoconstriction, leading to hypertension. Vagotomy abolished the rapid fall in FHR (p<0.001), and despite reduced diastolic filling time, increased both carotid (p<0.001) and femoral (p<0.05) blood flow during UCOs, secondary to carotid vasodilation (p<0.01) and delayed femoral vasoconstriction (p<0.05). Finally, vagotomy was associated with an attenuated rise in cortical impedance during UCOs (p<0.05), consistent with improved cerebral substrate supply. In conclusion, increased carotid and femoral blood flows after vagotomy are consistent with increased left and right ventricular output, which is incompatible with the hypothesis that labor-like UCOs impair ventricular filling. Overall, the cardiovascular responses to vagotomy do not support the hypothesis that the Bezold-Jarisch reflex is activated by UCO. The Bezold-Jarisch reflex is therefore mechanistically unable to contribute to intrapartum decelerations.

In Reply: Cerebral Blood Flow

PEDIATRICS ◽  
1982 ◽  
Vol 70 (6) ◽  
pp. 1013-1014
Author(s):  
RAUL BEJAR
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Gastrointestinal Tract ◽  
Ductus Arteriosus ◽  
Left Ventricular ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Left Ventricular Output ◽  
Patent Ductus

Baylen and Emmanouilides give the impression that their abstract was misquoted in our commentary. We would like to explain our interpretation of their data. In the abstract, Baylen et al indicate that they measured regional blood flows (RBF) in premature fetal lambs, expressing them as a percentage of the left ventricular output (LVO) before and after patent ductus arteriosus (PDA) closure. Their results (percent of LVO) before and after PDA closure were: lung, 42.7% vs 8.4% (P &lt; .01); carcass, 35% vs 55% (P &lt; .01); heart, 5.5% vs 10.2% (P &lt; .05); gastrointestinal tract, 5.1% vs 9.3% (P &lt; .05); brain, 2.7% vs 3.4% (P = NS); kidney, 2.2% vs 3.3% (P = NS); liver, 3.2% vs 5.7% (P = NS).

Effects of hypercapnia on uterine and umbilical circulations in conscious pregnant sheep

1976 ◽  
Vol 41 (5) ◽  
pp. 727-733 ◽  
Author(s):  
A. M. Walker ◽  
G. K. Oakes ◽  
R. Ehrenkranz ◽  
M. McLaughlin ◽  
R. A. Chez
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Co2 Concentration ◽  
Arterial Pco2 ◽  
Physiological Regulation ◽  
Blood Flows ◽  
Umbilical Blood ◽  
Pregnant Sheep ◽  
Near Term ◽  
Vascular Catheters

Changes in the uterine and umbilical circulations during induced hypercapnia were studied in nine unanesthetized near-term pregnant sheep. Blood flows were measured with electromagnetic flow transducers and arterial pressures with vascular catheters implanted under anesthesia 2–16 days prior to experiments. Hypercapnia was induced in the fetus alone by giving acetazolamide iv to the fetus, 100–200 mg/kg. Mean fetal arterial Pco2 increased from49.5 to 63.4 mmHg but no significant changes in umbilical blood flowoccurred. Stepwise increases in both maternal and fetal arterial Pco2 were induced by increasing maternal inspired CO2 concentration to a maximum of 12%. Nodignificant changes occurred in uterine or umbilical circulations until hypercapnia was severe (maternal arterial Pco2 greater than 60 mmHg, fetal arterial Pco2 greater than 70 mmHg). With severe hypercapnia uterine vascular resistance increased significantly and uterine blood flow decreased despitean increase in maternal arterial pressure; fetal arterial pressure and umbilical blood flow increased significantly, but umbilical vascular resistancedid not. We conclude that hypercapnia in conscious pregnant sheep is associated with significant changes in uterine and umbilical circulations, but only when hypercapnia is severe. Carbon dioxide is unlikely to be a factor innormal physiological regulation of the uteroplacental circulation in this species.

Hemodynamic effects of leukotriene C4 in ovine fetus

1990 ◽  
Vol 259 (6) ◽  
pp. E851-E855
Author(s):  
B. A. Meyer ◽  
S. W. Walsh ◽  
V. M. Parisi
Keyword(s):  
Blood Flow ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
In Vivo Studies ◽  
Leukotriene C4 ◽  
Blood Flows ◽  
Before And After ◽  
Placental Blood ◽  
Near Term

Leukotrienes are synthesized during pregnancy and produce cardiovascular effects in adults. We hypothesized that leukotriene C4 would cause vasoconstriction in the fetus and placenta. Eight near-term, unanesthetized ovine fetuses were studied before and after infusion of 10 micrograms leukotriene C4 (LTC4) into the fetal vena cava. Cardiovascular monitoring of maternal and fetal arterial pressures and heart rates was performed. Fetal blood flows were measured by the radioactive-microsphere technique. Sustained elevations in systolic and diastolic blood pressure and decreased fetal heart rate began by 1 min and returned to baseline by 30 min. Arterial pH fell from 7.33 +/- 0.01 to 7.29 +/- 0.01 at 15 min (P less than 0.05) and to 7.29 +/- 0.01 at 30 min (P less than 0.05), with a significant increase in base deficit from 0.7 +/- 0.7 to 3.5 +/- 0.7 at 15 min (P less than 0.05) and to 2.9 +/- 1.0 at 30 min (P less than 0.05). Fetal PO2 and PCO2 were unchanged. Significant decreases in blood flow and resistance were seen in the umbilical placental circulation as well as in fetal skeletal muscle and intestine. Blood flow and resistance were unchanged in the renal and adrenal vascular beds. Fetal administration of LTC4 caused no changes in maternal cardiovascular parameters. These findings represent the first in vivo studies of the effects of a lipoxygenase metabolite on fetal-placental blood flow.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

Sign in / Sign up

Export Citation Format

Share Document