Heat transfer pathways between fetal lamb and ewe

1985 ◽  
Vol 59 (2) ◽  
pp. 634-638 ◽  
Author(s):  
R. D. Gilbert ◽  
H. Schroder ◽  
T. Kawamura ◽  
P. S. Dale ◽  
G. G. Power

Heat produced by the fetus exists to the mother by one of two principal routes: by fetal-maternal exchange in the placenta or through the fetal skin to the amniotic fluid and uterine wall. We measured heat conductances along each pathway to estimate the fraction of total heat exiting each route. Thermistors were placed in the fetal aorta, two different sites in the amniotic fluid, and in a maternal artery. Five days after surgery we injected a total of 280 ml of ice-cold saline into the two separate amniotic fluid sites during a 45-s interval and measured the temperature response for the next hour. After one or two such injections the fetus was killed to cut off umbilical blood flow, and the experiment was repeated to measure the heat fluxes in the absence of placental heat exchange. Experimentally obtained temperature curves were compared with the predictions of a mathematical model. Heat conductances of the skin and uterine wall, as well as the fetal heat production, were estimated in the model using least-squares parameter optimization. In 10 fetal lambs, weighing 3.73 +/- 0.40 (SE) kg, total fetal heat production averaged 3.75 +/- 0.33 W X kg-1. The heat conductance of the uterine wall, 6.6 +/- 0.8 W X degrees C-1, was lower than that of the fetal skin, 10.2 +/- 1.0, and of the placenta, 25.7 +/- 2.9 W X degrees C-1, temperature gradient. We estimated that 84.5% of total fetal heat production exists by fetal-maternal exchange in the placenta with the remaining 15.5% exiting through the fetal skin.

1988 ◽  
Vol 65 (1) ◽  
pp. 460-468 ◽  
Author(s):  
H. Schroder ◽  
R. D. Gilbert ◽  
G. G. Power

We constructed and used a mathematical model of maternal-fetal heat exchange in the sheep to explore the effects of changes in certain parameters on steady-state fetal temperatures and to determine whether the fetus in the model has any potential to control its own temperature. The model took into account both fetal and placental heat production and exchange of heat in the placenta, across the fetal skin, via amniotic fluid, and through the uterine wall. The maternal ewe was assumed to be a constant temperature heat sink. Changes in placental or fetal heat production were calculated to change the ratio of heat exiting across the placenta or fetal skin significantly but to have little effect on fetal core temperature, e.g., a rise of only 0.8 degrees C was predicted after a twofold increase in fetal heat production. Fetal placental blood flow was calculated to affect fetal temperature the most of any flow, a reduction to zero causing fetal temperature to rise 5.0 degrees C. Changes in heat conductances between fetal skin and amniotic fluid, or between amniotic fluid and uterine wall, had minimal effect on fetal temperature. From the model calculations here and because heat exchange within the sheep placenta has previously been calculated to be extremely efficient, we conclude that the fetal sheep has little ability to control its temperature by changes in heat dissipated through extraplacental pathways. Thus the model predicts an effective heat clamp that closely links fetal to maternal temperature.


1980 ◽  
Vol 239 (1) ◽  
pp. R115-R122 ◽  
Author(s):  
R. H. Lorijn ◽  
L. D. Longo

In an effort to determine if placental diffusion reserves exceed fetal O2 requirements, we increased fetal O2 consumption (VO2) by infusing 1.7-11.5 microgram of norepinephrine (NE) . min-1. After 50 min of infusion VO2 rose 25% to 10.2 from 8.2 ml . min-1 . kg fetal wt-1. Placental CO diffusing capacity remained essentially unchanged from control, 0.49 +/- 0.05 (SE) ml . min-1. Torr-1 . kg-1, During the first 5 min of NE infusion fetal arterial blood pressure increased 29%, while heart rate decreased 15%. In addition, coronary, pulmonary, and umbilical blood flow, expressed per kilogram of fetal weight as determined by use of labeled microspheres, increased 50, 162, and 25%, respectively (P less than 0.05), although fetal cardiac output remained constant at 538 +/- 23 (SE) ml . min-1 . kg-1. Finally, we determined the NE-blood pressure dose-response relations for the fetus; Blood pressure increased with doses up to 1 microgram . min-1 . kg-1, but failed to rise further with higher doses. We conclude that 1) fetal VO2 increases with NE infusion 2) the placental reserve for O2 diffusion exceeds normal requirements, and 3) NE infusion is associated with increased blood pressure, bradycardia, and a redistribution of blood flows to the heart, lungs, and placenta despite a constant cardiac output.


1973 ◽  
Vol 116 (1) ◽  
pp. 48-56 ◽  
Author(s):  
James W. Goodwin ◽  
John E. Milligan ◽  
Bruce Thomas ◽  
John R. Taylor

1994 ◽  
Vol 267 (1) ◽  
pp. E150-E155 ◽  
Author(s):  
R. R. Moores ◽  
B. S. Carter ◽  
G. Meschia ◽  
P. V. Fennessey ◽  
F. C. Battaglia

Plasma serine disposal rate (DR), decarboxylation, and conversion to fetal plasma glycine by the placenta were measured in six fetal lambs at 72 +/- 1 days gestation. L-[1-13C]serine, L-[U-14C]serine, and 3H2O were infused over 3 h into the fetal circulation, the latter for measurement of uterine and umbilical blood flow. The fetal plasma serine DR was 8.7 +/- 1.0 mumol/min or 61.8 +/- 4 mumol.min-1.kg fetus-1. Approximately 90% of the DR represented placental uptake of fetal serine. There was no detectable release of fetal serine into the maternal circulation. The fetal arterial plasma glycine-to-serine enrichment ratio was approximately 0.30. The conversion rate of fetal serine to fetal plasma glycine by the placenta was 5.8 +/- 0.7% of the serine DR. Fetal and placental CO2 production from fetal plasma serine carbon was 1.9 +/- 0.4 and 1.2 +/- 0.4 mumol/min, respectively. Thus, at midgestation, there is a rapid fetoplacental serine exchange that constitutes most of the fetal plasma serine turnover. Placental conversion of serine to fetal glycine and serine oxidation together account for only 10% of the placental uptake of fetal serine.


1968 ◽  
Vol 22 (5) ◽  
pp. 595-603 ◽  
Author(s):  
JAMES W. GOODWIN ◽  
WILLIAM A. MAHON ◽  
DAVID W. J. REID

1991 ◽  
Vol 164 (4) ◽  
pp. 1118-1126 ◽  
Author(s):  
Klaus G. Schmidt ◽  
Mariarosaria Di Tommaso ◽  
Norman H. Silverman ◽  
Abraham M. Rudolph

1982 ◽  
Vol 242 (3) ◽  
pp. H429-H436 ◽  
Author(s):  
R. B. Wilkening ◽  
S. Anderson ◽  
L. Martensson ◽  
G. Meschia

The effect of variations of uterine blood flow (F) on placental transfer was examined in six chronic sheep preparations by measuring the placental clearances of ethanol (CE) and antipyrine (CA) at different levels of F. Norepinephrine infusion, hemorrhage, and occlusion of the terminal aorta were used to reduce F below normal. The reduction of F had no appreciable effect on umbilical blood flow (f). In each ewe, CE significantly correlated with F. The CE vs. F relationship at constant f was curvilinear with convexity toward the clearance axis. Regression analysis showed that the equation 1/CE = 1/.911 F + 1/.831 f could account for most of the CE variance (r2 = 0.97). Implicit in this relation is the concept that, given a certain level of placental perfusion, an F/f ratio congruent to 1 is optimal for the exchange of highly diffusible inert molecules between mother and fetus [CE/(F + f) was maximum at F/f = 0.955]. CA was not significantly different from CE at low clearance level but became smaller than CE at clearance values greater than 300 ml/min. This suggests that a high rates of perfusion placental permeability was a factor in limiting CA.


2021 ◽  
Vol 22 (15) ◽  
pp. 8150
Author(s):  
Amelia R. Tanner ◽  
Cameron S. Lynch ◽  
Victoria C. Kennedy ◽  
Asghar Ali ◽  
Quinton A. Winger ◽  
...  

Deficiency of the placental hormone chorionic somatomammotropin (CSH) can lead to the development of intrauterine growth restriction (IUGR). To gain insight into the physiological consequences of CSH RNA interference (RNAi), the trophectoderm of hatched blastocysts (nine days of gestational age; dGA) was infected with a lentivirus expressing either a scrambled control or CSH-specific shRNA, prior to transfer into synchronized recipient sheep. At 90 dGA, umbilical hemodynamics and fetal measurements were assessed by Doppler ultrasonography. At 120 dGA, pregnancies were fitted with vascular catheters to undergo steady-state metabolic studies with the 3H2O transplacental diffusion technique at 130 dGA. Nutrient uptake rates were determined and tissues were subsequently harvested at necropsy. CSH RNAi reduced (p ≤ 0.05) both fetal and uterine weights as well as umbilical blood flow (mL/min). This ultimately resulted in reduced (p ≤ 0.01) umbilical IGF1 concentrations, as well as reduced umbilical nutrient uptakes (p ≤ 0.05) in CSH RNAi pregnancies. CSH RNAi also reduced (p ≤ 0.05) uterine nutrient uptakes as well as uteroplacental glucose utilization. These data suggest that CSH is necessary to facilitate adequate blood flow for the uptake of oxygen, oxidative substrates, and hormones essential to support fetal and uterine growth.


2003 ◽  
Vol 189 (6) ◽  
pp. S218
Author(s):  
Zeev Weiner ◽  
Rula Hamisa ◽  
Allan Fisher ◽  
Allan Bombard ◽  
Eliezer Shalev

Sign in / Sign up

Export Citation Format

Share Document