Heat stress during pregnancy in sheep is associated with respiratory a
lkalosis in both the mother and fetus, and, if prolonged, fetal growth
is retarded. In seven pregnant sheep at 130-137 days gestation we use
d 15 mu m diameter radioactive microspheres to determine the effect of
raising the environmental temperature from 20 to 43 degrees C for 8 h
on uteroplacental blood flows and the distribution of cardiac output
in the ewe and fetus. Fetal cardiac output increased slightly from 47
. 0 +/- 3 . 2 (mean +/- S.E.M.) to 54 . 0 +/- 3 . 6 ml min(-1) (100 g
tissue)(-1), fetal arterial pressure and heart rate were unchanged, an
d total vascular conductance in the fetus increased significantly from
12397 +/- 1111 to 14732 +/- 1569 ml min(-1) kg(-1) mmHg(-1) (P < 0 .
01). Tissue blood flows (in ml min(-1) (100 g)(-1)) increased signific
antly (P < 0 . 05) in the fetal body (e.g. nasal mucosa, torso and for
eleg skin, adrenal, thyroid and thymus glands, brown and omental fats,
heart, urinary bladder and carcass) and the fetal brain (e.g. cerebel
lum, cerebral grey matter, cervical spinal cord and pituitary gland).
These regional vasodilatations occurred despite a significant fall (P
< 0 . 01) in fetal arterial O-2 saturation (55 . 2 +/- 1 . 8 vs. 38 .
6 +/- 2 . 4%), P-O2 (18 . 1 +/- 0 . 7 vs. 13 . 5 +/- 0 . 8 mmHg) P-CO2
(51 . 0 +/- 1 . 8 vs. 36 . 1 +/- 2 . 3 mmHg); under normothermic cond
itions hypoxia is associated with peripheral vasoconstriction. Because
hypocapnia would also be expected to cause cerebral vasoconstriction
it is suggested that during hyperthermia, hypoxia- and hypocapnia-indu
ced vasoconstrictions are reduced by the release of vasodilator substa
nces, or a decrease of sympathoadrenal effector responses. Blood flow
to the fetal and maternal sides of the placenta did not change during
the heat stress, suggesting that perfusion-dependent transfer of heat
from fetus to mother across the placenta does not increase under hyper
thermic conditions.