Cardiovascular responses to heat stress in late gestation fetal sheep.
Heat stress during pregnancy in sheep is associated with respiratory alkalosis in both the mother and fetus, and, if prolonged, fetal growth is retarded. In seven pregnant sheep at 130-137 days gestation we used 15 microns 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, and 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 significantly (P < 0.05) in the fetal body (e.g. nasal mucosa, torso and foreleg skin, adrenal, thyroid and thymus glands, brown and omental fats, heart, urinary bladder and carcass) and the fetal brain (e.g. cerebellum, cerebral grey matter, cervical spinal cord and pituitary gland). These regional vasodilatations occurred despite a significant fall (P < 0.01) in fetal arterial O2 saturation (55.2 +/- 1.8 vs. 38.6 +/- 2.4%), PO2 (18.1 +/- 0.7 vs. 13.5 +/- 0.8 mmHg) and PCO2 (51.0 +/- 1.8 vs. 36.1 +/- 2.3 mmHg); under normothermic conditions 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-induced vasoconstrictions are reduced by the release of vasodilator substances, 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 hyperthermic conditions.