Cardiovascular responses to heat stress in late gestation fetal sheep

Abstract

SUMMARYHeat 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 ,um diameter radioactive microspheres to determine the effect of raising the environmental temperature from 20 to 43°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-' (100 g tissue)-', 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-kg-mmHg-' (P <0.01). Tissue blood flows (in ml min-' (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 02 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.

Effects on fetal and maternal body temperatures of exposure of pregnant ewes to heat, cold, and exercise

“…We believe that the circumstances in which uteroplacental blood flow decreases, rather than increases, during heat stress are those in which the ewe's own thermal status is so threatened that she abandons the homeothermy of her fetus. In a transition zone of maternal heat stress, uteroplacental blood flow may remain unchanged, as has been reported for sheep (30) and for human mothers (29).…”

“…Umbilical and uterine blood flow have been measured by others, although only for short time periods, using hard-wired techniques in restrained mothers or using microspheres in terminal experiments. As we would have predicted, studies of ewes during environmental heat stress showed increases in umbilical blood flow (6,30) and uterine blood flow (2). Lublin and Wolfenson (18) found a 50% increase in maternal blood flow to the placenta of pregnant rabbits during mild heat stress.…”

Catecholamines Mediate Multiple Fetal Adaptations during Placental Insufficiency That Contribute to Intrauterine Growth Restriction: Lessons from Hyperthermic Sheep

“…Near term, blood flow to the brain and heart of hyperthermic fetuses is increased by 50% and 8%, respectively, at the expense of flow to the liver, lungs, small intestine, pancreas, and adipose tissue, which decreases noticeably [80, 81]. Additionally, slower rate of umbilical blood flow caused by increased resistance [82] increases transplacental oxygen and glucose gradients, aiding extraction from maternal circulation [32, 34, 83, 84] (Figure 6).…”

Bem-estar durante o período gestacional de ovelhas: uma breve revisão

“…Segundo Bell et al (1989), as mudanças biológicas em decorrência do estresse por calor retardam o crescimento fetal e placentário, bem como reduzem a secreção de lactogênio e progesterona placentários. No feto, a transferência de calor ocorre por meio da circulação sanguínea materno-fetal, o que contribui para o incremento de calor para a fêmea gestante (Walker et al, 1995). Sendo assim, neste período o estresse térmico tem efeitos mais pronunciados tanto na ovelha quanto nos fetos, podendo acarretar o nascimento de cordeiros mais leves e menos desenvolvidos, o que eleva as chances de mortalidade (Brown et al, 1977;Hopkins et al, 1980).…”