Walker D W, Hale J R, Fawcett A A, Pratt N M
Department of Physiology, Monash University, Clayton, Victoria, Australia.
Exp Physiol. 1995 Sep;80(5):755-66. doi: 10.1113/expphysiol.1995.sp003884.
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.
绵羊孕期热应激与母羊和胎儿的呼吸性碱中毒有关，若持续时间过长，胎儿生长会受到抑制。在7只妊娠130 - 137天的怀孕绵羊中，我们使用直径15微米的放射性微球来确定将环境温度从20℃提高到43℃持续8小时对子宫胎盘血流以及母羊和胎儿心输出量分布的影响。胎儿心输出量从47.0±3.2（平均值±标准误）略增至54.0±3.6毫升·分钟⁻¹（100克组织）⁻¹，胎儿动脉压和心率未变，胎儿总血管传导率从12397±1111显著增至14732±1569毫升·分钟⁻¹·千克⁻¹·毫米汞柱⁻¹（P<0.01）。胎儿身体（如鼻粘膜、躯干和前肢皮肤、肾上腺、甲状腺和胸腺、棕色脂肪和网膜脂肪、心脏、膀胱和胴体）和胎儿大脑（如小脑、大脑灰质、颈脊髓和垂体）的组织血流量（毫升·分钟⁻¹（100克）⁻¹）显著增加（P<0.05）。尽管胎儿动脉血氧饱和度（55.2±1.8对38.6±2.4%）、氧分压（18.1±0.7对13.5±0.8毫米汞柱）和二氧化碳分压（51.0±1.8对36.1±2.3毫米汞柱）显著下降（P<0.01），这些局部血管舒张仍发生；在常温条件下，低氧与外周血管收缩有关。由于低碳酸血症也预计会导致脑血管收缩，因此有人提出在高温期间，低氧和低碳酸血症诱导的血管收缩通过血管舒张物质的释放或交感肾上腺效应反应的降低而减轻。热应激期间胎盘胎儿侧和母体侧的血流量未发生变化，这表明在高温条件下，胎儿通过胎盘向母体的灌注依赖性热传递不会增加。
