Department of Animal Sciences, University of Florida, Gainesville, 32611, USA.
Department of Animal Sciences, University of Florida, Gainesville, 32611, USA.
Theriogenology. 2020 Jul 1;150:471-479. doi: 10.1016/j.theriogenology.2020.03.011. Epub 2020 Mar 19.
In dairy cattle, the final weeks before parturition are physiologically challenging and an important determinant of subsequent production performance. External stressors should be carefully managed during this period to avoid adding strain on the animals. Late-gestation heat stress impairs productivity in the dam and exerts transgenerational effects on progeny. Physiological responses are complex and detriments to performance are multifaceted. Late-gestation heat stress blunts mammary gland involution in the first half of the dry period and impairs cell proliferation as calving approaches. Moreover, cows that were exposed to prepartum heat-stress exhibit reduced adipose tissue mobilization and a lower degree of insulin resistance during early lactation. Prepartum heat exposure also depresses immune function and evidence links this decrease to altered prolactin signaling under heat stress. Placental functions are also impaired as reflected in a higher cotyledon mass but lower maternal circulating estrone sulfate concentrations, potentially resulting in lower nutrient supply and reduced calf birth weight. In addition, calves born to heat-stressed dams show impaired immune function and therefore higher disease susceptibly. Novel evidence reported that intrauterine heat stress alters the methylation profile of liver and mammary DNA, which may also contribute to the poorer performance during adulthood of calves exposed to heat stress in utero. Understanding the contribution of all altered biological systems during late-gestation heat stress can be used as a basis for improving cow management during the dry period. This article provides a review of the impacts of late-gestation heat stress and of the emerging understanding of the biological mechanisms that underlie the observed impairments of performance.
在奶牛中，分娩前的最后几周在生理上具有挑战性，是后续生产性能的重要决定因素。在此期间，应仔细管理外部应激源，避免给动物增加压力。晚期热应激会损害母体的生产力，并对后代产生跨代效应。生理反应很复杂，对性能的损害是多方面的。晚期热应激会使干奶期前半段的乳腺退化变钝，并在接近产犊时损害细胞增殖。此外，经历产前热应激的奶牛在泌乳早期表现出脂肪组织动员减少和胰岛素抵抗程度降低。产前热暴露还会抑制免疫功能，有证据表明，这种下降与热应激下催乳素信号的改变有关。胎盘功能也受到损害，表现为胎盘中叶质量增加，但母体循环雌酮硫酸酯浓度降低，可能导致营养供应减少和小牛出生体重降低。此外，来自热应激母牛的小牛表现出免疫功能受损，因此更容易患病。新的证据表明，宫内热应激会改变肝脏和乳腺 DNA 的甲基化谱，这也可能导致在子宫内暴露于热应激的小牛在成年期表现较差。了解晚期热应激期间所有改变的生物系统的贡献，可以作为改善干奶期奶牛管理的基础。本文综述了晚期热应激的影响，以及对潜在表现受损的生物学机制的新认识。
