Late gestation heat stress alters O₂ regulation in placenta and neonatal heifers

Maternal hyperthermia (i.e. heat stress) can adversely affect placental development and function, with severity varying based on pregnancy stage. During the last half of pregnancy, cow uterine blood flow increases 4.5-fold, and decreased maternal blood circulation can reduce placental diffusion capacity, impacting fetal growth.

Milk removal was discontinued (i.e. dried off) in multiparous pregnant Holstein cows 54 ± 5 days before expected calving and assigned to cooling (CLD) or heat stress (HT) treatments. Oxygen measurements were taken within ±3 h after birth (n = 7 per group) using the Rad-G Pulse Oximeter. RNA sequencing of cotyledonary tissue examined pathways and genes related to gas and oxygen transport.

Heifers exposed to late gestation in utero hypoxia (HT) had significantly lower oxygen saturation at birth compared with those from dams with normal (CLD) oxygen levels (83.4 % vs. 90.7 %, p = 0.03). The peripheral index of oxygen diffusion was also lower in HT-exposed heifers (2.04 % vs. 4.84 %, p = 0.01). Gene enrichment analysis of cotyledonary tissue revealed affected pathways, including response to hypoxia, oxygen transport, and VEGF signaling. Late gestation HT potentially influenced blood circulation and nitric oxide biosynthesis pathways, with various genes showing upregulation and downregulation.

The placenta is vital for fetal development, and late gestation hyperthermia can significantly affect its function, reducing fetal oxygen delivery and altering genes regulating placental gas and oxygen transport. These disruptions may result in fetal hypoxemia and growth restriction.