Corticosteroids are essential for fetal maturation in mammals. Cortisol stimulates structural and functional changes in many tissues to facilitate the transition from intra- to extrauterine life [Fowden et al. 1998); it also initiates the final endocrine cascade that leads to the onset of myometrial contractions and delivery in some species. Before birth, there is a gradual increase in fetal Cortisol concentrations over the last few weeks, initiated by activation of the fetal hypothalamo-pituitary-adrenal axis, and a decrease in Cortisol binding globulin concentrations. Animals not exposed to the prenatal Cortisol rise have deficient enzyme activities in key bodily organs, particularly the lungs, leading to respiratory distress syndrome (RDS) and widespread organ dysfunction. Horses are different to other animals because fetal Cortisol concentrations increase only during the final 24-48 h before delivery, and continue to increase after birth [Fowden et al. 1998). Foals that fail to complete this final maturational process display many features of immaturity. Premature foals typically have low body weights, adrenal insufficiency, hypoglycaemia associated with low body glycogen stores, hypothermia and low T3 concentrations, a poor suck reflex, inability to digest enteral feeds, lung and renal dysfunction, incomplete ossification and deficient muscular-skeletal development. Not surprisingly, premature foals have a worse prognosis for survival than full term neonatal foals suffering from other conditions [sepsis, PAS, HIE], even with high level intensive care. Moreover, post natal treatment with corticosteroids does little to induce adrenocortical activity and tissue maturation because of a deficiency in adrenal P450C17 enzyme activity.
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