Perinatal thyroid activity in farm animals and the role of iodocompounds in maternal milk (minireview).

There is a sudden rise in serum thyroid hormone concentrations immediately after birth, with some species differences related to the degree of the increase and to the iodothyronine involved. Extrauterine cooling stimulates TSH release; however, the marked release of the thyroid hormones from the gland is somewhat dependent on the process of transition from fetal to neonatal state. It seems that hemodynamic changes together with the sympathetic nervous system, which comes in force at the moment of cord cut, are indispensable co-factors of TSH action. Four factors, at least, may attribute to the immediate postnatal hyperiodothyroninemia: abrupt depletion of the preformed fetal hormonal iodine stores, preferential T3 secretion, increase in the T4 to T3 monodeiodination in the peripheral tissues, a release of TH content from peripheral reservoirs to plasma. The course of the postnatal hyperiodothyroninemia is dependent on the maturation level reached at birth, food intake, and cooling relative to extrauterine environment. One of the physiological significances of the postnatal thyroid hyperactivity lies in the metabolic thermostability mediated by iodothyronines and adrenaline in the thyroxine types of newborns, in contrast to newborns in which thyroxine does not results in an increase of oxygen consumption (noradrenaline type). Measurable quantities of T3 and T4 are present in colostrum and milk but their contribution to normal hormone production so far calculated does not exceed 7% of daily requirement for an individual hormone.