Studies on Acute Stimulatory Effect of Cold on Thyroid Activity and Its Mechanism in the Guinea Pig

Abstract

In an attempt to study an acute thyroid response to cold and the mechanism through which cold is effective, I131 was injected ip and changes of plasma PBI131 were measured in guinea pigs acclimatized to various room temperatures, and in guinea pigs receiving thyroid, thyroid plus TSH (thyroid-stimulating hormone), and animals with hypothalamic lesions or large lesions in other parts of the brain. It was demonstrated that plasma PBI131 was significantly higher at 2 hr., maximal at 4 hr., and remained high for up to 48 hr. after exposure to cold, and that this increase of PBI131 subsided markedly within 4 hr. after removing animals from the cold. The rapidity and magnitude of thyroid response to cold was largely governed by the temperature to which the animals were acclimatized previously. In addition to the secretion of organic iodine, a significant amount of iodide was also secreted very rapidly after exposure to cold. A similar increase of iodide secretion was found after TSH administration. It is suggested that the thyroidal response to cold may be necessary for the acute phase of cold adaptation. Since plasma PBI131 significantly decreased in thyroidectomized, thyroxine-maintained animals 2 hr. after exposure to cold, and since thyroid hormone could prevent increased release of hormonal iodine in the cold, it is suggested that an increased rate of peripheral utilization resulting in a lowered blood level of hormone may act via the feedback mechanism to produce increased TSH secretion. Hypothalamic lesions prevented increased TSH release in the cold, but large brain lesions, including the dorsal part of cerebral cortex, much of the hippocampus, part of the thalamus and all of the habenular nuclei, failed to prevent TSH release. The essential role of the hypothalamus in producing thyroid hyperactivity in the cold is discussed.