Effects of thyrotropin upon thyroidal iodide; studies using thyroid venous cannulation and two radioiodine isotopes.

Abstract

Studies in dogs have indicated that after the injection of thyrotropin (TSH) there is an enhanced release into thyroid venous blood of inorganic iodine in addition to the expected secretion of hormonal iodine (1, 2). Plasma iodide that has been newly accumulated by the thyroid iodide "trap" and still exists in the gland in inorganic form (transported iodide) does not appear to be the major source of the iodide released after TSH stimulation. The published data [reviewed in (3) ] suggest that the iodide so released is produced within the gland and is derived from deiodination of glandular organic compounds.However, a release of transported iodide into thyroid venous blood after TSH administration also has been demonstrated by studies in which organic binding of iodide was blocked (4, 5). The mechanism for the release of transported iodide and its relationship to the generation and release of iodide produced within the gland from organic precursors remain unresolved. It has been suggested (5) that the effect of TSH upon the release of transported iodide may be a consequence of the formation of iodide from glandular organic stores.The purpose of this report is to present data that provide more precise characterization of the effect of TSH upon glandular iodide release and of the * Submitted for publication October 22, 1965; accepted January 25, 1966. Supported by research grants A-2585 and A-5589 from the National Institute of Arthritis and Metabolic Diseases.Presented in part at the Forty- relationship of iodide derived from intraglandular organic stores to that newly accumulated from the circulation. Experiments were performed in which these two sources of glandular iodide were individually labeled in the same animal with different radioiodine isotopes whose flux between thyroid and circulation was estimated from differences between the radioiodide concentrations of arterial and thyroid venous plasma. Related studies on the acute effect of TSH on unidirectional (blood to thyroid) radioiodide clearance and on the sensitivity of iodide release to exogenous TSH stimulation are also reported. MethodsPentobarbital-anesthetized male mongrel dogs, weighing 30 to 50 pounds, were used in all experiments. The inferior thyroid vein of one lobe was cannulated, and continuous serial samples of thyroid venous blood were obtained by methods previously reported (1). The duration of each sampling period was usually 4 to 6 minutes; this was reduced to 2 to 3 minutes in the clearance experiments. Femoral arterial blood was drawn at the midpoint of each venous sample. Intravenous injections were given through a femoral vein cannula.Radioactivity measurements were made with a scintillation well counter and spectrometer. All samples were counted at a final volume of 1.0 ml. Separate 'I and 'I standards were made from suitable dilutions of the same isotope solutions administered to the animals. The activity present at each of two different energy levels was determined for each plasma sample and isotope standard with spectrometer wi...

A new method for the measurement of thyroidal iodine release in man

“…The abrupt outpouring of 'I from the thyroid gland after TSH stimulation, primarily represented a marked augmentation in the release of I-from the thyroid in addition to hormonal release. This augmentation in the I-leak from the thyroid gland stimulated with TSH has been previously observed in laboratory animals (19). This view is supported by the observation that there was a rapid return of the ratio values to base line as would be expected if I-had been the predominating release product.…”

“…The daily fluctuations in thyroidal iodine release are accountable almost entirely by variations in the I-leak from the thyroid gland. Under normal conditions, the magnitude and timing of the I-leak serves as a sensitive indicator of the state of thyroid glandular stimulation (19). The technique is primarily qualitative although some semiquantitative interpretation may be made by the exogenous administration of known amounts of TSH.…”

Effect of Perchlorate and Methimazole on Iodine Metabolism

“…While considerable varia¬ tion was present in individual patients, for the entire group perchlorate ap¬ peared to act only by blocking thyroidal uptake of iodide from plasma. It is reported (Isaacs et al 1966) that the perchlorate ion, when infused in large concentrations intravenously directly into the dog thyroid, can also accelerate release of intrathyroidal iodine. This might not be apparent in our patients because of a species difference or because the amount of iodine release is too small to be detected in the in vivo studies performed.…”

“…By preventing uptake of iodide from blood, it presumably should completely inhibit recirculation of iodide derived from degradation of thyroid hormone in peripheral tissues. Isaacs et al (1966) report that in the dog perchlorate also causes a discharge of some iodide derived from intrathyroidal sources (pre¬ sumably from the deiodination of iodotyrosine). The extent of this discharge and its mechanism are unknown.…”

Human thyroid blood flow response to endogenous, exogenous human, and bovine thyrotrophin measured by electromagnetic flowmetry

“…Other investigators found no change in TBF after administration of TSH to rabbits (Campbell et al 1960;Taurog et al 1964), cats (Taurog et al 1964), dogs (Rosenberg et al 1960(Rosenberg et al , 1961Dumont & Rocmans 1964;Stark et al 1965;Isaacs et al 1966;Dumont 1971;Roc¬ mans et al 1978), or rats (Goldman 1963). Gold¬ smith et al (1965) found no change in TBF in a dog after injection of 10000 mlU TSH but noted a temporary decrease after 5000 mlU.…”