Effect of passive immunization with an antiserum to thyrotropin (TSH)-releasing hormone on plasma TSH levels in thyroidectomized rats.

Abstract

The role of TRH in mediating the rapid rise of plasma TSH which occurs upon interruption of short term negative feedback inhibition by exogenous thyroid hormone in thyroidectomized (TX) rats was investigated by passive immunization with rabbit antiserum to TRH (TRH-AS). Administration of triiodothyronine (T3), 10 μg/kg ip to TX adult male rats with indwelling right atrial catheters, led within 24 h to a suppression of plasma TSH from hypothyroid to near euthryoid levels. Upon discontinuation of T3 after one or two daily injections, plasma TSH remained maximally suppressed for 24 h, but began to rise by 32 h after the last dose of T3 and returned to hypothyroid levels within 36–48 h. Intravenous administration of 1 ml TRH-AS, 24 h after the last dose of Ta, failed to abolish the subsequent TSH rise. TRH antibody titers in rat plasma 12–48 h after passive immunization were equal to or greater than those which had previously been found adequate to inhibit the acute rise of TSH after cold exposure. To explore the possibility that an early effect of TRH-AS had disappeared by 12 h, antiserum was administered to untreated TX and age-matched normal control rats. Plasma TSH was suppressed within 15–30 min in both groups; the duration of this suppression was between 2 and 4 h in TX and between 8 and 24 h in normal rats. The rate of fall of plasma TSH was consistent with a complete cessation of pituitary TSH secretion in normal rats, but suggested only a partial suppression in TX rats. TRH antibody titers were higher in TX than in normal rats at all times during the 24 h period after antiserum administration and, therefore, could not account for the less prolonged and incomplete suppression of plasma TSH. The similar disappearance rates of TRH antibody from plasma of TX and control rats also argue against the hypersecretion of TRH after thyroidectomy. These results suggest that although TRH exerts a role in maintaining basal levels of TSH secretion, the hypersecretion of TSH in TX rats is to a large extent independent of TRH control. (Endocrinology102: 799, 1978)