Hypothyroidism attenuates stress-induced prolactin and corticosterone release in septic rats

We investigated the effects of sepsis, through the lipopolysaccharide (LPS)-induced inflammatory response, on plasma corticosterone and prolactin (PRL) levels during acute immobilization stress in normal and thyroidectomized rats. Thyroidectomized (TX) or sham-operated (N) rats were subjected to 120 min of immobilization stress. Rats were treated with an intraperitoneal injection of either LPS (250 microg (100 g body wt)(-1)) or the same volume of vehicle (saline solution), 90 min before the induction of stress. Blood samples for hormone assays were collected before sepsis and stress induction for baseline measures (-90 min), and during sepsis and immobilization stress for the measurement of prolactin and corticosterone levels by radioimmunoassay. Our results show that the thyroid hormones are necessary for a proper response of PRL and corticosterone release during immobilization stress. Although sepsis enhanced PRL secretion, this was not true of corticosterone release in either group of rats. Low levels of thyroid hormones partially block the release of PRL, but do not block corticosterone secretion during sepsis.