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...

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Veröffentlicht in:Experimental physiology 2003-11, Vol.88 (6), p.755-760
Hauptverfasser: Rodriguez, T. T., Albuquerque-Araújo, W. I. C., Reis, L. C., Antunes-Rodrigues, J., Ramalho, M. J.
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container_end_page 760
container_issue 6
container_start_page 755
container_title Experimental physiology
container_volume 88
creator Rodriguez, T. T.
Albuquerque-Araújo, W. I. C.
Reis, L. C.
Antunes-Rodrigues, J.
Ramalho, M. J.
description 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 µg (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. Experimental Physiology (2003) 88.6, 755-760.
doi_str_mv 10.1113/eph8802621
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T. ; Albuquerque-Araújo, W. I. C. ; Reis, L. C. ; Antunes-Rodrigues, J. ; Ramalho, M. J.</creator><creatorcontrib>Rodriguez, T. T. ; Albuquerque-Araújo, W. I. C. ; Reis, L. C. ; Antunes-Rodrigues, J. ; Ramalho, M. J.</creatorcontrib><description>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 µg (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. 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subjects Animals
Corticosterone - blood
Full Length Papers
Hypothyroidism - blood
Hypothyroidism - complications
Hypothyroidism - immunology
Lipopolysaccharides
Male
Prolactin - blood
Rats
Rats, Wistar
Sepsis - blood
Sepsis - chemically induced
Sepsis - complications
Sepsis - immunology
Stress, Physiological - blood
Stress, Physiological - complications
Stress, Physiological - immunology
title Hypothyroidism attenuates stress-induced prolactin and corticosterone release in septic rats
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