English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

It is generally accepted that acute injury results in an outpouring of adrenocortical hormones 5 (1, 2), and that these hormones play an important role in the response of the total organism to such injury. The marked increase in urinary nitrogen excretion which characteristically occurs immediately following acute injury is usually considered to result from the catabolic action of the adrenocortical hormones on protein metabolism (3). Supporting this concept are recent studies correlating the negative nitrogen balance following surgical trauma in man with the rise in 17-hydroxysteroid excretion (4). The participation of the thyroid gland in the response to acute injury in man is less well delineated. Certain observations have suggested that there may be an increase in circulating thyroid hormone in man following trauma (5,6); other investigators have been unable to confirm this finding (7, 8). The role of the thyroid is particularly difficult to evaluate following injury because the increased output of adrenocortical hormones may affect some of the methods used to assay thyroid function (9-11 ), and may also tend to inhibit thyroid activity (9, 11-14). Goldenberg, Lutwak, Rosenbaum, and Hayes (15) have recently proposed that the catabolic response to injury is due primarily to excess thyroid hormone rather than adrenocortical hormones.

Thyroid-Adrenocortical Interrelations: Failure to Demonstrate Antagonism Between Triiodo-thyronine and Hydrocortisone in Man1