DEXAMETHASONE-INDUCED ADRENAL-CORTEX ATROPHY AND RECOVERY OF THE GLAND FROM PARTIAL, STEROID-INDUCED ATROPHY

This study aims to examine the effects of low dexamethasone (DX) doses on cellular and functional changes in the rat adrenal cortex and to o bserve the recovery of the gland from DX-induced partial atrophy. With in seven days doses of 15, 30 and 60 mug DX/100 g/day resulted in a do se dependent decrease in body and adrenal gland weight. Within two wee ks the lowest DX dose tested caused further decrease in adrenal weight . DX markedly lowered plasma ACTH and corticosterone (B) level, B cont ent in the gland and B output by adrenal slices. Adrenocortical atroph y induced by 15 mug DX was dependent upon the linear decrease in the v olume of fasciculata and reticularis zones, in the average volume of t he fasciculata cell and in the number of adrenocortical cells in the e ntire cortex. This dose of DX resulted in a prompt and potent inhibiti on of proliferative activity of adrenocortical cells as assessed by th e counting of metaphases per adrenal section. Partial adrenal atrophy evoked by 7 day DX-treatment was reversible within seven days of the d iscontinuation of the steroid treatment. Recovery of the gland depende d mainly on the increases in the volume of all adrenocortical zones, i n the average volume of fasciculata cell and in the number of parenchy mal cells in the gland. Seven days after discontinuation of DX adminis tration plasma ACTH was significantly higher than in controls. Plasma B and B secretion by adrenal slices were similar to the control group while B content in the gland was still depressed. These studies demons trated that within seven days low DX doses (15 mug/100 g/day) resulted in partial adrenocortical atrophy which is readily reversible within seven days of the discontinuation of DX administration.