Pituitary adrenal interactions in shorn sheep exposed to cold, wet conditions

Abstract

Newly shorn sheep were exposed to a cold (3°C) wet environment for 8 days; six out of 10 untreated animals died but there were no deaths in a group of 10 that was treated with cortisone. In two other experiments, nine out of 15 control sheep died, but only four out of 15 sheep treated with adrenocorticotrophin (ACTH). In a final experiment approximately one-third of exposed controls died compared with one-tenth of sheep treated with dexamethasone trimethylacetate. A significantly greater proportion (P < 0.05) of sheep given ACTH or 1.5 mg or more of dexamethasone trimethylacetate per kg had rectal temperatures higher than 37.8°C during the first 96 hr of exposure than the comparable controls. The adrenal glands of sheep that died in the cortisone and ACTH experiments were heavier than those taken from survivors that were killed after the experiment; macroscopically, the cortices of some of the adrenals from sheep that succumbed were haemorrhagic and resembled the glands seen in the Waterhouse-Friderichsen syndrome in man; all were heavily infiltrated with lipid when compared with the cortices of survivors. ß-Glucuronidase activity in the serum of cortisone-treated sheep (and in untreated survivors) was elevated during the first 2–3 days of exposure and returned to pre-exposure levels; untreated sheep that succumbed showed continuously increasing enzymatic activity. Acid phosphatase activity was initially depressed in steroid-treated sheep and returned to pre-exposure levels, whereas activity increased continuously in controls that died. Total leucocytes were lower during the first 72 hr of exposure in sheep treated with 1.5–2 mg dexamethasone trimethylacetate per kg, compared with untreated controls. We suggest that the enlarged, fat-laden haemorrhagic adrenals found in sheep that died from cold exposure resulted from excessive ACTH stimulation prior to death. The results suggested a state of adrenocortical insufficiency during the first 96 hr of cold exposure.