A dog was evaluated for clinical signs suggestive of hypercortisolemia. Serum biochemical testing revealed hypernatremia and hypokalemia. Serum cortisol concentration after injection of ACTH was less than the lower reference limit. An adrenal gland tumor was visualized via ultrasonography and computed tomography. Histologic examination confirmed that the mass was an adrenocortical carcinoma. Excess adrenal secretion of corticosterone was hypothesized to be the cause of the signs of glucocorticoid excess. Serum corticosterone secretion was high before and after ACTH injection, compared with clinically normal dogs and dogs with hypercortisolemia and classic hyperadrenocorticism. Hyperaldosteronemia was detected as well. Treatment with mitotane was instituted and successful for a period of 4-months until the dog was euthanatized for neurologic problems that were most likely unrelated to endocrine disease.

Summary Gastrin is the only hormone known to stimulate secretion of hydrochloric acid. It also has trophic effects on specific parts of the mucosa of the gastrointestinal tract. Using radioimmunoassay techniques, postprandial serum gastrin and insulin concentrations were measured in six adult horses to establish effects of different diets on gastrin concentrations. Insulin concentrations were measured to provide support to the patterns of gastrin secretion because patterns of insulin secretion were already known. The horses were fed coastal bermuda hay, or twice daily 5 kg of a complete pelleted ration, 5 kg of commercial sweet feed or 5 kg of the sweet feed together with hay. There was little change in serum gastrin or insulin concentrations after feeding hay alone. Rations containing more readily available nutrients (pellets, sweet feed) produced significant increases in postprandial serum gastrin and insulin concentrations. Gastrin concentrations also varied according to the duration of feeding each diet, but this was not seen with insulin. These results indicated that gastrin secretion, and therefore possibly gastric acid secretion, were markedly influenced by dietary composition and duration of feeding a diet. There appeared to be some adaptation of the stomach (gastrin secretion) to changes in diet, but this was not accompanied by indications of adaptation in the endocrine pancreas (insulin secretion).

Urine cortisokcreatinine ratios (UCCR) were determined from single urine samples obtained by cystocentesis in 47 cats allotted into 2 groups: 31 healthy cats and 16 sick, hospitalized cats with assorted clinical illnesses. The mean ( 2 standard deviation) UCCR for healthy cats was 5.9 2 7.0 (median, 3.2; range, 0.6 to 27.8). Age or gonadal status had no significant effect on the magnitude of UCCR within this group. However, sick cats had significantly higher UCCR ( P wareness of disorders of the hypothalamo-pituitary-

This new RIA method provides a commercially available, accurate, and sensitive method for measurement of the relatively low serum T4 concentrations of birds and snakes. Initial ranges for the species evaluated were established.

Summary Postprandial gastrin concentrations were assayed in serum samples from a group of six foals at one day, one week, one month and three months of age. Before sampling, each foal was prevented from feeding for 2 h and was then allowed to suck for 15 mins. Blood samples were taken at the start of the meal and at 30 min intervals for the next 3 h. Feeding increased serum gastrin concentrations at one day, one week and one month, with the greatest increases detected at one day. Mean pre‐feeding gastrin concentrations were 25.2 ± 2.3 pg/ml at one day, 22.8 ± 3.9 pg/ml at one week, 15.2 ± 2.3 pg/ml at one month and 15.6 ± 7.5 pg/ml at three months. Highest mean post prandial concentrations were at 60 mins on Day one (47.4 ± 15.2 pg/ml) and at 30 mins for the one week (44.4 ± 14.2 pg/ml) and one month (25.2 ± 4.1 pg/ml) old foals. There was no apparent post prandial increase in serum gastrin concentrations in foals at three months of age. Precise reasons for changes in postprandial serum gastrin concentrations remain unknown. Factors that could be important include maturation of G cell function, alterations in gastrin metabolism and excretion, and changes in gastrointestinal motility with increasing age.