The biochemical characterization of 22 cases of pituitary-dependent hyperadrenocorticism in the dog, is reported. The principal characteristics of the disease include excessive and non-rhythmic production of cortisol, decreased sensitivity of the hypothalamic-pituitary system to the suppressive effects of dexamethasone, decreased responsiveness of the pituitary-adrenocortical system to the stimulus of insulin-induced hypoglycaemia and increased responsiveness of the system to stimulation with lysine-vasopressin. From these observations it is concluded that pituitary-dependent hyperadrenocorticism in the dog is a valid model for study of the pathogenesis of the disease in man. For the diagnosis of hyperadrenocorticism itself, the measurement of the concentration of corticosteroids in a single sample of plasma obtained 8 h after intravenous injection of 0.01 mg dexamethasone/kg was sufficient. The level of 11-hydroxycorticosteroids was less than 140 nmol/1 plasma in normal dogs, whereas higher values were found in dogs with hyperadrenocorticism. For purposes of differential diagnosis, measurement of the level of corticosteroids in the plasma both before and 4 h after intravenous injection of 0.05 mg dexamethasone/kg is adequage: suppression is obtained only in cases of pituitary-dependent hyperadrenocorticism.

Reference values for 23 blood chemical parameters in racing pigeons (Columba livia domestica) were established for use in clinical pathology. The inner limits are given for the percentiles P(2).(5) and P(97.5) with a probability of 90%. A minimum of 50 blood samples collected between September and January from different animals aged between 6 months and 12 years (median 1.5 years) was used for each parameter. Reference values obtained in the present study are compared with values published previously.

The roles of plasma insulin-like growth factor I (IGF I) and growth hormone (GH) were studied in 7 beagle dogs before and during starvation and during refeeding. IGF I levels significantly decreased from 75.2 \ m=+-\5.9 ng/ml at 7 days prior to the start of starvation to 9 \m=+-\1.7 ng/ml at 19 days after the commencement of starvation (mean \ m=+-\ SEM; P < 0.0001). During refeeding IGF I significantly rose from 9 \m=+-\1.7 ng/ml to 55.5 \ m=+-\7.5 ng/ml within 9 days (mean \ m=+-\ SEM; P < 0.002). During starvation plasma GH levels significantly increased (P < 0.05) and these elevated levels returned to normal during refeeding. The dogs' GH secretory capacity significantly increased during starvation (P = 0.012) and became normal again during refeeding. The following conclusions can be drawn from this study: 1) starvation in the dog leads to a significant and drastic reduction of the circulating levels of IGF I, and 2) starvation in the dog, as in man, leads to increased circulating GH levels and to an increased GH-secretory capacity possibly brought about by a lack of a negative feedback normally exerted by IGF I.

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