Localization of brain-stem lesions inhibiting compensatory adrenal hypertrophy following unilateral adrenalectomy

Summary It has been attempted to determine in which parts of the brain-stem lesions have an inhibitory effect on the compensatory hypertrophy, which normally follows unilateral adrenalectomy. Lesions were made by means of the stereotaxic technique at 34 points in the mid-line of the brain-stem. The diameter of the lesions was approximately 1 mm. They were regularly distributed over the entire diencephalon, the septal area and the rostral part of the mesencephalon. Two days after the lesions had been placed the left adrenals were removed. Six days later the animals were sacrificed, compensatory hypertrophy values were determined and compared with those in control animals.Lesions in a remarkably large area had an inhibitory effect on compensatory hypertrophy. This area includes the entire diencephalon with the exception of a region in its dorsal part and it extends into the septal area and the mesencephalon. The most acceptable explanation of these findings is that the lesions inhibit compensatory hypertrophy not because they destroy a specific neuro-endocrine center but because they bring about a general disturbance of homeostatic mechanisms in the brain-stem.With technical assistance from Mr. L. Meijer.     

An electron-microscopic stereological study of the compensatory hypertrophy of the rat adrenal zona fasciculata after unilateral adrenalectomy

Summary The ultrastructural changes associated with the compensatory hypertrophy of the zona fasciculata cells on monoadrenalectomized rats were investigated by stereological techniques. It was found that these subcellular changes display a different pattern from those underlying the ACTH-induced adrenocortical cell growth in the intact rats. This result supports the view that compensatory adrenal hypertrophy does not involve activation of the hypothalamo-hypophyseal-adrenal axis.     

Morphometric investigations into the mechanism of the compensatory hypertrophy of the rat adrenal zona fasciculata after unilateral adrenalectomy

Summary Compensatory hypertrophy of the remaining gland in unilaterally adrenalectomized rats was investigated by morphometric techniques. It was observed that compensatory adrenal growth occurred in both dexamethasone-treated and hypophysectomized rats, receiving maintenance doses of ACTH. However, it was only half that found in intact animals. These results support the view that activation of the hypothalamo-hypophyseal axis is not the unique mechanism underlying adrenal compensatory hypertrophy in the rat.     

Compensatory hypertrophy in radiothyroidectomized dwarf rats.

The aim of the study was to clarify whether growth hormone and thyroid hormones play a role in compensatory organ hypertrophy. Radiothyroidectomized dwarf rats with serious disorder of growth hormone production due to the loss of thyroid function were used in the experiments. As regards growth hormone production these animals may be considered as having been "hypophysectomized". The loss of thyroid function and growth hormone deficiency did not affect the degree of compensatory hypertrophy of the kidney, the adrenal and the gonad. The observation indicates that the hormones under study are not of decisive importance in the mechanism of compensatory organ enlargement. Further investigations are needed to clarify whether organ enlargement in the hypometabolic rat occurring at the level observed in the controls is associated with enhanced function.     

Compensatory adrenal growth in dexamethasone treated rats

The changes in right adrenal weight and adrenocortical mitotic activity have been quantified in the early (up to 72 h) stages following left adrenalectomy or sham adrenalectomy in adult male Sprague Dawley rats. These have been compared with the changes seen in rats pretreated for 14 days with a daily intraperitoneal injection of the synthetic glucocorticoid, dexamethasone (200 micrograms/kg) body weight. The results indicate a significant proliferative response in both groups of animals, although basal proliferative activity and the amplitude of the response was lower in the dexamethasone treated animals. In addition, they suggest two waves of mitotic activity at 24 and 72 h.     

Ultrastructure of thymus and liver following adrenalectomy and replacement adrenal hormone therapy in rats

Prior research in this laboratory has shown that dexamethasone, aldosterone, and epinephrine interact in regulating the activity of ornithine decarboxylase (EC 4.1.1.17, ODC) in rat thymus and liver. The three primary adrenal hormones were administered alone and in various combinations to adrenalectomized rats. Liver and thymus samples were removed, prepared for electron microscopy, and morphometric analysis of thymic micrographs was performed. It was found that both corticosteroids induced thymic lympholysis and that concurrent administration of epinephrine 'rescued' the lymphocytes. Observations of liver micrographs indicated that changes in liver glycogen deposition vary in response to the hormone treatment regimen. The liver response to a combination of the glucocorticoid and catecholamine was different from the response to the mineralocorticoid and catecholamine, which indicated that the liver response to the two steroids may be mediated via different mechanisms. Evidence is provided to support the conclusion that the influence of the adrenal gland on rat thymus and liver is not restricted to glucocorticoids but may also involve mineralocorticoids and catecholamines.