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Evolution of the methods for suppression of adrenal hyperfunction has now made it possible to give up bilateral adrenalectomy in favour of portalization of the adrenal blood flow from the left adrenal by its autotransplantation with maintained blood supply into the transverse mesocolon and cryodestruction of the right adrenal. Analysis of the mortality showed two-stage suppression of adrenal hyperfunction to be advisable.
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We have studied glomerular zone involution in the rat's adrenal gland after a period of hyperfunction brought about by a low-sodium diet. The changes observed in this zone effect those organoids that are more directly involved in steroid genesis; mitochondria, smooth endoplasmic reticulum and liposomes. The Golgi complexes appear very developed, often, showing, a positive acid phosphatase activity. Lysosomes suffered a considerable increase in their number, and carried out their digestive function on liposomes. All those changes discussed here are seen as an accomodation of this zone to the new normofunctional situation.
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Three pregnant sows, being in the last quarter of gestation, were used in an experiment to study the changes induced in newborn piglets by T-2 toxin. One sow was used as control (C). The other two received 24 mg (sow A) and 6 mg (sow B) T-2 toxin, respectively, mixed in the feed, daily, up to the time of farrowing. The piglets of sow A became ill by 48-72 h after birth, while the litters of sow B and C remained healthy. The clinical symptoms included faintness, diarrhoea, decreased blood glucose level, and collapse followed by death. The milk and urine of sow A and the stomach contents of affected and dead piglets contained T-2 toxin and its metabolites. Pathological changes seen at necropsy included acute enteritis, degeneration of the liver and kidneys, and oedema of the mesentery. The stomach was filled with clotted milk. Histopathological and electron-microscopic findings consisted of reduced glycogen content and pathological simple fatty infiltration of the liver cells, lymphocyte depletion and necrosis in the lymphoid follicles of the intestinal mucosa, atrophy of the thymic cortex, and hyperfunction of the adrenal and thyroid glands compared to the control.
The plasma growth hormone response to the provocative agent, xylazine, was assessed in 4 dogs with spontaneous hyperadrenocorticism, before and after therapy. Before treatment of the hyperadrenocorticism, no significant increase in growth hormone concentration occurred in any of the dogs following the administration of xylazine. A significant increase in growth hormone concentrations following xylazine administration occurred in 2 of the 3 dogs with hypophysis (pituitary)-dependent hyperadrenocorticism after treatment with mitotane (o,p'-DDD) and in 1 dog after surgical removal of a hyperfunctional adrenal adenoma. Although the impaired growth hormone response persisted in 1 dog, the administration of xylazine was repeated in this animal after only 3 weeks of mitotane therapy; it is likely that growth hormone unresponsiveness would reverse if the hyperadrenocorticism were controlled for a longer period. These findings demonstrate that in dogs, as in persons, the excessive production of endogenous corticosteroids associated with either hypophysis-dependent hyperadrenocorticism or hyperfunctional adrenal tumor can induce suppression of growth hormone release which is reversible following treatment.
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The study was performed in albino rats treated during first two postnatal weeks with guanetidin isotonic solution injected subcutaneously in dose 20 mg/kg body weight to obtain desympathization. Control animals received similar volume of the solution during equal terms. Thyroid and adrenal glands were studied in 1- and 6-month-old rats both by light and electron microscopes. Serotonin and catecholamines were revealed by fluorescent-histochemical method. In experimental 1-month-old animals morphological indexes indicate the thyroid gland hyperfunction. In these animals serotonin and catecholamines content is lower in parafollicular endocrinocytes, mast cells and in adrenergic fibres, the density of which is significantly lower than that in control animals. The adrenal gland weight in experimental animals increases due to the medulla. Serotonin and catecholamine content is essentially higher. Thyroid gland in 6-month-old experimental rats is hyperfunctioning. Adrenal fibres density in its stroma is close to control indexes. Catecholamines and serotonin adrenal glands medulla grows with age and remains higher than the appropriate control level, which indicates active participation of adrenal glands in adaptive reactions is desympathized animals. Serotonin plays an important role in local regulation of thyroid glands. Parafollicular endocrinocytes perform the function of local biogenic amines-producers, while mast cells regulate the serotonin content.
An electrolyte-regulating corticoid has been identified and given the name aldosterone. This hormone may be produced in amounts above normal in adrenal cortical tumors in hyperplastic adrenal glands and in normal appearing adrenal glands. Overproduction of aldosterone is accompanied by certain characteristic clinical manifestations which should suggest the diagnosis. The diagnosis may be supported by examinations available in most well equipped clinical laboratories. Bioassay of aldosterone in the urine and estimation of exchangeable body sodium and potassium, using radioactive salts, are necessary for confirmation of the diagnosis.Since the description of this salt-retaining hormone by Simpson and Tait and the discovery of its chemical structure by Reichstein in 1954, reports of 14 cases have been published. Surgical removal of the offending tissue gives spectacular relief from the very distressing symptoms.
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