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A simple adrenalectomy technique is presented for the ferret (Mustela putorius furo). The adrenal glands were removed in two operations with an interim recovery period of approximately 1 week. The right adrenal should be removed first, as the surgery is complicated on that side by fascia which binds the adrenal to the inferior vena cava. Salt solution (1% NaCl) in place of water will maintain sodium balance.
Adrenal incompetence developed in rats 6 weeks after adrenalectomy without any salt and hormonal compensation. In individual fragments of the isolated glomeruli containing juxtaglomerular cells (JGC) renin activity increased 1.2 times on the average, and there was revealed renin-like activity (RLA) in the fragments containing mesangial cells (MC). Signs of intensified renin secretion (expressed in reduction of granule count, marked development of granular endoplasmic reticulum, Golgi complex and microtubules) were noted in the JGC. In MC such organoids were well developed, but no granules were revealed. The following occurred in 8 to 12 weeks with the restoration of the 11-OCS and sodium level in the plasma: renin JGC activity became normal, RLA activity in MC disappeared, and the initial ultrastructure of both of these cells was restored. The reserve role of MC as the source of renin-like substances was confirmed.
Four postmenopausal women are described in whom breast cancer responded both to bilateral adrenalectomy and bilateral oophorectomy, and subsequently, after relapse, to estrogen therapy. This paradoxical finding demonstrates the complexity of the response of breast carcinoma to hormone manipulations. Simple estrogen dependence and estrogen suppression of pituitary mammotrophins are seen to be inadequate explanations of this phenomenon. Seven fundamental observations are listed that have to be accounted for by hypotheses concerning the endocrinology of breast cancer. It is suggested that in the past we have perhaps overlooked (1) the difficulty of extrapolating observations on experimental animal tumours to spontaneous human neoplasms, (2) the fact that there may be more than one type of breast cancer, and (3) the important role that must be played by the different tissues bearing the metastases.
A three-step, pharmacist-taught education program for adrenalectomy patients is described. Twenty-three patients were trained during the two years of the project. Training included: (1) an explanation of the patient's disease state and need for supplementary medication; (2) an explanation of each medication taken; and (3) training on self-administration of an i.m. dose of dexamethasone. Blue Cross agreed to pay the hospital ø25 per patient trained. Thirteen patients were available for interviews designed to evaluate the program. All patients knew the signs and symptoms of adrenal crisis and had excellent recall of information about their medication. Eight patients had increased their oral steroid doses as instructed to avoid adrenal insufficiency during stress. Substantial cost savings resulted from the program. The costs saved by offering the program justified the cost of supplying the service.
The diurnal variation in cholesterol synthesis exhibited by rat liver has been examined in fed, fasted, and adrenalectomized animals. Fasting for 3 days caused a lowering of the rate of synthesis but did not abolish the diurnal rhythm. Adrenalectomy abolished the diurnal variation, and caused synthesis to remain at a uniformly high level. We suggest that corticosterone may play an essential role in the daily rhythm of cholesterogenesis.
Normal rats were subjected to unilateral adrenalectomy and were killed 3 hr later. The concentration and composition of the cholesteryl esters in adrenals removed at operation and after death were compared. The esterified cholesterol concentration was lower in the adrenals obtained 3 hr after surgery. Cholesteryl arachidonate decreased in concentration significantly more than any other ester, followed in order of magnitude by linoleate and oleate. The cholesteryl ester concentration of adrenals removed from sham-operated rats 3 hr after surgery was also greatly reduced. On the basis of comparison with other work on the hydrolysis of cholesteryl esters by adrenal homogenates, it is concluded that the apparent selectivity in depletion of cholesteryl esters is due to differences in their rates of hydrolysis.
Plasma corticosterone (CST) level and body weight were studied in male and female rats after bilateral pallidal lesion (GPL). The effect of high dose of glycocorticoids on body weight of food and water deprived, non-lesioned rats was also studied since high CST levels due to the stress caused by the aphagia and adipsia could be anticipated. Weight changes in lesioned-adrenalectomized animals were in investigated as well. A weight loss, higher in males than females, developed after the pallidal lesion and the CST level was higher in lesioned females than in lesioned males. This sex-difference was present in non-lesioned, food and water deprived animals as well. The weight loss was higher in lesioned males than in food and water deprived male/female controls. Adrenalectomy eliminated weight loss differences between the sexes after lesion, by reducing the weight loss in males. CST administration reduced body weight loss in food and water deprived males but not in familes, and cortisol facilitated it in both sexes.
A technique for anaesthesia of Pietrain pigs using thiopentone or ketamine, ventilation with nitrous oxide and oxygen and muscle relaxation with pancuronium, is described. Bilateral adrenalectomy was carried out by a mid line laparotomy and details of the surgical technique are illustrated. Four of the 10 animals died 7--13 hours after surgery with a hyperthermic response.
Aminoglutethimide and dexamethasone were administered for 3 months to 11 postmenopausal women with advanced breast cancer. During initial in-hospital studies, there was uniform suppression of plasma cortisol (0.23 microgram/100 ml), androstenedione (8.3 ng/ 100 ml), estrone (0.44 ng/100 ml), and estradiol (0.32 ng/100 ml) to concentrations indistinguishable from those after surgical adrenalectomy. Eight of the 11 patients maintained this degree of suppression for 3 months. The other three patients may have taken inadequate amounts of dexamethasone, as evidenced by plasma steroid patterns characteristic of aminoglutethimide alone, that is, partial cortisol suppression (3.6 microgram/100 ml) and markedly increased androstenedione (355 ng/100 ml) with low estrone (0.54 ng/100 ml) and estradiol (0.61 ng/100 ml) concentrations. This apparent block in the aromatization of androstenedione to estrogens may be a feature important to the effectiveness of the regimen in sporadically noncompliant patients. After 3 months of therapy, return of resting plasma cortisol values to normal occurred within 3 to 4 days after cessation of the regimen and pituitary-adrenal responsiveness to surgical stress was demonstrable. This regimen is capable of maintaining an effective, reversible suppression of plasma steroids considered to be relevant to estrogen-dependent breast cancer.
Activities of alpha-hydroxybutyrate- and lactate dehydrogenases (HBDH, LDH), aspartate- and alanine aminotransferases (AST, ALT), alkaline phosphatase, alpha-amylase as well as content of total proteins, glucose, cholesterol, triglycerides and Ca2+ were estimated sprectrophotometrically in blood serum of rat males within 2 hrs after thermic burns of the III degree involving 15% the body surface. The burns caused about 2-fold increase in activities of LDH, HBDH and AST and in content of triglycerides in blood serum but did not affect the other biochemical patterns. Adrenalectomy, carried out within 3 days before the burns, accelerated and pseudoadrenalectomy decreased the early postburn enzymatic activation. Preadministration of reserpine, phentolamine and obsidane (propranolol) decreased distinctly the hyperenzymic reaction observed after the burn stress.
A pituitary-dependent Cushing's syndrome in a young woman had an unusually protracted course and was extremely resistant to therapy. After unsuccessful pituitary irradiation, bilateral total adrenalectomy was performed. A piece of an excised adrenal gland was reimplanted into a buttock. Nevertheless, the patient went into adrenocortical failure and had to be given replacement therapy. After three years the Cushing's syndrome reappeared, this time combined with general hyperpigmentation. The implanted adrenal tissue was no longer to be found. Neither stereotactic pituitary coagulation nor implantation of 90-Yttrium into the pituitary resulted in remission of Cushing's syndrome. All attempts to localize the--very probably ectopic--cortisol-producing adrenocortical tissue failed. However, complete remission was finally achieved by treatment with o,p'-DDD.
A method of "thin slices" was developed for estimation of enzymatic activities in cells, in which relationship between structure elements was maintained and the cells were readily permeable for substrates. Activities of Na, K-ATPase and succinate dehydrogenase were markedly higher in thin slices than in homogenates; activities of choline esterase and lactate dehydrogenase were of the same value in both tissue preparations. As compared with controls, adrenalectomy caused a decrease in Na, K-ATPase activity in the tissue slices, activities of succinate- and lactate dehydrogenases were unaltered and the choline esterase activity was increased. Comparison of the enzymatic activities in homogenates and thin slices indicates that some contradictions in data on the effect of the adrenal cortex hormones on the activity of the enzymes involved in the ion transport porcesses are due mainly to unadequateness of the methods used.
Adrenalectomized rat kidney is commonly used for the study of mineralocorticoid mechanism of action in mammals. In this model, aldosterone is known to bind to two classes of binding sites: type I (mineralocorticoid) and type II (glucocorticoid). The study of the aldosterone binding in normal rat kidney requires the elimination of endogenous hormones bound to each type of receptor. Thus, a suitable technique was developed using in situ perfusion of the kidneys. The efficacy of this method was of about 85 to 90% at the level of both cytoplasm and nucleus. Aldosterone binding capacity was checked in normal rat kidney after in situ perfusion and was found to be 300 to 500% lower than in adrenalectomized rat kidney, both in cytoplasm and nuclei. Computer analysis of aldosterone binding parameters in the cytoplasm (30,000 X g supernatant) of rat kidney suggested that adrenalectomy might induce an important rise in the number of mineralocorticoid receptors (congruent to 260%). An increase in the number of glucocorticoid receptors was also observed but appeared to be lower. Aldosterone, when perfused during 24 h in adrenalectomized rats, lowered the number of type I sites to the same level as observed in normal rat kidney. This effect was fully reversible after interruption of aldosterone perfusion. These results suggested an aldosterone-induced down regulation of mineralocorticoid receptors.
In experiments after adrenalectomy and adrenal cortex hormone therapy the quantity of ACTH was ascertained in the hypophysis of cats by methods of microphotometry and radioimmunoassay. The deviation of increased or decreased amounts was studied in acute as well as in chronic physiological conditions of the cats. The different methods to measure the quantities are equally identifying the physiological conditions.
Endogenous opioid substances are activated in and may contribute to the cardiovascular depression of hemorrhagic shock. In order to determine the importance of the adrenal gland in the beneficial effects of the opiate antagonist naloxone in shock we studied 23 adrenalectomized dogs subjected to hemorrhagic shock. Adrenalectomy abolished the salubrious cardiovascular responses to naloxone. Naloxone responses (increased mean arterial pressure, cardiac output, and left ventricular contractility) were restored by giving hydrocortisone 50 mg intravenously before naloxone. Survival was also prolonged in animals receiving naloxone and hydrocortisone compared to naloxone or saline alone; hydrocortisone alone decreased survival. The adrenal glands are necessary for naloxone's beneficial effects, probably via adrenal corticosteroid secretion.
The effects of naloxone on endotoxic hypotension in adrenalectomized and selectively adrenal demedullated rats were evaluated. In sham-operated rats, naloxone administered intracerebroventricularly (ICV) and intravenously (IV) produced an elevation of arterial pressure in this conscious rat model of endotoxemia. By contrast, both adrenalectomy and selective adrenal demedullation (wherein cortical function remained) not only enhanced the sensitivity to endotoxin-induced hypotension at least 10- to 15-fold, but also completely prevented the pressor response to ICV or IV naloxone. These results indicate that 1) adrenal enkephalins are probably not the endogenous opiates responsible for shock hypotension since their removal enhances shock susceptibility; 2) pituitary-derived endorphins in the circulation also appear to be uninvolved since naloxone fails to reverse shock hypotension despite reported elevations of circulating beta-endorphin in adrenalectomized rats; 3) since evidence indicates that naloxone acts centrally in intact endotoxemic rats and fails to do so following adrenal demedullation, we suggest that endotoxic shock results in an endogenous opiate inhibition of central autonomic sites regulating sympatho-medullary outflow. Naloxone, by reversing these actions, may result in the increased release of pressor substances from the adrenal medulla.
The gastric ulcerogenic effect of the glucocorticoid, prednisolone, was studied in albino rats. Shay operation in forestomachectomized rats with intact adrenals induced acute gastric ulcers in the corpus, whereas adrenalectomy prevented the development of gastric ulcers in another group of forestomachectomized Shay rats. Only superficial erosion of gastric epithelium was noticed in 66.67% of these rats. Administration of prednisolone to another group of similarly operated rats increased the number and severity of gastric ulceration, whether the adrenals were ablated or otherwise. From the observation of acid and mucous content of the stomach, it is postulated that the reduced mucous secretion may be an important predisposing factor in gastric ulcerogenic effect of steroids.
Unilateral medullosclerosis associated with splanchnicosympathectomy was applied in 60 cases of severe essential arterial hypertension. In 21 patients this was associated with contralateral adrenalectomy. No deaths were recorded. The late results (2 to 20 years) varied in terms of the anatomoclinical stage of the disease when surgery was performed. Systolic pressures fell to 30-50 mm Hg, hypertensive oscillations disappeared, mean adrenalinaemia values decreased by 47.9% after unilateral medullosclerosis and slanchnicosympathectomy and by 72.2% after bilateral interventions in two stage. The constitutional hyperadrenergic psychosomatic background was modified and became normohypoadrenergic. There was no case of adrenocortical insufficiency, the secretion of corticoids being insured by activity of the hexose-6-mono-phosphate dehydrogenase shunt.