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PubMed1991

Effects of adrenalectomy and nephrectomy on adrenal regeneration hypertension in the rat.

The involvement of the regenerating adrenal gland and kidney, and the contribution of deoxycorticosterone (DOC) and prostaglandin E2 (PGE2), in the development of adrenal regeneration hypertension (ARH) was evaluated in young female Sprague-Dawley rats. Based on tail-cuff plethysmographic measurement, animals subjected to nephrectomy and adrenalectomy on the right side and adrenal enucleation (removal of the adrenal cortex) on the left side developed significant (P less than 0.05, n = 12) hypertension within 6 weeks following operation. Subsequent left nephrectomy in these ARH rats produced a further elevation, whereas a secondary adrenalectomy resulted in an acute and discernible reduction in blood pressure within 24-36 hours. It is interesting to note that the progressive increase in blood pressure following left nephrectomy was significantly reversed by PGE2 (10 or 20 micrograms/kg, i.p.). At the same time, the reduction in blood pressure after secondary adrenalectomy was significantly retarded by deoxycorticosterone trimethylacetate (2 mg/kg, i.p.). These data demonstrated that both the kidney and the regenerating adrenal cortex are involved in the pathogenesis of ARH. Furthermore, it is probable that the secretion of DOC by the regenerating adrenal cortex is responsible for the elevation in blood pressure, in a process that is balanced by PGE2, possibly secreted by the kidney.

Adrenal Glands↗
PubMed1977

Plasma ACTH in rats following medical adrenalectomy.

We have previously reported that surgically adrenalectomized nonstressed rats showed delayed secretion of the expected increase in plasma ACTH concentrations following adrenalectomy.(1) However, increased plasma ACTH concentrations were always detected when these animals were subjected to severe stress, and their responsiveness increased again seven days or more following surgical adrenalectomy. We are now reporting similar results which were obtained following prolonged systemic glucocorticoid administration (medical adrenalectomy) in similar groups of rats.

Adrenal Glands↗
PubMed1990

Hypophysial trophic hormone response to adrenalectomy and ether stress in rats bearing anterior pituitary tissue in third ventricle of the brain.

Inhibitory effect of anterior pituitary tissue implanted into the brain on trophic hormone secretion was studied under resting conditions and after adrenalectomy or ether stress. The weight of pituitary gland in rats bearing anterior pituitary graft in the third ventricle was decreased and the body weight gain was retarded. The levels of ACTH, PRL and GH, but not those of FSH and LH in plasma were significantly lower as compared with all control groups. There was a pituitary ACTH, PRL and GH response to adrenalectomy and ether stress in these rats. Besides supporting literary data on the inhibitory effect of additional pituitary grafts on the adenohypophysis, these findings indicate that pituitary implants did not cause any appreciable alteration of pituitary responsiveness, at least to adrenalectomy or ether stress.

Adrenal Glands↗
PubMed1979

Effects of adrenalectomy on hormone action on hepatic glucose metabolism. Impaired glucagon activation of glycogen phosphorylase in hepatocytes from adrenalectomized rats.

The effects of adrenalectomy on glucagon activation of liver glycogen phosphorylase and glycogenolysis were studied in isolated hepatocytes. Adrenalectomy resulted in reduced responsiveness of glycogenolysis and phosphorylase to glucagon activation. Stimulation of cAMP accumulation and cAMP-dependent protein kinase activity by glucagon was unaltered in cells from adrenalectomized rats. Adrenalectomy did not alter the proportion of type I and type II protein kinase isozymes in liver, whereas this was changed by fasting. Activation of phosphorylase kinase by glucagon was reduced in hepatocytes from adrenalectomized rats, although the half-maximal effective concentration of glucagon was unchanged. No difference in phosphorylase phosphatase activity between liver cells from control and adrenalectomized rats was detected. Glucagon-activated phosphorylase declined rapidly in hepatocytes from adrenalectomized rats, whereas the time course of cAMP increase in response to glucagon was normal. Addition of glucose (15 mM) rapidly inactivated glucagon-stimulated phosphorylase in both adrenalectomized and control rat hepatocytes. The inactivation by glucose was reversed by increasing glucagon concentration in cells from control rats, but was accelerated in cells from adrenalectomized rats. It is concluded that impaired activation of phosphorylase kinase contributes to the reduced glucagon stimulation of hepatic glycogenolysis in adrenalectomized rats. The possible role of changes in phosphorylase phosphatase is discussed.

Adrenalectomy↗
PubMedDate not supplied

[Changes in the ultrastructure of rat hepatocyte nucleoli during bilateral adrenalectomy and after administration of cortisol].

Nucleolar ultrastructure of the rat hepatocytes after bilateral adrenalectomy and cortisol stimulation has been studied by the electron-microscopic method Traits of nucleolar inactivation (a decrease of granular component enlargement of fibrillar centres, condensation of peri- and intranucleolar chromatin, etc.) are observed in hepatocyte nucleoli 5 days after adrenalectomy. Cortisol stimulation of hepatocytes of the adrenalectomized rats leads to nucleolar activation (4h, 5h, 8h after the hormone injection). Adrenalectomy with following cortisol injection is a useful model to study inactivation and activation of ribosomal genes in the target cells.

Adrenalectomy↗
PubMed1989

[Effect of ACTH, dexamethasone, and adrenalectomy on the secretion of testosterone in the rat].

The effect of ACTH (100 micrograms/animal/day, i.p.), dexamethasone (75 micrograms/animal/day, s.c.), both for three consecutive days, and adrenalectomy, with or without dexamethasone, maintained according to the group, one, two or three days, on the plasmatic testosterone and corticosterone levels, has been studied in adult male Wistar rats. ACTH and adrenalectomy produced a high decrease in testosterone levels (p less than 0.001 for the three days studied). Dexamethasone produced lower testosterone levels in the first day followed by partial recuperation between the second and the third days of its administration. Dexamethasone produced the effects mentioned for intact animals. The changes in corticosterone levels were according to an adequate response of the hypothalamus-pituitary-adrenal system under these experimental circumstances. ACTH exerts an inhibitory effect on testosterone secretion in the rat, so that such an effect from the data obtained after adrenalectomy and simultaneous dexamethasone injections, does not seems to be mediated either by the presence of adrenals or high corticosterone levels.

Adrenalectomy↗
PubMed1989

Long-term studies on compensatory adrenal growth in the female hamster induced by unilateral adrenalectomy.

The study was designed to explain the cellular aspects of compensatory adrenal growth in the female hamster in the course of long-term unilateral adrenalectomy. Animals were autopsied 3, 6, 9, 18 and 36 days after unilateral adrenalectomy. Removal of the left adrenal gland within 36 days did not change both the absolute and relative adrenal gland weight of the female hamster. Also the volume of particular adrenocortical zones and the number of parenchymal cells in the zones and in the entire cortex were unchanged in unilaterally adrenalectomised hamsters. Moreover, in the course of experiments the volumes of the glomerulosa and fasciculata cells were unchanged in relation to the control group. On the contrary, a marked increase in the volume of the zona reticularis cells was observed, with the highest rate of increase within the first 9 days after unilateral adrenalectomy.

Adrenal Glands↗
PubMed1989

Effect of glucocorticoid replacement on tumor growth after adrenalectomy in mice.

We studied the effects of glucocorticoid replacement on tumor growth after adrenalectomy of Meth A sarcoma in mice. Tumor growth was inhibited in the adrenalectomized mice when a minimum dose of corticosterone, 0.3 mg/day, was given for replacement, and higher doses led to an even greater inhibition. Corticosterone had no effect on tumor growth in the irradiated mice. Sinecomitant immunity in the case of growth of the retransplanted excised tumor was compromised in the adrenalectomized mice. In vivo neutralization and immunosuppressive activities were absent in the spleen cells of the adrenalectomized mice. It would thus appear that adrenalectomy suppresses tumor growth by mechanisms other than glucocorticoid ablation. For optimum tumor control, glucocorticoid replacement after adrenalectomy should be in excess of the minimum daily requirements.

Adrenalectomy↗
PubMed1987

The effect of bilateral adrenalectomy on metabolism and tissue distribution of ascorbic acid in the rat.

Adult, male, Sprague-Dawley rats were injected with [1-14C] -ascorbic acid 11 days post bilateral adrenalectomy or sham-adrenalectomy, and immediately placed in metabolism chambers. Excreta (CO2 and urine) were collected for 48 hours. The animals were then sacrificed and 10 tissues were processed and assayed for total ascorbic acid (AA) and radioactivity. There was no significant difference in weight gain between groups post-operation. Adrenalectomized rats excreted significantly less radioactivity, resulting in a significantly longer estimated half-life of AA (173 +/- 7 h) than the sham-adrenalectomized controls (141 +/- 7 h). Weights of tissues were similar between groups. The concentration of AA was significantly higher (43%) in the heart and lower (17%) in the liver in adrenalectomized animals. This group of animals also had significantly higher levels of radioactivity in the heart (51%), kidney, and spleen (19%). The specific activity of AA (% dose/mg AA) was not different between groups for any tissue examined. These results demonstrate that adrenalectomy affects the degradation of AA and its concentration in selected tissues, with a profound effect on the heart.

Adrenalectomy↗
PubMedDate not supplied

Changes in calcitonin secretion and in serum magnesium following adrenalectomy in rats.

The level of serum magnesium and also thyroid of calcitonin content was followed up in the conditions of adrenalectomy after hydrocortisone replacement as well as after calcium propranolol administration. Six days after adrenalectomy a significant decrease both of calcitonin secretion and of serum magnesium was noted. Hydrocortisone replacement reestablished the levels of both parameters to the levels found in controls. Adrenalectomy also reduced the calcitonin secretory response consequent to calcium loading, but calcium excess simultaneously determined hypermagnesemia. Propranolol, a beta blocker with direct action on the secretory tonus of the thyroid C cells, completely annulled the stimulation effect of calcium in adrenalectomized animals but not the hypermagnesemic response. The adrenocortical hormones interfere in the calcitonin-magnesium secretory antagonism, together with the sympathetic -adrenergic system, ensuring the secretory control of calcitonin especially by blocking the occurrence of an excess of magnesium which reduces calcitonin secretion.

Adrenal Cortex↗
PubMed1966

Effect of adrenalectomy and glucocorticoids on the secretion and absorption of hydrogen ion.

The effect of bilateral adrenalectomy on the secretion and absorption of acid in Heidenhain pouch dogs has been investigated. It was found that bilateral adrenalectomy significantly decreased the acid output to varying doses of histamine and did not alter the relation between hydrogen ion concentration and the volume rate of secretion. The absorption of acid by the gastric mucosa was not changed by adrenalectomy. Glucocorticoids but not mineralocorticoids restored secretion to normal levels. These experiments indicate that the impaired secretion of acid in response to histamine in adrenalectomized dogs is not attributable to increased leakage of secreted acid from lumen to blood.

Adrenal Cortex Hormones↗
PubMed1983

Cushing's disease treated by total adrenalectomy: long-term observations of 43 patients.

Forty-three patients were treated by total adrenalectomy for pituitary-dependent Cushing's disease. The median period of observation was 10 years (range one to 20 years). Thirty-eight patients (88 per cent) had rapid and lasting remissions. Of the 38 in remission, 21 became pigmented but without pituitary enlargement, 11 became pigmented with evidence of further pituitary expansion (Nelson's syndrome) and six neither became pigmented nor showed pituitary expansion. Pituitary expansion was associated with high plasma ACTH values, and treatment of pituitary tumours by surgery or radiotherapy gave poor results. However, when compared with alternative methods of treatment, total adrenalectomy for Cushing's disease is still satisfactory for many patients, despite advances in pituitary surgery, and has advantages over 'medical adrenalectomy' with drugs.

17-Ketosteroids↗
PubMed1984

Hypertension after brainstem (A1) lesions in normal rats and in rats with adrenalectomy, sympathectomy or diabetes insipidus.

Lesions of the ventrolateral medulla coinciding with the A1 noradrenaline cell group, in either the rabbit or the rat, cause hypertension and bradycardia accompanied by 50-fold increases in plasma vasopressin and adrenaline and a two-to-four-fold increase in plasma noradrenaline. Following adrenalectomy in normal rats, the A1 hypertension and bradycardia were unchanged. In Brattleboro rats with diabetes insipidus, A1 hypertension was not altered but the bradycardia was reduced by 40%. In Brattleboro rats subjected to adrenalectomy, the hypertension was reduced by 50%. In normal rats, chemical sympathectomy with intravenous 6-hydroxydopamine (6OHDA) reduced the hypertension by about 50%, and when combined with adrenalectomy it abolished the hypertension altogether. In Brattleboro rats, 6OHDA reduced the hypertension after A1 lesions by about 40%. We suggest that A1 hypertension is predominantly mediated through increased activity of sympathetic vasoconstrictor nerves, and that circulating adrenaline and vasopressin only make a minor contribution to the increase in pressure.

Adrenal Glands↗
PubMed1978

[Early effect of adrenalectomy and castration on the demethylating activity of the liver microsomal fraction in male rats].

The author examines three indices in liver microsomal fraction during the first five days after castration and adrenalectomy of male rats: demethylation in vitro of amidophen, amount of cytochrome P450 and cytochrome b5. Demethylating activity is lowered significantly to the respective control on the second day after adrenalectomy--73%, on the fifth day--61%; after castration on the third day--71%, on the fifth day--75%; after simultaneous castration and adrenalectomy after two days--53%, but on the fifth day--22%. The amount of cytochrome P450 diminishes parallely to the demethylating activity is due to the reduced amount of cytochrome P450, but the reduction of the latter is explained by the lowered activity of aminolevulanatsynthetase--the limiting enzyme in the synthesis of heme of cytochrome P450. Androgens and corticoids are inductors of microsomal oxidative enzymes and probably on the basis of this action the activity of aminoevulinatsynthetase is affected.

Adrenal Glands↗
PubMed1995

[Laparoscopic adrenalectomy in pheochromocytoma].

Standard adrenalectomy for pheochromocytoma was until recently performed via the transperitoneal open approach. The disadvantage of the open procedure is a more painful and longer recovery. With good surgical experience in laparoscopic techniques and in endocrine surgery, laparoscopic adrenalectomy can be performed safely without complications. The advantage of the laparoscopic technique is excellent vision of the operative field with magnification even of very small vessels. The first two cases of laparoscopic right adrenalectomy at our institution are described.

Adrenal Gland Neoplasms↗
PubMed1995

[Adrenalectomy under celioscopy. Experience of 25 operations].

OBJECTIVES: Determine the indications for laparoscopic adrenalectomy on the basis of our experience. METHODS: We performed 25 laparoscopic adrenalectomies for primary hyperaldosteronism (n = 10), non-ACTH-dependent hypercortisolism (n = 6), Cushing's disease (n = 2 including one bilateral operation), pheochromocytoma (n = 1) and tumoral formation (n = 5). RESULTS: The operation required conversion to an open procedure in 4 cases (16%). The post-operative period was uneventful in 19 and was clearly less painful. Improved delay to normal intestinal function and rapid return to normal activities was also beneficial in these patients with no parietal damage. Complications occurred in two cases: one local asymptomatic collection and one localized pancreatitis requiring surgical drainage of an abscess. COMMENTS: Compared with our experience with open procedures, the inconvenience of a long laparoscopic procedure (2h 45 min for unilateral adrenalectomy), is counterbalanced by the reduction in risk to complications in 64% of the cases due to the simplicity and lack of parietal damage. We currently propose the laparoscopic procedure for tumours under 6 cm in diameter and for certain pheochromocytomas and rely on the open procedure for proven or suspected corticoadrenalomas.

Adrenal Gland Neoplasms↗
PubMed1995

Transperitoneal laparoscopic versus open adrenalectomy for benign hyperfunctioning adrenal tumors: a comparative study.

In our retrospective study we compare the effectiveness and safety of transperitoneal laparoscopic versus open adrenalectomy in 40 patients with benign hyperfunctioning unilateral adrenal tumors. Patients 1 to 20 underwent open adrenalectomy between July 1988 and July 1992, and patients 21 to 40 underwent the laparoscopic procedure between September 1992 and January 1994. Student's t test for unpaired data was used to compare intraoperative and postoperative results, and morbidity observed in the 2 groups. The affected adrenal gland was successfully removed in all cases. Mean operative time was significantly longer for laparoscopy, although it shortened progressively due to the learning curve effect. Blood loss was significantly less with laparoscopy, while only 3 patients undergoing open surgery required blood transfusions. Overall invasiveness and analgesic requirement were significantly lower with laparoscopy. The intervals to oral intake and ambulation, hospital stay and return to preoperative normal activity were shorter with laparoscopy. Major complications were noted only in open surgery patients. At 3 months all patients in both groups were cured of the underlying adrenal disease. We conclude that transperitoneal laparoscopic adrenalectomy is equally effective and less invasive than open surgery, and that it should be considered the first choice therapy for benign hyperfunctioning adrenal tumors.

Adrenal Gland Neoplasms↗
PubMed1994

[Results of unilateral adrenalectomy for primary hyperaldosteronism].

From 1970 to 1992, 57 patients underwent unilateral adrenalectomy for primary hyperaldosteronism. All were hypertensive and the biochemical profile was diagnosed in all cases but two. 44 out of 57 were operated on using to the posterior Young Mayor approach. The present series included 44 macroadenomas > or = 1 cm in diameter (21 > 2 cm; 23 < or = 2 cm), 7 microadenomas (< 1 cm), 3 associations of macro and microadenomas and 3 cases of unilateral hyperplasia. All were biochemically cured. 4/57 patients remained hypertensive postoperatively (3/44 macroadenomas and 1/3 unilateral hyperplasia). There were two late recurrences, which were both clinical and biochemical (2 macroadenomas < or = 2 cm), and one of these was reoperated on for contralateral multiple "adenomas". Pathological background was defined by preoperative imaging studies with a sensitivity of 100% for MRI (23 cases), 96% for CT-scan (52 cases), 73% for NP 59 scanning (15 cases), 38% for sonography (16 cases) and 85% for venous sampling (7 cases). Cure of hyperaldosteronism or hypertension after unilateral adrenalectomy was therefore not predictable by the pathological background. If a firm diagnosis of primary hyperaldosteronism has been made and the unilaterality of the disease has been established, the patient should be operated. Even adrenalectomy for unilateral hyperplasia can lead to cure, and the syndrome can recur after removal of a solitary macroadenoma.

Adrenalectomy↗