Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENALECTOMY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,171 records · Page 65Linked to original sources
PubMed2001

Central CRH suppresses specific antibody responses: effects of beta-adrenoceptor antagonism and adrenalectomy.

Central corticotropin releasing hormone (CRH)-induced activation of the sympathetic nervous system and/or the pituitary-adrenal axis is hypothesized to mediate suppression of in vivo specific antibody responses. To test whether beta-adrenergic receptor activation is involved in the immunosuppressive effects of central CRH, rats were pretreated with propranolol or saline before intracerebroventricular infusion of CRH and immunization with keyhole limpet hemocyanin (KLH). KLH (3 microg/kg) immunization induced significant increases in circulating levels of antigen-specific IgM and IgG. Central infusion of CRH (200 pmol) suppressed both IgM and IgG responses. Pretreatment with propranolol (20 mg/kg IP) reversed CRH-induced suppression of IgG responses but had no effect on IgM levels. To test whether adrenal activation also plays a role in the effects of KLH on specific antibody responses, a separate group of animals underwent adrenalectomy prior to CRH infusion and immunization with KLH. As compared to nonadrenalectomized control rats, adrenalectomized rats showed a reduction of antibody responses, and CRH failed to induce a further suppression of IgM or IgG responses in adrenalectomized animals. Collectively, these data suggest that beta-adrenoceptors mediate the suppression of primary antibody responses induced by central CRH. Moreover, the adrenals may promote optimal primary antibody responses after exposure to physiological levels of antigen.

Adjuvants, Immunologic↗
PubMed1999

The level and phosphorylation of Hsp70 in the rat liver cytosol after adrenalectomy and hyperthermia.

Hepatic heat shock protein Hsp70 synthesis and in vitro phosphorylation were studied in the liver cytosol of intact, adrenalectomized and dexamethasone-administered adrenalectomized rats after 41 degrees C whole body hyperthermic stress. Hsp70 was detected by immunoblotting with N27F3-4 monoclonal antibody recognizing both constitutive and inducible forms of the protein. A comparison between basal and heat stress-induced levels of the protein in the liver cytosol of the three groups of animals suggested that glucocorticoid hormones stimulate the basal synthesis of Hsp70 and inhibit its induction by stress. In both unstressed and hyperthermia-exposed animals, hepatic Hsp70 was detected as a phosphoprotein. The extent of its in vitro phosphorylation was found to be significantly reduced by heat stress or adrenalectomy, but dexamethasone failed to restore it to the original level.

Adrenalectomy↗
PubMed1997

Immunosuppressive phenotype of corticotropin-releasing factor transgenic mice is reversed by adrenalectomy.

Stress elicits a wide range of physiological changes involving the nervous, endocrine, and immune systems. Corticotropin-releasing factor (CRF) plays a key role in orchestrating this response, activating both the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis, resulting in release of corticosteroids. The present study examines the immunological phenotype and responsiveness of CRF-transgenic (CRF-Tg) mice. The immune system of the CRF-Tg animals has profound changes compared to littermate controls, including a marked reduction in both cell number and immune responsiveness. There were also phenotypic changes in the lymphocytic composition of the various lymphoid organs, most notably in the spleen, where CRF-Tg mice had a greater percentage of T lymphocytes compared to littermate controls. Adrenalectomy of CRF-Tg reversed the immunological phenotype observed and restored immune responsiveness. These results demonstrate that CRF overexpression leads to profound impairment on lymphocyte development and function mediated via corticosteroids.

Adrenalectomy↗
PubMed1993

Adrenalectomy and steroid replacement in a small macropodid marsupial, the quokka (Setonix brachyurus): metabolic and renal effects.

Contrary to previously accepted observations, the quokka (Setonix brachyurus), a small macropodid marsupial, survival bilateral adrenalectomy indefinitely if injected with appropriate doses of cortisol and aldosterone, either singly or combined. Normal behavior and plasma solute concentrations could be maintained indefinitely by daily i.m. injection of 0.2 mg cortisol acetate and 0.01 mg aldosterone/kg. Plasma glucose concentration was maintained at the control value when the supplement contained cortisol but was significantly reduced with only a mineralocorticoid. Cortisol also caused a dose-related enhancement of food intake. There was no significant effect of supplementation on plasma urea concentration. Deoxycorticosterone, with or without cortisol, caused Na+ retention but aldosterone had this effect only when combined with cortisol. Urinary K+ excretion was not significantly affected by any of these corticosteroids. Withdrawal of hormone supplements caused muscular weakness and cessation of food intake within 3-6 days, accompanied by a moderate fall in Na+ and rise in K+ concentration of blood plasma as well as instability of plasma glucose concentration with hypoglycemic episodes. Renal excretion of both Na+ and K+ exceeded intake only when food intake had declined to negligible levels. Glomerular filtration rate (GFR) and renal plasma flow (RPF) fell when corticoids were withheld, without change in inulin space. However, p-aminohippurate (PAH) space fell, as did the intercompartmental exchange parameters of both inulin and PAH. Cortisol and aldosterone or aldosterone alone restored GFR, but not RPF, to the normal range. The fractional reabsorption of K+, but not Na+, was reduced in the absence of corticoids. It is suggested that, in this species, the circulatory effects of corticoids are essential for normal tissue perfusion and their influence on renal circulation is important in the control of salt and water balance. Metabolic effects are probably mainly permissive, as in other macropodid marsupials.

Adrenal Cortex Hormones↗
PubMed2000

Pharmacological adrenalectomy with mitotane.

The potential of mitotane (ortho, para'-DDD, commonly used to treat adrenal carcinomas in humans and dogs) was investigated as an alternative to surgical adrenalectomy in birds, salamanders, and lizards. House sparrows (Passer domesticus) were injected twice daily with vehicle or one of two doses of mitotane (225 or 450 mg/kg), and basal and stress-induced levels of corticosterone (CORT) were measured 3 and 5 days after injections. Mitotane reduced basal CORT levels to nondetectable and abolished stress-induced CORT increases by the 3rd day of treatment. In another study, a single injection of mitotane was effective in lowering endogenous CORT levels 36 h later, but levels had apparently recovered by 10 days after the injection. Mitotane did not effect testicular weights and had no detectable effect on testosterone levels. In contrast to its effects on house sparrows, mitotane did not lower endogenous CORT levels in either tiger salamanders (Ambystoma tigrinum) or tree lizards (Urosaurus ornatus), even at doses much higher than those used in house sparrows.

Adrenalectomy↗
PubMed1988

Hormonal regulation of muscle protein catabolism in acutely uremic rats: effect of adrenalectomy and parathyroidectomy.

To examine the role of glucocorticoids and PTH on the enhanced protein catabolism of acute uremia, rats were rendered uremic and had their adrenals or their parathyroid glands concomitantly removed. Adrenalectomy resulted in a marked reduction of urea generation in uremic animals due to decrease of myofibrillar protein breakdown as indicated by lower serum levels of Nt-methylhistidine and a reduction in the activity of the myofibrillar proteinase from skeletal muscle. This reduced urea formation was accompanied by marked hypoglycemia. Parathyroidectomy, on the other hand, caused no change of those parameters of protein catabolism, suggesting that PTH does not account for the protein degradation observed in acutely uremic rats.

Acute Disease↗
PubMed1987

Effect of glucocorticoid deficiency after adrenalectomy on antitumor immunity.

We studied the effect of corticosterone after adrenalectomy on antitumor immunity in immunogenic tumors in mice. Antitumor immunity in the glucocorticoid deficient adrenalectomized mice (ADX mice) examined via comitant immunity and cytotoxic activity of spleen cells was compromised. Antitumor immunity was detected in ADX mice receiving sufficient supplementary doses of corticosterone. Loaded stress compromised the cytotoxic activity of the spleen cells in the ADX mice receiving adequate corticosterone, and the failure also contributed to the glucocorticoid deficiency because the activity was not affected by stress in the sham ADX mice. A matured effector cell activity was transferred to the glucocorticoid deficient ADX mice. We conclude that glucocorticoid deficiency compromises the antitumor immune response and that glucocorticoid might play an important role in the maturation of immunocompetent cells.

Adrenalectomy↗
PubMed1977

Formaldehyde-ozone-induced fluorescence in pituitary ACTH cells: effect of adrenalectomy.

ACTH and MSH cells of the pituitary are rich in peptides with NH2-terminaltryptophan, as revealed by fluorescence histochemistry. Adrenalectomy stimulates the ACTH cells but not the MSH cells. As a result, ACTH as well as tryptophyl-peptides disappear from the ACTH cells but not from the MSH cells. It is concluded that the tryptophyl-peptides are stored together with the respective hormone in the ACTH and MSH cells and that tryptophyl-peptides in the ACTH cells are released together with the hormone.

Adrenal Glands↗
PubMed1991

Quantitative non-radioactive in situ hybridization. Model studies and studies on pituitary proopiomelanocortin cells after adrenalectomy.

Non-radioactive in situ hybridization using biotinylated oligodeoxynucleotides and a detection protocol involving monoclonal antibiotin antibodies and the alkaline phosphatase-anti-alkaline phosphatase system was employed for quantitation by image analysis. Calibrations of the image analysis system with neutral density filters revealed that the grey levels recorded were strongly linearly correlated to the absorbance (r2 = 0.97) in the range studied in tissue specimens (0-0.8 optical density or absorbance units). Several methodological parameters, including light source stability, section thickness, probe concentration and development time were initially optimized. Model systems revealed that the grey level measured varied linearly with the logarithm of the target concentration. Moreover, histophysiological studies on adrenalectomized and sham-operated rats documented that previous biochemical data on an 8- to 10-fold increase in anterior lobe proopiomelanocortin (POMC) mRNA levels 8 days after adrenalectomy are accounted for both by an increased ACTH cell concentration and content of POMC mRNA, as well as by increases in ACTH cell sizes and cell numbers. Also in agreement with biochemical data, image analysis did not reveal significant differences between OD's of melanotrophs in adrenalectomized and sham-operated animals. To our knowledge, these data are the first to document that non-radioactive in situ hybridization can be employed for relative quantitation. A particular advantage of this approach is the good morphological definition which permits parallel analyses of densitometric values, cell sizes and cell areas/cell numbers.

Adrenal Glands↗
PubMed1989

Effect of adrenalectomy on diazinon-induced changes in carbohydrate metabolism.

Treatment with diazinon resulted in hyperglycaemia and depletion of glycogen from cerebral and peripheral tissues 2 h after its administration in rats; the changes were maximal after 40 mg/kg diazinon, administered intraperitoneally. The activities of glycogen phosphorylase and phosphoglucomutase were significantly increased in brain and liver, while that of glucose-6-phosphatase was not altered. The activities of the glycolytic enzymes hexokinase and lactate dehydrogenase were increased only in brain. The cholinesterase activity of the brain was reduced by treatment with diazinon. The activities of hepatic gluconeogenic enzymes (fructose 1,6 diphosphatase and phosphoenolpyruvate carboxykinase) were also significantly increased in diazinon-treated animals. The level of lactate was increased in brain and blood while that of pyruvate was not changed. The activity of glucose-6-phosphate dehydrogenase was not significantly changed. Cholesterol and ascorbic acid contents of adrenals were depleted in diazinon-treated animals. Adrenalectomy abolished the hyperglycaemia and changes in carbohydrate metabolism, suggesting the possible involvement of adrenals in the induced changes in diazinon-treated animals.

Adrenalectomy↗
PubMed1983

Effect of adrenalectomy, pretreatment with SKF 525-A, phenobarbital and diethyl maleate on the acute toxicity of fenitrothion in male rats.

The effect of adrenalectomy (Adx), SKF 525-A, phenobarbital (PB), and diethyl maleate (DEM) on the acute toxicity of fenitrothion was investigated in male rats by assessing the degree of plasma cholinesterase activity. PB, 60 mg/kg/day for 3 days, exerted no protective effect on the toxicity of fenitrothion (100 mg/kg, p.o.) given 24 h after the last injection. In adrenalectomized and SKF 525-A-pretreated rats, the toxicity of fenitrothion was lower than that of the controls. Fenitrothion toxicity was increased by administration of DEM (1 ml/kg), which depletes hepatic glutathione (GSH) levels. In vitro, the rates of fenitrothion decomposition and fenitrooxon formation by microsomes were markedly affected by PB, SKF 525-A and Adx. The decomposition of fenitrooxon by the microsomal fraction and GSH-dependent decomposition of fenitrooxon by the soluble fraction were not affected by PB, SKF 525-A and Adx pretreatment. The GSH-dependent decomposition of fenitrothion and fenitrooxon was increased by addition of GSH to the incubation mixture. The present results indicate that the GSH-dependent metabolic pathway plays an important role in the detoxication of fenitrothion.

Adrenalectomy↗
PubMed1984

The effect of adrenalectomy and dexamethasone on the antinociceptive effects of physostigmine.

The tail-flick procedure was used to study the antinociceptive effects of physostigmine in adrenalectomized and sham-operated rats. At 5 days after surgery, they were tested 30 min after either 0.32 or 0.45 mg/kg IP physostigmine. Adrenalectomized animals showed significantly greater elevation of TF scores from predrug latencies than the sham controls at both doses of physostigmine. Following 3 days of dexamethasone replacement therapy on days 18, 19, and 20 post-surgery the antinociceptive effects of physostigmine were uniformly attenuated across doses or surgical groups. On the other hand, animals receiving saline injection instead of dexamethasone did not manifest any reduction of the physostigmine antinociceptive effect. The potentiation by adrenalectomy and the reduction following dexamethasone of the antinociceptive effects of physostigmine suggest that these effects may be mediated through hypothalamic-pituitary-adrenal mechanisms and are consistent with beta-endorphin-induced sensitization of opiate or cholinergic receptors.

Adrenalectomy↗
PubMed1993

Immunocytochemical localization of glucocorticoid receptors in the spinal cord: effects of adrenalectomy, glucocorticoid treatment, and spinal cord transection.

1. Studies were performed to determine the changes in immunoreactive (IR) type II glucocorticoid receptors of the ventral horn of the spinal cord produced by adrenalectomy (ADX), dexamethasone (DEX) treatment, and spinal cord transection in rats. 2. These treatments did not significantly affect the number of IR neurons of the ventral horn; however, staining intensity was enhanced after ADX and decreased following 4 days of DEX. A similar response pattern was observed for glial-type cells. 3. In control rats, about half of the ventral horn motoneurons were surrounded by immunoreactive glial perineuronal cells. These perineuronal cells increased after ADX (77% of counted neurons) and decreased following DEX treatment (32%; P < 0.05). 4. Two days after transection, staining was intensified in ventral horn motoneurons and glial cells located in the spinal cord below the lesion. Immunoreactive perineuronal cells increased to 85% of counted neurons, from a value of 66% in sham-operated rats (P < 0.05). 5. These findings suggest considerable plasticity of the spinal cord GCR in response to changes in hormonal levels and experimental lesions. It is possible that factors involved in cell to cell communication with transfer of hypothetical regulatory molecules may play roles in GCR regulation and the increased immunoreaction of glia associated with neurons following transection and ADX.

Adrenalectomy↗
PubMed1991

The effects of adrenalectomy and thermal stress on glutamic acid decarboxylase activity in different regions of the rat brain.

Glutamic acid decarboxylase (GAD) enzyme activity was measured in synaptosomes prepared from the hypothalamus, the hippocampus, the striatum and the cerebral cortex of control, adrenalectomized and rats exposed to a thermal stress. Adrenalectomy caused a statistically significant decrease in the enzyme activity in the striatum, while it had no effect in the other three brain areas. On the other hand, exposure to the thermal stress resulted in a dramatic increase of GAD specific activity in all brain areas examined. This thermal stress-induced increase in enzyme activity was observed in both non-operated and adrenalectomized animals, which implies that it is not mediated by glucocorticoids.

Adrenalectomy↗
PubMed1981

Effect of castration and adrenalectomy on the ultrastructure of pinealocytes in the female garden dormouse (Eliomys quericnus L.) under different conditions of lighting and temperature during the normal period of hibernation.

The ultrastructure of the female garden dormouse pinealocyte has been studied during the period of hibernation in normal, castrated, castrated and adrenalectomized hibernant animals and non-hibernant ones living under a L-D = 10-14 photoperiodicity or continuous lighting. Continuous illumination on the one hand, and gonad and adrenalectomy on the other, have similar effects on the ultrastructure of pinealocytes. Especially a striking reduction of liposomes, an increased development of the Golgi apparatus and of cisterns formed by the rough endoplasmic reticulum were observed. The observations suggest that the liposomes are involved in a perhaps indoleaminergic antigonadotropic secretory process whereas the peculiar dilated cisterns of the rough endoplasmic reticulum may be related with a pineal polypeptidergic gonadotropic secretory process.

Adrenalectomy↗
PubMed1996

Effect of adrenalectomy and corticosterone substitution on glucose and glycogen metabolism in rat brain.

In non-nervous tissues, glucocorticoids (GCs) counteract the effects of insulin and stimulate gluconeogenesis. The present study was designed to investigate whether or not adrenalectomy (ADX) and glucocorticoid substitution influence the pathway of both glucose and glycogen metabolism in cerebral parietotemporal cortex and hippocampus, and if so how. The activities of respective key enzymes, such as hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK), glucose-6-phosphatase (G6Pase) and phosphorylase a (PLa), and the concentrations of the intermediates, such as glucose (Glu), glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), fructose-1,6-bisphosphate (F16PP), pyruvate (Pyr), lactate (Lac), glycogen (Glyc) and glucose-1-phosphate (G1P), were measured in the brains of 1-year-old male Wistar rats under controlled conditions 3 days after ADX or sham operation and in a pilot study after ADX and substitution with corticosterone (CST) suspended in sesame oil or after ADX and subcutaneous administration of the vehicle only. An increase in both glycolytic flux and glycogen breakdown and a decrease in gluconeogenesis in cerebral cortex but not in hippocampus were observed after ADX. After substitution with CST in adrenalectomized rats the effect of ADX on enzyme activities was reversed: significant differences from adrenalectomized rats that received vehicle only was shown for PK and G6Pase activities in both areas of the rat brain investigated.

Adrenalectomy↗
PubMed1995

Proliferation of pituitary corticotrophs following adrenalectomy as revealed by immunohistochemistry combined with bromodeoxyuridine-labeling.

Proliferation of corticotrophs following adrenalectomy (ADX) was studied by a combination of bromodeoxyuridine (BrdU)-labeling and immunohistochemistry. Rats were adrenalectomized, allowed to survive for 1, 3, 7, and 14 days and given 100 mg/kg body wt BrdU 3 h before sacrifice. BrdU and adrenocorticotropic hormone (ACTH) were detected in the same sections of the anterior pituitary using double-labeling immunohistochemistry. BrdU-labeled cells in the pituitary showed a tendency to increase until 1 week after ADX and slightly decreased at 2 weeks. Corticotrophs were increased to about 1.5 times of the control level 1-2 weeks after ADX. The number of cells double-labeled with both BrdU and ACTH increased markedly after ADX, suggesting active mitosis of existing corticotrophs. On the other hand, the ratios of these double-stained cells to all BrdU-labeled cells and to all corticotrophs were 5-7% and 0.9-1.3%, respectively, even after ADX, suggesting that the majority of corticotrophs which were increased after ADX were recruited from some other type of immature cells. The extent to which the two mechanisms are involved in hyperplasia of corticotrophs after ADX remains to be elucidated.

Adrenalectomy↗
PubMed1981

Medical adrenalectomy in patients with advanced breast cancer resistant to anti-oestrogen treatment.

Fifty-three women with actively progressing advanced breast cancer, who had all previously received tamoxifen, were treated with aminoglutethimide to induce medical adrenalectomy. Sixty-nine percent of the patients who had previously responded to tamoxifen subsequently responded to aminoglutethimide, while thirty-five percent of the nonresponders to tamoxifen subsequently responded to aminoglutethimide. The median duration of remission to aminoglutethimide was 12 months with a range from 4 to 22 + months. The drug was well tolerated and would appear to be the treatment of choice in tamoxifen responsive cases of advanced breast cancer.

Adrenalectomy↗