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PubMed1989

Quantitative electron microscopy of carcinogen-induced alterations in hepatocyte rough endoplasmic reticulum. II. Modulation of the effects of 3'MeDAB by adrenalectomy and adrenal corticosteroids.

A quantitative electron microscope study was made of the effects of bilateral adrenalectomy (ADX) and deoxycorticosterone acetate (DOCA) on the state of aggregation of hepatocyte rough ER cisternae in both untreated and 3'MeDAB-fed Leeds strain rats. Disaggregation of hepatocellular rough ER appears to be a common response of the rat liver to hepatocarcinogenic insult, while ADX and DOCA treatment are known to inhibit the chemical induction of neoplasia in this species. In untreated animals both ADX and DOCA significantly increased the mean number of cisternae per array or stack, while an even more pronounced effect was obtained from a combination of the two. The carcinogen 3'MeDAB induced a highly significant loss of aggregation, which was prevented by the combination of ADX and DOCA. In a separate experiment, a single dose of cortisone acetate was also found to partially reverse 3'MeDAB-induced rough ER disaggregation. In the rat hepatocyte, rough ER stacking or aggregation appears to be at least partially under hormonal control.

Adrenalectomy↗
PubMed1989

Studies on the mechanism of the decreased guanine nucleotide stimulatory effects on adenylate cyclase after adrenalectomy in rat adipocytes.

In adipocyte membranes from adrenalectomized rats: (i) the defect in the stimulatory effects of guanine nucleotides on adenylate cyclase is greater with GTP than with GppNHp and appears to concern the GS-C complex and not the HR-GS-C ternary complex; (ii) the GTP-ase activity is enhanced; (iii) maximal alpha S-C interaction (tested by the responses to forskolin, cholera toxin or NaF) is unaltered and (iv) the alpha S affinity for guanine nucleotides and the GDP/GppNHp exchange reaction are both unimpaired. These data suggest that the enhanced GTP-ase activity together with a decrease in the catalytic activity of the alpha S-GTP-C complex are the likely mechanisms whereby adrenalectomy causes a defect in the fat cell adenylate cyclase response to guanine nucleotides.

Adenylyl Cyclases↗
PubMed1989

Adrenal cortex transplantation after bilateral total adrenalectomy in the rat.

An experimental animal model with adrenal cortex transplantation was developed to study adrenal cortex replacement therapy in patients with multiple endocrine neoplasia type 2 who have had bilateral adrenalectomy for pheochromocytomas. Adrenal cortex of syngenetic rats was isolated from the medulla by collagenase digestion and a defined sedimentation. The cell suspension of the cortical cells was implanted under the kidney capsule of untreated syngenetic rats. After two weeks the recipients were bilaterally adrenalectomized. Serum corticosterone levels were measured as an estimate of function of the grafts. All recipients were healthy throughout the observation period, whereas all adrenalectomized controls died within 18 days. Vital cortex cells could be demonstrated in the explanted grafts by immunohistochemistry. Corticosterone levels of transplanted animals were nearly normal (9.5 ng/100 mL +/- 0.4) compared to the controls (0.20 ng/mL +/- 0.06). This animal model of adrenal cortex transplantation allows the separation of medullary from cortical cells. After transplantation, these cortical cells survived for eight weeks and were able to replace the adrenal cortex function.

Adrenal Cortex↗
PubMed1986

An improved method for adrenalectomy of suckling rats. The influence of thrombin treatment and deoxycorticosterone substitution on survival and on hepatic and renal enzyme activities.

Adrenalectomy of suckling rats is complicated by a high mortality rate, caused by the loss of blood (early mortality) and by the disturbed sodium-potassium balance (late mortality). Treatment of the abdominal cavity with a thrombin solution and a daily administration of deoxycorticosterone glucoside (DOC) decrease the total mortality remarkably. DOC treatment has no influence on renal beta-glucosidase and beta-galactosidase as well as on hepatic tyrosine aminotransferase activity, whereas hepatic serine dehydratase activity exhibits a time- and dosage-dependent response to this hormone. The DOC effect is very likely a consequence of the glucocorticoid-like action of the synthetic hormone, which competes with the endogenous glucocorticoids for the hepatic receptor molecules.

Adrenal Glands↗
PubMed1985

Corticosterone secretion by rats after adrenalectomy.

Using high pressure liquid chromatography (HPLC) and/or gas liquid chromatography (GLC), corticosterone plasma levels were determined in rats at various periods after adrenalectomy. Lowest levels could be found 24 to 48 hours after the operation.

Adrenalectomy↗
PubMed1987

[Morphofunctional changes in the parietal cells of the stomach after adrenalectomy].

As demonstrated experiments performed in 150 white male rats by means of light and electron microscopy, cytochemistry with successive morpho-, cytophotometric and biochemical analysis, after bilateral adrenalectomy, inhibition of proliferative processes of cervical epitheliocytes and their differentiation into parietal cells take place. This results in decreasing amount of the latter, in appearance among them not completely differentiated forms. Dystrophic processes develop, manifesting as a decreasing balance of the secretory membranes and destruction of the mitochondrial apparatus, accompanied with a sharp drop in activity of the main oxidoreductases and ATP-ase. The gastric juice acidity decreases. These changes depend mainly on deficiency of glucocorticoid hormones, but not mineralocorticoids.

Adenosine Triphosphatases↗
PubMed1987

Effect of alloxan diabetes and adrenalectomy on carrageenin-induced pleurisy in the rat.

1. The effect of alloxan diabetes and adrenalectomy on the acute inflammatory response was investigated in rats using the carrageenin-induced pleurisy model. 2. Diabetic rats had reduced exudate volume (-85%) and inflammatory cell accumulation (-50%), especially polymorphonuclear leucocytes (-60%) in the pleural cavity 24 h after stimulation in relation to control values. Subcutaneous insulin administration 2 h after the inflammatory stimulus restored these parameters to normal levels. In contrast, all three measures of the response were potentiated 1.5 to 4-fold in adrenalectomized animals. 3. Results obtained by other investigators using different experimental models point to a possible pro-inflammatory function of insulin for the vascular component of inflammation. The present data show that insulin also has a significant effect on the cellular component of inflammation, especially the polymorphonuclear one, by increasing its accumulation at the affected site.

Acute-Phase Reaction↗
PubMed1988

Hypophysectomy and adrenalectomy decrease Ca2+-induced swelling of rat liver mitochondria.

Hypophysectomized rats showed significant modifications in Ca2+-induced swelling and MgATP-induced contraction of liver mitochondria. Two-three months after operation, maximal swelling (MS), rate of swelling (VS), maximal contraction (MC) and rate of contraction (VC) were decreased by 77 (MS), 83 (VS), 79 (MC) and 62 (VC) % (in all cases P less than 0.05 as compared with normal rat mitochondria). Treatment of hypophysectomized rats with bovine pituitary extract, for two weeks, counteracted the effect of hypophysectomy, whereas treatment with bovine growth hormone was ineffective. Adrenalectomy produced similar though less extensive modification of Ca2+-induced swelling but failed to affect the MgATP-dependent mitochondrial contraction. Substrate oxidation by hypophysectomized or adrenalectomized rat mitochondria showed no modification of the energy-yielding mechanisms, capable of explaining the observed changes in mitochondrial swelling.

Adrenal Glands↗
PubMed1988

Adrenalectomy exacerbates paw edema without interfering with desensitization induced by PAF-acether in rats.

Subcutaneous injection of PAF-acether into the rat's paw leads to a local inflammatory response (edema) followed by desensitization after repeated injections of the substance. The desensitizing effect was not modified by previous adrenalectomy, whereas the inflammatory response observed after the first injection of PAF-acether was exacerbated. This finding suggests that adrenal hormones may act as modulators of PAF-induced inflammatory reactions. Because LY 171883, an LTD4 blocker, inhibited the edema which follows the first injection of PAF-acether, we suggest that leukotrienes may play an important role in the phenomenon.

Adrenalectomy↗
PubMed1988

Effect of corticosterone treatment and adrenalectomy on phenylethanolamine N-methyltransferase and catecholamines in brain stem and hypothalamic nuclei and superior cervical ganglion of rats.

The effects of corticosterone treatment and adrenalectomy with or without corticosterone replacement on the activity of phenylethanolamine N-methyltransferase (PNMT) and catecholamine content has been studied in isolated brain stem nuclei containing adrenergic and noradrenergic nerve cell bodies, hypothalamic nuclei and in the superior cervical ganglion (SCG) of adult rats. Changes of PNMT activity were found only in a few brain stem areas. In adrenalectomized rats, PNMT activity was decreased in Cl area and in the locus coeruleus, but after corticosterone replacement it returned to the control values. The treatment of rats with corticosterone resulted in a rise of PNMT activity only in C2 area. No significant changes in PNMT activity were seen in the hypothalamic areas in any experimental group of rats. The observed changes of PNMT activity occurred without any measurable changes of noradrenaline (substrate) or adrenaline (product of the reaction catalysed by PNMT). Our results may suggest the involvement of brain stem adrenaline and noradrenaline producing neurons in the central modulation of the pituitary-adrenal function. The basal PNMT activity in SCG of adult rats was very low, but the treatment of rats with high dose of corticosterone or corticosterone replacement to adrenalectomized rats increased PNMT activity in the SCG to the same extent.

Adrenal Glands↗
PubMed1987

[Evaluation of the hypotensive effect of unilateral adrenalectomy in patients with low-renin hyperaldosteronism].

The antihypertensive effect of unilateral adrenalectomy was analyzed in 19 patients with arterial hypertension and primary hyperaldosteronism diagnosed by way comparing clinical findings, a degree of hypokalemia, activity of plasma renin and aldosterone concentration and CT data. A follow-up period after operation was 8-14 mos. Clinical and biochemical findings were compared with the results of morphological investigation of the adrenal glands and kidneys. An antihypertensive postoperative effect was observed in 12 patients: good in 6, moderate in 6, the absence of an antihypertensive effect in 7. Different forms of adrenocortical hyperplasia revealed during histomorphological investigation, endocrine nephropathy of various degree and vascular changes of hypertensive genesis in the renal parenchyma were discussed as causes of residual hypertension.

Adrenal Glands↗
PubMed1987

Effect of diabetes, adrenalectomy and hypophysectomy on D-3-hydroxybutyrate dehydrogenase activity and substrate oxidation by rat mitochondria.

In good agreement with previous observations, D-3-hydroxybutyrate dehydrogenase (OHBD) activity in disrupted liver mitochondria decreased significantly in chronic diabetic rats, whereas insulin treatment prevented this decrease. Similar effects were observed with kidney mitochondria. Adrenalectomy increased OHBD activity in liver and brain mitochondria from normal rats and in liver mitochondria from diabetic rats. Corticosterone depressed OHBD activity in liver mitochondria of normal rats and restored the normal level of OHBD in adrenalectomized rats. Hypophysectomy increased OHBD activity in normal rats, this effect being further increased by growth hormone administration. D-3-hydroxybutyrate (OHB) oxidation by liver mitochondria from diabetic, adrenalectomized or hypophysectomized rats varied as expected from OHBD activity in disrupted mitochondria, but to a relatively lesser degree. Submitochondrial particles from diabetic rats showed significant diminution in OHB-, succinate- and NADH-oxidase activities, whereas mitochondria from diabetic rats oxidized succinate and L-malate + L-glutamate at a slower rate than the corresponding controls.

3-Hydroxybutyric Acid↗
PubMed1987

Adrenalectomy-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons: anatomic, peptide, and steroid specificity.

Following adrenalectomy (ADX), corticotropin-releasing factor (CRF) and vasopressin immunoreactivity are jointly expressed by a population of parvocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus (PVH). Because these cells stain positively for CRF, but not for vasopressin, after pretreatment with colchicine, the results suggest the existence of state-dependent alterations in the expression of peptides by neuroendocrine neurons. The present study sought to determine whether other neuropeptides (e.g., neurotensin, met-enkephalin) that have been colocalized with CRF in the parvocellular division of the PVH are influenced similarly by ADX; whether the enhancement of CRF and/or vasopressin immunoreactivity after ADX is limited to neurons of the PVH; and what factors might be involved in the regulation of the expression of these peptides in the PVH. The results confirmed that CRF and vasopressin immunoreactivity are both enhanced, and may be colocalized in a substantial population of parvocellular neurosecretory neurons after ADX; no comparable enhancement of staining for met-enkephalin or neurotensin was observed. The effect of ADX on CRF immunoreactivity was not limited to cells in the PVH, as neurons in the cerebral cortex, amygdala, and the bed nucleus of the stria terminalis also showed heightened CRF immunostaining after ADX; vasopressin immunoreactivity was never colocalized with CRF in these extrahypothalamic sites. Hypophysectomy produced an enhancement of CRF and vasopressin staining in the PVH that was comparable to that seen after ADX, implicating adrenal steroids as primary regulators of peptide expression in this system. Corticosteroid replacement studies in ADX rats indicated that lower doses of dexamethasone attenuated, and higher doses essentially abolished, the expected enhancement of both CRF and vasopressin immunoreactivity after ADX. The relative potency of steroids in mitigating these effects was dexamethasone greater than corticosterone greater than deoxycorticosterone greater than aldosterone. Collectively, these results indicate that the ADX-induced enhancement of CRF and vasopressin immunoreactivity in parvocellular neurosecretory neurons is at least somewhat specific to these peptides and to this cell type. Both peptides would appear to be regulated similarly by adrenal steroids, with glucocorticoids playing a primary role.

Adrenal Cortex Hormones↗
PubMed1987

Fine structural alterations induced in the rat hepatocyte by adrenalectomy: influence of deoxycorticosterone acetate or fasting.

Electron microscopy was used to investigate the changes induced by bilateral adrenalectomy (ADX) in rat hepatocytes. Animals were killed at 1 week post-ADX, either with or without a prior 24 h fast. Further studies were carried out at 4 to 5 weeks after ADX to investigate the effect of administering deoxycorticosterone acetate (DOCA) for 4 weeks on the ADX-induced alterations. At 1 week, fasting had a profound effect on the response of hepatocytes to ADX in that either fasting or ADX alone caused proliferation of smooth endoplasmic reticulum (ER) and reduced glycogen but did not alter the rough ER, while ADX together with fasting resulted in the total depletion of glycogen, the virtual absence of smooth ER and the disaggregation of the rough ER into single cisternae. In contrast to the changes seen at 1 week after ADX in unfasted animals, at 4 weeks the hepatocytes contained increased glycogen in large, dense areas and had a scanty smooth ER, suggesting that some endogenous source of steroid hormones active in carbohydrate metabolism becomes available in male ADX rats by this time. This interpretation was consistent with the finding that DOCA-treatment of ADX rats prevented the glycogen accumulation seen at 4 weeks and also induced some smooth ER proliferation.

Adrenalectomy↗
PubMed1987

[Study of rat pulmonary macrophages as affected by hydrocortisone administration and adrenalectomy].

The blood clearance rate of inert colloidal particles and the number of rat lung interstitial phagocytic cells decrease considerably on the 7th day after daily subcutaneous hydrocortisone acetate (HC) injection at a dose of 125 mg/kg. The number of cells in the bronchoalveolar lavage (BAL) increases more than 5-fold, and the absolute quantity of neutrophils is 66 times higher than in the control. Phagocytic and microbicidal activity of HC-treated animal alveolar macrophages (AM) decreases. Stimulation with zymosan led only to the recovery of the normal parameters of mononuclear phagocytosis system (MPC) and its pulmonary compartment activity. The parameters of MPS and AM studied increase on the 7th day after bilateral adrenalectomy (AE). The number of BAL cell increases 1.4-fold due to the animals' death immediately after intravenous zymosan injection because of total hemorrhage. The data obtained testify to the influence of glucocorticoids on the composition and activity of bronchoalveolar space cells, which in turn determine the resistance of the lung tissue.

Adrenal Cortex Hormones↗
PubMed1985

Survival and causes of death after adrenalectomy for Cushing's disease.

A consecutive series of 79 patients with Cushing's disease, treated by bilateral adrenalectomy (subtotal, total initially, or total finally) between 1953 and 1980, were studied to determine the survival and mortality rates and causes of death as long as 28 years after surgery. There were three early postoperative deaths, the last in 1974, caused by coma of unknown cause, severe diarrhea, and pulmonary embolism, respectively. The actuarial survival rates at intervals of 1, 2, 3, 5, 10, 15, and 20 years after surgery were approximately 87%, 83%, 82%, 79%, 72%, 68%, and 62%, respectively. These are significantly less than the rates for the general population (p less than 0.001). There were no differences between the sexes or between the types of operation (p greater than 0.05). The commonest causes of death were cardiac or vascular lesions (11 patients) and the local effects of pituitary tumors (four patients). These long-term results of an established method of treatment provide a standard by which other, especially newer, methods may be compared.

Actuarial Analysis↗
PubMed1985

[Effect of adrenalectomy of the recipients of allogeneic lymphocytes on the inactivation of endogenous colony-forming cells in mice].

Intravenous injection of lymph node cells from the parental C57BL/6 mouse line in doses of 2 X 10(6) or 5 X 10(6) into sublethally irradiated (CBA X C57BL/6) F1 hybrids produced more demonstrable suppression of endogenous colony-formation in adrenalectomized recipients as compared with that seen in sham-operated on ones (P less than 0.01). The recipients' adrenalectomy itself was accompanied by an over 2-fold increase in the number of the endogenous colony-forming cells in the spleen as compared with sham-operated on mice. Possible mechanisms, by which the killer action of lymphocytes on the endogenous colony-forming cells is potentiated, are under discussion.

Adrenal Glands↗
PubMed1985

Effects of adrenalectomy on gonadal hormone-induced changes in hepatic microsomal carboxylesterase activities in rats.

Hepatic microsomal carboxylesterase (E.C. 3.1.1.1) showed a different capacity for the hydrolysis of various substrates in rats. Adrenalectomy in castrated male rats slightly decreased the activities towards p-nitrophenyl-acetate and malathion. The magnitude of testosterone-induced changes in the hydrolase activities by liver microsomes in adrenalectomized-castrated male rats was markedly decreased castrated male rats. However, when 5 alpha-dihydrotestosterone was administered to adrenalectomized-castrated male rats, malathion and p-nitrophenylacetate hydrolase activities were significantly increased. But in all cases, isocarboxazid and acetanilide hydrolase activities were not affected by physiological states. These results suggest that hepatic microsomal carboxylesterases may be, at least in part, regulated by adrenal gland and gonadal hormones which exert different effects on the several isozymes of carboxylesterases.

Adrenalectomy↗