Analysis Of Adrenal Glands Research Articles

Results of Structural and Bacteriological Analysis of the Mouse Adrenal Glands in a Sepsis Model.

The article presents the results of histological and bacteriological analysis of the adrenal glands in two models of sepsis caused by intraperitoneal administration of Pseudomonas aeruginosa strains 1623 and 5266 to sexually mature male C57BL/6 mice. In both models, histological changes in the adrenal glands in the dynamics of sepsis consist in cell destruction and decrease in the absolute areas of the zona glomerulosa, columnar part of the zona fasciculata, and medulla, the development of venous congestion in the absence of pronounced signs of leukocytic infiltration. Most adrenocortical cells of the zona glomerulosa and chromaffin cells of the medulla show signs of destruction. The columnar part of the zona fasciculata loses normal architectonics, the cells undergo degeneration and apoptosis, a significant part of cells in the deep layers of the zona fasciculata remain intact, but do not show tinctorial and ultrastructural signs of steroidogenesis. The active growth of P. aeruginosa colonies from adrenal homogenates in both models already in the first hours after infection of animals makes it possible to associate the revealed structural changes in the adrenal glands with the direct negative effect of P. aeruginosa, and high levels of mRNA of proinflammatory cytokines in the adrenal tissues raise the question of the possible synthesis of these modulators of inflammation in the adrenal parenchyma of septic animals.

New insights into morphological, stereological and functional studies of the adrenal gland under exposure to the potent goitrogen thiourea.

Thiourea (thiophen-3-yl-acetic acid) is a well established antithyroid drug used for treating hyperactivity of the thyroid gland as it blocks the conversion of thyroxine (T4) to triiodothyronine (T3) in peripheral tissues. Human exposures to thiourea include contaminated drinking water and vegetables for its extensive use in fertilizers. Chronic thiourea exposure can cause thyroid dysfunction leading to redox imbalance. However, such effects on morphological, quantitative, functional and hypothalamo-pituitary-adrenocortical axis (HPA) analysis of the adrenal gland are yet to be explored. The aim was to explore the effect of thiourea on structural and functional status of the adrenocortical region with special reference to the HPA axis. Control rats were fed a normal laboratory standardized diet whereas to experimental rats, thiourea at a dose of 0.3 mg/day/Kg body weight was administered orally, once every day for consecutive 28 days. Histology and histometry, including morphometry of the adrenal, adrenal Δ5 3β HSD and 17β HSD activity, LPO level and serum corticosterone profile were assessed. Statistical significance was studied by ‘Mann-Whitney U’ test at p<0.05. Hypertrophy and hyperplasia of the adrenocortical cells was found especially in the layer zona fasciculata (p=0.0027) and enhanced adrenal Δ5 3β HSD activity (p=0.0067) in comparison to that of the control. Increased lipid peroxidation (p=0.0054) and up-regulated corticosterone release (p=0.0064) through adrenocortical stress signalling pathway were also noted. Stereological analysis of the left adrenal gland showed significant increase in volume (p=0.0025) and mass of cells (p=0.0031) in adrenocortical region in comparison to that of control animals. This study concludes that thiourea, in addition to its antithyroidal activity, develops stress in the adrenal as evident by enhanced lipid peroxidation in the gland that in turn through the HPA axis causes hypertrophy and hyperplasia of adrenocortical cells to enhance synthesis and release of corticosterone secretion to counteract the stress developed under the influence of this potent chemical agent.

The influence of adrenal medullectomy on the development of ethanol-induced cardiac hypertrophy.

Cardiac hypertrophy was assessed in adrenal medullectomized and sham control rats given ethanol in a liquid diet mixture, intragastrically, in severely intoxicating doses at 8-h intervals for 48 and 96 h. The ethanol treatments produced increases of some 20% in wet and dry proportional heart weights in the control animals, but this rapid development of hypertrophy was less apparent in the medullectomized rats. Hearts of the medullectomized animals given ethanol were heavier than those of pair-matched controls given isocaloric maltose-dextrin in the diet mix. These increases were not statistically significant. The ethanol treatments produced, in addition, equivalent increases in the weight of the adrenal glands of both medullectomized and control animals. Medullectomy was evaluated by analysis of adrenal glands and urine samples for catecholamines. The majority of adrenals from the demedullated group had nondetectable amounts of catecholamines and minimal quantities were found in the remainder. Adrenaline was not detected generally in urine samples from this group. The adrenaline contents of adrenals from sham controls given ethanol were markedly reduced by the ethanol treatments, whereas the quantities in urine were many times greater than those from rats given maltose-dextrin. Urinary noradrenaline levels were increased in both control and medullectomized rats given ethanol. The results of this study identify that adrenal medullary catecholamines participate in the rapid development of cardiac hypertrophy that results from severe, continuing ethanol intoxication in the rat.

The role of energy metabolism in calcium-evoked secretion from the adrenal medulla.

1. Experiments were carried out on cat adrenal glands perfused with Locke solution to study the effects of inhibition of metabolism on calcium-evoked catecholamine release.2. In the presence of sodium cyanide (CN, 0.2 mM), a low concentration of glucose (1 mM) prevented the gradual decline in the secretory response to sequential exposures to calcium. Furthermore, when the secretory response was almost completely blocked by perfusing with a glucose-deprived solution containing CN, restoration of secretion was correlated with the glucose concentration in the perfusion medium.3. In the presence of CN, 2-deoxyglucose blocked both the protective effect and the restorative effect of glucose. The deoxyglucose inhibition of the glucose-dependent restoration of secretion was antagonized by a higher concentration of glucose.4. Restoration of calcium-evoked secretion was also observed after the washout of CN. The extent of this restoration was not at all related to the glucose concentration and was not affected by various inhibitors of carbohydrate metabolism, including deoxyglucose.5. Analysis of adrenal glands which had been perfused first with a glucose-free solution containing CN and subsequently with the normal medium indicated that no discernible synthesis of catecholamines had taken place during the experimental procedures.6. The data provide further evidence that the action of calcium to trigger medullary secretion requires the presence of metabolic energy and support the hypothesis that an interaction between calcium and high-energy nucleotides is a step in the sequence of events leading to the extrusion of catecholamines from the chromaffin cell.