• Clinical and Experimental Pediatrics
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• v.57 no.10
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• pp.425-433
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• 2014

Adrenal and thyroid hormones are essential for the regulation of intrauterine homeostasis, and for the timely differentiation and maturation of fetal organs. These hormones play complex roles during fetal life, and are believed to underlie the cellular communication that coordinates maternal-fetal interactions. They serve to modulate the functional adaptation for extrauterine life during the perinatal period. The pathophysiology of systemic vasopressor-resistant hypotension is associated with low levels of circulating cortisol, a result of immaturity of hypothalamic-pituitary-adrenal axis in preterm infants under stress. Over the past few decades, studies in preterm infants have shown abnormal clinical findings that suggest adrenal or thyroid dysfunction, yet the criteria used to diagnose adrenal insufficiency in preterm infants continue to be arbitrary. In addition, although hypothyroidism is frequently observed in extremely low gestational age infants, the benefits of thyroid hormone replacement therapy remain controversial. Screening methods for congenital hypothyroidism or congenital adrenal hyperplasia in the preterm neonate are inconclusive. Thus, further understanding of fetal and perinatal adrenal and thyroid function will provide an insight into the management of adrenal and thyroid function in the preterm infant.

• Korean Journal of Veterinary Research
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• v.15 no.1
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• pp.39-45
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• 1975

The authors believe that farm livestok will be greatly affected by the marked increasing use of organic phosphate. This study was carried out to observe the clinical signs and histopathological changes of mouse, guinea pig, hamster and rabbit that were orally administered with diazinon used usually as agricultural insecticide, and cholinesterase (ChE) activity was histochemically examined in the liver, heart, kidney, adrenal gland, duodenum and salivary gland of these experimental animals administered with diazinon. The results obtained were as follows: 1. Clinical signs such as dullness, severe salivation, ataxia, dyspnea, irregular slight convulsion and inappetance and as the histopathological changes cloudy swelling, congestion and hemorrhage of parenchymal organs, catarrh or local necrsois of the gastrointestinal tract, congestion or hemorrhage of the other organs were observed. Especially, hemorrhage of adrenal glands (rabbit, guinea pig) and pulmonary congestion and hemorrhage were necessarily constant. 2. In the histochemical study, ChE activity appeared intensely in the liver, heart, medulla of adrenal glands and salivary glands (submaxillary and parotid) of control animals, but ChE activity was negative or markedly decreased in experimental animals administered with diazinon. There was no marked difference between the control and experimental animals in ChE activity of the kidney. 3. Histochemical observation of ChE activity was helpful to explain the clinical signs and histopathological changes and was regarded as a diagnostic method for organic phosphate poisoning.

• Natural Product Sciences
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• v.13 no.1
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• pp.68-77
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• 2007

The aim of the present study was to examine the effects of green tea extract (CUMS6335) on the release of CA evoked by cholinergic stimulation and direct membrane-depolarization in the perfused model of the adrenal gland isolated from the spontaneously hypertensive rats (SHRs), and to establish the mechanism of action. Furthermore, it was also to test whether there is species difference between animals, and between CUMS6335 and EGCG, one of biologically the most powerful catechin compounds found in green tea. CUMS6335 $(100\;{\mu}g/ml)$, when perfused into an adrenal vein for 60 min, time-dependently inhibited the CA secretory responses evoked by ACh (5.32mM), high $K^+$(56 mM), DMPP $(100\;{\mu}M)$, and McN-A-343 $(100\;{\mu}M)$ from the isolated perfused adrenal glands of SHRs. However, CUMS6335 itself did fail to affect basal catecholamine output. Also, in adrenal glands loaded with CUMS6335 $(100\;{\mu}g/ml)$, the CA secretory responses evoked by Bay-K-8644 $(10\;{\mu}M)$ and cyclopiazonic acid $(10\;{\mu}M)$ were also inhibited in a relatively time-dependent fashion. However, in the Presence of EGCG $(8.0\;{\mu}g/ml)$ for 60 min, the CA secretory response evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were not affected except for last period. Collectively, these results indicate that CUMS6335 inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by direct membrane-depolarization from the perfused adrenal gland of the SHR. It seems that this inhibitory effect of CUMS6335 is exerted by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself. It seems likely that there is much difference in mode of the CA-releasing action between CUMS6335 and EGCG.

• Clinical Endoscopy
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• v.55 no.2
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• pp.302-304
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• 2022

Adrenal gland infection is a clinical entity of great importance, but it is a largely unrecognized pathology. Immunosuppressed individuals are at a higher risk of presentation. Herein, we describe a young female patient, recently diagnosed with HIV, who presented with severe sepsis due to methicillin-resistant Staphylococcus aureus, associated with a left adrenal abscess. She was initially treated with antibiotics; however, due to the persistence of the systemic inflammatory response and bacteremia, endoscopic ultrasound-guided drainage was performed. This procedure was successful in resolving the clinical situation. Endoscopic ultrasound-guided adrenal gland drainage can be a safe, efficacious, and minimally invasive option for managing antibiotic-refractory adrenal abscesses in immunosuppressed patients.

• Archives of Pharmacal Research
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• v.28 no.6
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• pp.699-708
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• 2005

The present study was designed to investigate the effect of naloxone, a well known opioid antagonist, on the secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane-depolarization in the isolated perfused rat adrenal glands, and to establish its mechanism of action. Naloxone ($10^{-6}\~10^{-5}$ M), perfused into an adrenal vein for 60 min, produced dose- and time-dependent inhibition of CA secretory responses evoked by ACh ($5.32\times10^{-3}$ M), high K+ ($5.6\times10^{-2}$ M), DMPP ($10^{-4}$ M) and McN-A-343 ($10^{-4}$ M). Naloxone itself also failed to affect the basal CA output. In adrenal glands loaded with naloxone ($3\times10^{-6}$ M), the CA secretory responses evoked by Bay-K-8644, an activator of L-type $Ca^{2+}$ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic $Ca^{2+}$-ATPase, were also inhibited. In the presence of met-enkephalin ($5\times10^{-6}$ M), a well known opioid agonist, the CA secretory responses evoked by ACh, high $K^+$, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly inhibited. Taken together, these results suggest that naloxone greatly inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as that by membrane depolarization. It seems that these inhibitory effects of naloxone does not involve opioid receptors, but might be mediated by blocking both the calcium influx into the rat adrenal medullary chromaffin cells and the uptake of $Ca^{2+}$ into the cytoplasmic calcium store, which are at least partly relevant to the direct interaction with the nicotinic receptor itself.

• Archives of Pharmacal Research
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• v.25 no.4
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• pp.511-521
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• 2002

The purpose of this study was to determine whether bromocriptine affects the catecholamines (CA) secretion evoked in isolated perfused rat adrenal glands, by cholinergic stimulation, membrane depolarization and calcium mobilization, and to establish the mechanism of its action. The perfusion of bromocriptine ($1~10{\;}{\mu}M$) into an adrenal vein, for 60 min, produced relatively dose-dependent inhibition in the secretion of catecholamines (CA) evoked by acetylcholine (ACh, 5.32 mM), DMPP ($100{\;}{\mu}M$ for 2 min), McN-A-343 ($100{\;}{\mu}M$ for 2 min), cyclopiazonic acid (CPA, $10{\;}{\mu}M$ for 4 min) and Bay-K-8644 ($10{\;}{\mu}M$ for 4 min). High $K^+$ (56 mM)-evoked CA release was also inhibited, although not in a dose-dependent fashion. Also, in the presence of apomorphine ($100{\;}{\mu}M$), which is also known to be a selective $D_2$-agonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were also significantly depressed. However, in adrenal glands preloaded with bromocriptine ($3{\;}{\mu}M$) in the presence of metoclopramide ($15{\;}{\mu}M$), a selective $D_2$-antagonist, the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid considerably recovered as compared to that of bromocriptine only. Taken together, these results suggest that bromocriptine can inhibit the CA secretion evoked by stimulation of cholinergic receptors, as well as by membrane depolarization, in the perfused rat adrenal medulla. It is thought this inhibitory effect of bromocriptine may be mediated by inhibiting the influx of extracellular calcium and the release from intracellular calcium stores, through the activation of dopaminergic $D_2$-receptors located in the rat adrenomedullary chromaffin cells. Furthermore, these findings also suggest that the dopaminergic $D_2$-receptors may play an important role in regulating adrenomedullary CA secretion.

• The Korean Journal of Physiology and Pharmacology
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• v.11 no.3
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• pp.97-106
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• 2007

The present study was attempted to investigate the effect of nicorandil, which is an ATP-sensitive potassium ($K_{ATP}$) channel opener, on secretion of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused rat adrenal glands. The perfusion of nicorandil ($0.3{\sim}3.0mM$) into an adrenal vein for 90 min produced relatively dose-and time-dependent inhibition in CA secretion evoked by ACh (5.32 mM), high $k^+$ (a direct membrane depolarizer, 56 mM), DMPP (a selective neuronal nicotinic receptor agonist, $100{\mu}M$ for 2 min), McN-A-343 (a selective muscarinic $M_1$ receptor agonist, $100{\mu}M$ for 4 min), Bay-K-8644 (an activator of L-type dihydropyridine $Ca^{2+}$ channels, $10{\mu}M$ for 4 min) and cyclopiazonic acid (an activator of cytoplasmic $Ca^{2+}$-ATPase, $10{\mu}M$ for 4 min). In adrenal glands simultaneously preloaded with nicorandil (1.0 mM) and glibenclamide (a nonspecific $K_{ATP}$-channel blocker, 1.0 mM), the CA secretory responses evoked by ACh, high potassium, DMPP, McN-A-343, Bay-K-8644 and cyclopiazonic acid were recovered to the considerable extent of the control release in comparison with that of nicorandil-treatment only. Taken together, the present study demonstrates that nicorandil inhibits the adrenal CA secretion in response to stimulation of cholinergic (both nicotinic and muscarinic) receptors as well as by membrane depolarization from the isolated perfused rat adrenal glands. It seems that this inhibitory effect of nicorandil may be mediated by inhibiting both $Ca^{2+}$ influx and the $Ca^{2+}$ release from intracellular store through activation of $K_{ATP}$ channels in the rat adrenomedullary chromaffin cells. These results suggest that nicorandil-sensitive $K_{ATP}$ channels may play an inhibitory role in the regulation of the rat adrenomedullary CA secretion.

• Advances in pediatric surgery
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• v.1 no.2
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• pp.204-208
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• 1995

Neonatal adrenal hemorrhage is frequently associated with birth trauma or perinatal hypoxia. Hemorrhagic necrosis of the adrenal glands is often found at autopsy and many small lesions are usually asymptomatic. A palpable abdominal mass and jaundice are the usual presenting signs. Ultrasound is very useful in the diagnosis of this lesion; however, if the mass has mixed echoic pattern, magnetic resonance imaging (MRl) is helpful for the differential diagnosis from neuroblastoma. We present the case of a female newborn who was found to have a abdominal mass on physical examination. The patient showed anemia and hyperbilirubinemia. An ultrasonogram disclosed a $3.8{\times}3.0$ cm suprarenal mass with mixed echoic pattern. The mass was initially suspected to be neuroblastoma. An abdominal computed tomogram was not able to differentiate the mass. Magnetic resonance imaging revealed markedly increased signal intensity on T1 and T2-weighted sequences. This finding was consistent with adrenal hemorrhage. Serial sonogram demonstrated the mass that resolved completely by 12 weeks of age.

• Korean Journal of Animal Reproduction
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• v.4 no.1
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• pp.35-45
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• 1980

The purpose of this experiment was to investigate the effects of castration and administration of testosterone propionate(TP) on the development of the thyroid, adrenal glands and the testis in immature male rats, 25 days immatured, weighing 64.1${\pm}$2g, were divided into two groups of control and castrated, each sub-divided into 30 rats again, treated and untreated with TP respectivity. Each rat was given 20$m\ell$ of TP subcutaneously at two weeks interval. Six rats among each group were randomly sacrificed at 7, 21, 35, 49, and 63 days after treatment, of which their thyroid, adrenal glands and testis were collected for cytometric observation. The results obtained were as follows. 1. The size of the follicle of thyroid glands had a tendency to increase proportionally to the treatment period in every group. However, in castration group, the follicular size of the untreated with TP were significantly increased from 49 days (p<0.05) after treatment than that of the treated with TP, while in control group, the treated with TP were not increased during the treatment period. Regarding the height of the follicular epithelial cell in thyroid gland, the treated with TP had a tendency to increase than the untreated with TP in both castration and control group. 2. Regarding the size of the follicle of thyroid gland in relation with the increment period, the untreated with TP in control group were slightly increased from 49 days after treatment, but the treated with TP were not changed significantly. Castration group had a tendency to increase significantly than the control group, especially the untreated with TP in castration group were significantly increased. 3. As for the change of the relative height of thyroidal follicular epithelial cell in relation with the increment of treatment period, the untreated, A and C group, in both castration and control group were increased at 35 days 63 days after treatment while the treated, B and D group had tendency to increase from 21 days after treatment. 4. Regarding the thickness fo adrenal cortex, the castration group had a tendency to increase than the control group until 21 days after treatment. But, at 35 days, the change of the thickness was reversed; Mean while at 49 days and 63 days, especially C group in castration were significantly increased than any other groups although there were no significant differences among the every group during the whole treatment period. Regarding the thickness of adrenal cortex in relation with the increment of treatment period, A, B and C group had a tendency to increase until 21 days after treatment. After that period, there was no significant increment in all groups. Especially, in D group, there were no significant changes from 7 days to 63 days after treatment. 5. As for the tickness of adrenal medulla, there were no significant changes in every group of castration and TP treatment, except that the castration group had a tendency to increase continually than the control throughout the whole treament period. 6. In terms of the number, diameter and thickness of seminiferous tubule in testis of control group, the treated group with TP were distinctly reduced than those of the untreated group from 49 days after treatment respectively.

• The Journal of the Korean dental association
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• v.21 no.3 s.166
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• pp.253-259
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• 1983