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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of short-term dexamethasone administration (8 mg daily for 3 days) on thyroid hormone response to exogenous TSH (bovine TSH, 5 IU i.m.) was studied in 16 euthyroid volunteers. Serum T3 and T4 concentrations were measured by radio-immunoassay prior to and 2, 6, 12, 24, and 49 hr after bTSH injection, both under basal conditions and during dexamethasone treatment. In all subjects bTSH administration raised both T3 and T4 concentrations significantly. Dexamethasone treatment induced a slight depression of endogenous TSH (m +/- SEM = 2.0 +/- 0.4 versus 1.6 +/- 0.3 muU/ml) and T4 (6.8 +/- 0.4 versus 6.1 +/- 0.2 mug/100 ml) basal values and a significant decrease in T3 value (1.16 +/- 0.09 versus 0.64 +/- 0.06 ng/ml, p = 0.005). The mean increment of both T3 and T4 after bTSH injection was percentually unchanged during dexamethasone treatment but, due to lowered basal value, T3 levels at each time interval after TSH + dexamethasone were significantly lower than the corresponding values observed after TSH alone. The present data show that high dexamethasone doses decrease T3 serum levels significantly without inhibiting T3 response to TSH stimulation. Only a slight lowering was observed in T4 levels.
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PMID:Effect of dexamethasone on thyroid hormone response to TSH. 118 94

Our previous observations have shown that calcitonin (CT) stimulates beta-endorphin, ACTH, and cortisol secretion. In order to give further information on the supposed hypothalamic pituitary involvement in this effect, we studied the influence of dexamethasone on this stimulative influence of CT. Six healthy women aged 50-65 years were investigated. All the subjects received 100 U CT salmon (Sandoz) i.v. at 0800 (0 time). Plasma beta-endorphin, ACTH, and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassays. The same subjects were evaluated a second time, at the same intervals, when 1 mg dexamethasone was administered per os at 11 PM the previous night and CT i.v. at 0800 the next morning. Beta-endorphin, ACTH, and cortisol levels (mean +/- SEM) rose significantly after 100 U CT from 5.6 +/- 0.17 to 16.75 +/- 1.8 pmol/L (p less than 0.001); from 39.6 +/- 6 to 88.0 +/- 3.1 pg/ml (p less than 0.0001) (from 8.7 +/- 1.3 to 19.4 +/- 0.7 pmol/L); and from 13.1 +/- 1.6 to 23.8 +/- 3.0 micrograms/dl (p less than 0.0001) [374 +/- 45 to 680 +/- 85 nmol/L], respectively. Dexamethasone suppressed almost completely the stimulatory effect of CT beta-endorphin rose from 4.9 +/- 0.12 to 6.3 +/- 1.3 pmol/L (n.s.), ACTH from 38.6 +/- 5.1 to 42.6 +/- 6.2 pg/ml (n.s.) (from 8.5 +/- 1.1 to 9.4 +/- 0.9 pmol/L) and cortisol from 0.88 +/- 0.23 to 0.88 +/- 0.18 microgram/dl (n.s.) (from 25.1 +/- 6.5 to 25.0 +/- 5.1 nmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dexamethasone suppression of the calcitonin induced beta-endorphin, ACTH and cortisol secretion. 131 84

Glucocorticoids act upon the hypothalamic paraventricular nucleus (PVN) and anterior pituitary in a classic negative feedback loop to regulate ACTH biosynthesis and secretion. Evidence exists to indicate that glucocorticoid feedback may be attenuated during late gestation in the sheep fetus to allow the preterm rise in fetal plasma cortisol necessary for parturition in this species. The present studies were undertaken to determine the effect of glucocorticoids placed adjacent to the fetal PVN on messenger RNA (mRNA) for CRH in the PVN and mRNA for POMC in the anterior pituitary during late gestation. We performed our studies at two critical stages during late gestation to determine if gestational age related changes occur in the efficacy of negative feedback regulation of expression of CRH and subsequently POMC. Dexamethasone (DEX) implants were placed bilaterally 2 mm lateral to the fetal PVN at 105 to 107 days gestational age (dGA; group I, n = 4) and 121-123 dGA (group II; n = 4). Gestational-age matched, sham implanted fetuses were used as controls (CONT) for both groups (n = 4 per group). Fetuses were recovered at 126-128 (group I) and 136 dGA (group II). Fetal PVN were isolated by micropunching, and the anterior pituitary was separated from neurointermediate and posterior lobes after necropsy. Total RNA was subjected to Northern analysis using specific complementary DNA probes to CRH and POMC, and specific message was normalized to actin mRNA content in each individual sample. Anterior pituitary POMC mRNA was not different in DEX fetuses compared to CONT for either group I (78 +/- 26% of CONT; mean +/- SEM) or group II (84 +/- 17% of CONT). PVN CRH mRNA content was lower in DEX fetuses in group I (28 +/- 14% of CONT; P less than or equal to 0.01) and group II (65 +/- 12% of CONT; P less than or equal to 0.01). The degree to which DEX suppressed mRNA for CRH was greater in group I compared to group II (P less than or equal to 0.05). We conclude that 1) CRH expression in the PVN of fetal sheep is suppressible by glucocorticoids; 2) suppression can occur directly at the level of the PVN and 3) that the efficacy of negative feedback decreases with increasing gestational age. Furthermore, the lack of effect of hypothalamic administration of DEX on anterior pituitary POMC mRNA indicates that basal expression of POMC in fetal sheep may be independent from support from the PVN at this stage of gestation.
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PMID:Effect of implantation of dexamethasone adjacent to the paraventricular nucleus on messenger ribonucleic acid for corticotropin-releasing hormone and proopiomelanocortin during late gestation in fetal sheep. 154 33

The Ah receptor regulates induction of cytochrome P450IA1 and mediates certain toxicities of polyhalogenated aromatics such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). It has been characterized previously in continuous cell lines, notably the mouse hepatoma line Hepa 1, the human squamous cell carcinoma line A431, and the human liver cell line Hep G2. The present work extends our knowledge of the Ah receptor in continuous human liver cell lines. Ah receptor can be detected in Mz-Hep-1, a hepatitis B virus-negative cell line derived from a Thorotrast-induced hepatocellular carcinoma. The mean concentration of Ah receptor in Mz-Hep-1 cells was 341 +/- 22 fmol/mg cytosol protein (mean +/- SEM, nine separate determinations). This is equivalent to approximately 30,000 sites per cell. The concentration of Ah receptor in Mz-Hep-1 cells is similar to that in Hepa 1 cells and approximately three times higher than that in Hep G2 cells. The Mz-Hep-1 Ah receptor sedimented in continuous sucrose gradients at approximately 9 S. Specificity of binding by [3H]TCDD was demonstrated by competitive binding of non-radiolabeled 2,3,7,8-tetrachlorodibenzofuran, 3-methylcholanthrene (MC), and dibenz[a,h]anthracene in 50-fold molar excess. Phenobarbital, which is not a substrate for P450IA1, did not compete with [3H]TCDD for binding to Mz-Hep-1 Ah receptor. Dexamethasone and estradiol also did not compete with [3H]TCDD for binding, suggesting non-identity of Ah receptor with glucocorticoid or estrogen receptor. In separate experiments, glucocorticoid receptor was identified in Mz-Hep-1 cells. By Scatchard plot analysis, the apparent equilibrium dissociation constant (Kd) for binding of [3H]TCDD to Mz-Hep-1 Ah receptor was estimated to be 4.4 nM, compared to 0.8 nM in Hepa 1 cells. By Woolf plot analysis the Kd was 5.4 nM, compared to 1.2 nM in Hepa 1 cells. The [3H]TCDD.Ah receptor complex extracted from nuclei of Mz-Hep-1 cells incubated with [3H]TCDD in culture at 37 degrees sedimented at approximately 6 S under conditions of high ionic strength. Aryl hydrocarbon hydroxylase (AHH) activity was detectable in Mz-Hep-1 cells after pretreatment with inducing chemicals. Mz-Hep-1 cells have the highest concentrations of Ah receptor in any continuous human liver cell line thus far investigated. The Mz-Hep-1 Ah receptor is similar physicochemically to that described in murine systems. AHH activity is inducible in Mz-Hep-1 cells.
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PMID:Ah receptor mediating induction of cytochrome P450IA1 in a novel continuous human liver cell line (Mz-Hep-1). Detection by binding with [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin and relationship to the activity of aryl hydrocarbon hydroxylase. 165 Feb 14

A number of neuropeptides including neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), and beta-calcitonin gene related peptide (beta-CGRP) are known to influence insulin secretion. In order to investigate whether they might have a local autocrine/paracrine effect within the islets of Langerhans we screened isolated islets by Northern blot analysis and RIA for a number of peptides and found evidence for the presence of messenger RNA (mRNA) encoding NPY, VIP, and beta-CGRP. Dexamethasone treatment for 12 days increased the content of NPY, VIP, and beta-CGRP significantly from 1.3 +/- 0.3 to 19.8 +/- 1.6; 0.25 +/- 0.03 to 0.91 +/- 0.1; 2.2 +/- 0.2 to 4.8 +/- 0.1 fmol/islet respectively, mean +/- SEM (n = 4, P less than 0.05) and remained elevated 24 h after recovery. However when the results were normalized and expressed as a ratio of insulin content only NPY and VIP were significantly raised. Five days post treatment VIP was still significantly elevated compared to controls. mRNA for NPY increased 10-fold and for VIP increased 2 1/2 times after dexamethasone whereas mRNA for beta-CGRP was not significantly different from controls. Neither capsaicin nor 6-hydroxydopamine affected islet content or message of NPY, VIP, and beta-CGRP. Immunoreactive NPY and its mRNA were detected in two cultured beta-cell lines, HIT T-15 and RIN m5F cells whereas VIP and beta-CGRP were undetectable. The local islet synthesis of neuropeptides, which are known to influence islet hormone release pharmacologically, suggests the possibility that they may play a role in intraislet paracrine regulation.
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PMID:Peptide contents of neuropeptide Y, vasoactive intestinal polypeptide, and beta-calcitonin gene-related peptide and their messenger ribonucleic acids after dexamethasone treatment in the isolated rat islets of Langerhans. 195 11

We studied the circadian rhythm and the response of the hypothalamic-pituitary-adrenal (HPA) axis to ovine corticotrophin releasing hormone (oCRH) stimulation and dexamethasone suppression in 32 children with grade II-III marasmus. Children were studied prior to and after nutritional rehabilitation. Mean baseline plasma cortisol concentrations were elevated at admission and decreased significantly after nutritional rehabilitation. Mean +/- SEM plasma cortisol response to oCRH increased from a basal of 480 +/- 41 to a peak of 582 +/- 58 nmol/l at the time of admission, and from a basal of 234 +/- 27 to a peak of 532 +/- 41 nmol/l after caloric rehabilitation. Dexamethasone suppression in the malnourished group was associated with a decrease in the mean +/- SEM basal plasma cortisol concentration from 397 +/- 44 to 171 +/- 44 nmol/l. After caloric rehabilitation, basal cortisol levels decreased from 259 +/- 27 to 22 +/- 5 nmol/l following dexamethasone. Our results support the concept that malnutrition is associated with decreased responsiveness to oCRH and incomplete dexamethasone suppression, and that these abnormalities are restored after nutritional rehabilitation.
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PMID:The hypothalamic-pituitary-adrenal axis in infantile malnutrition. 211 70

Prostaglandins (PGs), interleukin 1 beta (IL-1 beta), and tumor necrosis factor alpha (TNF alpha) are likely mediators of local inflammatory reactions. We measured PGE2, PGI2, IL-1 beta, and TNF concentrations in paired cerebrospinal fluid (CSF) samples (on admission, CSF1, and 18 to 30 hours later, CSF2) from 80 infants and children with bacterial meningitis. Forty patients received dexamethasone sodium (0.6 mg/kg per day in four intravenous doses) and 40 received an intravenous saline placebo. In CSF1, PGE2, PGI2, IL-1 beta, and TNF were detected in 90%, 56%, 98%, and 71% of specimens with mean (+/- SEM) concentrations of 462 +/- 65, 377 +/- 62, 1266 +/- 242, and 799 +/- 227 pg/mL, respectively. Concentrations of PGE2 correlated significantly with PGI2, IL-1 beta, TNF, and lactate and inversely correlated with glucose concentrations in the first CSF specimens. The PGE2, PGI2, IL-1 beta, and TNF were still detected in 40%, 18%, 97%, and 60%, respectively, of second CSF specimens obtained from placebo-treated patients. Compared with patients who had detectable PGI2 or TNF alpha concentrations in CSF2 specimens, those placebo-treated patients with no detectable PGI2 or TNF alpha activity in CSF2 had a lower incidence of neurological sequelae. Dexamethasone-treated patients had significantly lower PGE2, IL-1 beta, and lactate concentrations and higher glucose concentrations in CSF 18 to 30 hours later, shorter duration of fever, and a lower incidence of neurological sequelae than did placebo-treated patients.
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PMID:Cerebrospinal fluid prostaglandins, interleukin 1 beta, and tumor necrosis factor in bacterial meningitis. Clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients. 211 86

The present study documents the effects of hypophysectomy and the effects of dexamethasone substitution on the NaCl-stimulated release and on the basal secretion rates of ANP from the rat atria in vitro. We also measured the concentration of mRNA in the atria after hypophysectomy. Rats (n = 12) were subjected to hypophysectomy by a parapharyngeal approach. One group of rats (n = 6) received dexamethasone 0.2 mg s.c. daily for 4 weeks, while the other group was left unsubstituted. After 4 weeks, the atrial block (n = 10) was excised, placed in an organ bath (field stimulation 4 s-1, 20 V, 1 ms; resting tension = 5 mN) and superfused (7 ml min-1) either with a physiological buffer solution (295 mosmol kg-1) or with a hyperosmotic NaCl solution (330 mosmol kg-1). The atria from the hypophysectomized rats did not respond to the stimulus: the concentration of ANP in the 1-min samples of the perfusate was under 100 pg ml-1. Dexamethasone treatment significantly (P less than 0.05) increased the ANP concentration to a maximum of 165 +/- 17 (mean +/- SEM) pg ml-1 during the superfusion while the control concentration was 110 +/- 19 pg ml-1. The ANP mRNA/18 S RNA ratios did not differ between the atria of hypophysectomized and control rats. In conclusion, glucocorticoids are required in the stimulus-induced release of ANP and the impaired release of ANP after hypophysectomy does not depend on an impaired synthesis of ANP.
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PMID:Adrenal cortex contributes to the regulation of NaCl-stimulated ANP release in the rat. 214 74

We evaluated the role of the hypothalamic paraventricular nucleus (PVN) in control of ACTH secretion in fetal sheep. Dexamethasone (DEX, 700 micrograms) (n = 6) or cholesterol (CHOL, 700 micrograms) (n = 5) implants were placed bilaterally 2 mm lateral to PVN of fetal sheep at 108 to 111 days of gestation (dga). After 5 days recovery, fetuses were challenged with: 1) hypotension (50% drop of blood pressure), 2) hypoxemia (fall of greater than 5 mm Hg in fetal PaO2), and 3) corticotropin-releasing hormone (CRH) (10 micrograms iv, single injection to fetus). Hypotension and hypoxemia were repeated after 125 dga. Compared with CHOL, DEX fetuses had lower average concentrations of ACTH in plasma after hypotension [23 +/- 0.5 vs. 149 +/- 83.8 and 31 +/- 13.1 vs. 101 +/- 31.3 pg ml-1 at less than 125 and more than 125 dga, respectively (mean +/- SEM, P less than 0.05)] and during hypoxemia [11 +/- 1.6 vs. 292 +/- 152.8 and 33 +/- 9.4 vs. 304 +/- 91.3 pg ml-1 at less than 125 and more than 125 dga, respectively (P less than 0.05)]. DEX and CHOL responses to CRH at 122 to 127 dga (10 micrograms iv) were not different (38 +/- 23.9 vs. 92 +/- 26.7 pg ml-1, respectively). Immunocytochemistry demonstrated that CRH was decreased in PVN and eliminated from median eminence in DEX, but not in CHOL fetuses. Arginine vasopressin (AVP) immunostaining of PVN of DEX and CHOL fetuses was similar; however, unlike CHOL, DEX fetuses showed no AVP immunostaining of the external zone of median eminence. These results show that, in fetal sheep, high concentrations of glucocorticoid near the fetal PVN prevent increases in plasma ACTH secretion seen in controls in response to hypotension and hypoxemia, and exert at least part of their effect at the level of the CRH- and AVP-producing neurons located in the PVN.
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PMID:Hypothalamic glucocorticoid implants prevent fetal ovine adrenocorticotropin secretion in response to stress. 217 38

Steroids reduce permeability of the blood-brain barrier and inhibit active sodium transport by brain capillaries in vitro. Since the rate of edema formation during the early stages of ischemia is related to the rate of sodium transport from blood to brain, this study was designed to determine whether steroids reduce ischemic edema formation by inhibiting blood-brain barrier sodium transport. Dexamethasone was compared with progesterone since the latter is a more potent inhibitor of sodium transport in isolated capillaries. Sprague-Dawley rats were treated with vehicle (n = 22) or 2 mg/kg of either dexamethasone (n = 22) or progesterone (n = 17) 1 hour before occlusion of the middle cerebral artery. After 4 hours of ischemia, brain water content and blood-brain barrier permeability to [3H] alpha-aminoisobutyric acid and sodium-22 were determined. In controls, mean +/- SEM water content of tissue in the center of the ischemic zone was 82.4 +/- 0.2%. Brain edema was significantly reduced following pretreatment with either dexamethasone (80.6 +/- 0.1%, p less than 0.001) or progesterone (81.5 +/- 0.3%, p less than 0.05). There was also a significant reduction in blood-brain barrier permeability to alpha-aminoisobutyric acid in normal brain following either treatment (e.g., 2.21 +/- 0.19 and 1.37 +/- 0.10 microliters/g/min, p less than 0.001, for control and dexamethasone treatments, respectively), but no effect on the permeability to sodium (e.g., 1.19 +/- 0.05 and 1.12 +/- 0.11 microliters/g/min for control and dexamethasone treatments, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of steroids on edema and sodium uptake of the brain during focal ischemia in rats. 238 1


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