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PubMed1997

Ovarian and extraovarian sources of immunoreactive inhibin in the chicken: effects of dexamethasone.

The present study investigates whether besides the ovary, extragonadal sources contribute to the total amount of immunoreactive inhibin in the plasma of the domestic hen. A comparison of the inhibin content of different organ shows that, expressed per milligram of tissue, the adrenal ranks second only to the ovarian granulosa layer. To explore the contribution of the adrenals to plasma inhibin, dexamethasone (100 micrograms/kg BW) was injected i.v. into intact, ovariectomized, and sham-operated hens. Control animals of each experimental group were injected with saline (0.9% (w/v) NaCI). Dexamethasone significantly (P < 0.05) decreased plasma inhibin concentrations in the three groups. The suppressive effect of dexamethasone in intact hens, however, was caused by a direct effect of this synthetic glucocorticoid on the gonads. Indeed, dexamethasone decreased the production of inhibin by granulosa cells in vitro and also lowered the immunoreactive inhibin concentration in ovariectomized animals. The decreased plasma inhibin concentration in ovariectomized animals is probably due to a direct effect of dexamethasone on the adrenals. Adrenal cells produced immunoreactive inhibin in vitro. The inhibin secretion by adrenal cells was significantly (P < 0.05) depressed by dexamethasone. In conclusion, the ovary is the major source of plasma immunoreactive inhibin in the laying hen. The presence of substantial amounts of immunoreactive inhibin in the adrenal, the secretion of inhibin by cultured adrenal cells, and the decreased immunoreactive inhibin in ovariectomized animals treated with dexamethasone indicate that the adrenal is a likely source of extragonadal inhibin. The nature and the role of this adrenal inhibin remain to be investigated.

Adrenal Glands↗
PubMed1999

Dexamethasone-induced hypertrophy in rat neonatal cardiac myocytes involves an elevated L-type Ca(2+)current.

The mechanism responsible for dexamethasone-induced hypertrophy in infants has not been defined. In this study, we have investigated the role of L-type Ca(2+)currents in the development of dexamethasone-induced hypertrophy in rat neonatal cardiac myocytes. Using cytoplasmic membrane capacitance measurements, we have shown that the size of the cells treated with dexamethasone were larger than those of the control cells. In addition, treating the cells with 1 microM dexamethasone for 48 h increased L-type Ca(2+)current density significantly, without affecting the voltage-dependent activation and steady state inactivation of the current. The increase in current density was associated with an elevation of the mRNA transcript encoding the L-type Ca(2+)channel subunit alpha(1)C. Dexamethasone treatment also resulted in an increase in the peak amplitude of the intracellular Ca(2+)transient measured by fura-2/epifluorescence. Finally, we have demonstrated that the hypertrophic effect of dexamethasone, characterized by the ratio of protein content per cell, was blocked by the L-type specific antagonist, nifedipine. In conclusion, an elevation of L-type Ca(2+)current is involved in the process of dexamethasone-induced cardiac myocyte hypertrophy in neonatal rats.

Animals↗
PubMed2001

Dexamethasone prevents acute cadmium-induced hepatic injury but exacerbates kidney dysfunction in rabbits.

Cadmium is a potent hepatotoxicant for which neither effective preventive methods nor the mechanism of toxicity has been established. We investigated the preventive effect of dexamethasone against cadmium toxicity on cadmium-induced liver injury in rabbits. Pretreatment with dexamethasone at 1 mg/kg increased the rate of survival in rabbits administered 2.5 mg/kg iv cadmium. Cadmium induced acute severe liver injury characterized by hepatocellular necrosis, infiltration by inflammatory cells, and increases of plasma GOT, GPT, LDH, and LDH5. Dexamethasone mitigated the acute hepatotoxic effect of cadmium, but exacerbated cadmium-induced kidney dysfunction, with destruction of renal tubular cells and increases in excretion of protein, glucose, and amino acids into urine. The cadmium concentration in liver and kidney of rabbits administered cadmium was not changed by dexamethasone pretreatment. Although metallothionein mRNA expression induced by cadmium was not affected by dexamethasone in liver or kidney, cadmium-induced metallothionein protein production was augmented at the early phase in liver and decreased at the later phase in kidney. Neutrophilia observed after cadmium administration was enhanced initially by dexamethasone pretreatment. These results indicate that dexamethasone pretreatment potently prevented cadmium-induced liver injury, but exacerbated renal tubular dysfunction.

Amino Acids↗
PubMed1994

The effects of topical dexamethasone on experimental brain tumors and peritumoral brain edema.

To determine if topical dexamethasone administered to brain tumor beds would not only control peritumoral edema and suppress tumor growth but also prevent systemic steroid complications, we studied experimental brain tumors produced in 102 rabbits by implanted VX2 carcinoma cells. We separated 58 animals into three groups: 1) untreated rabbits (n = 15), 2) systemic dexamethasone-treated (4 mg/kg/day) rabbits (n = 18), and 3) topical dexamethasone-treated (2.5 microliters/h, osmotic pump) rabbits (n = 25). We administered systemic or topical dexamethasone from the third day or from the seventh day after tumor implantation, and sacrificed the animals on the 13th day. We compared survival in these three groups with that of another 44 rabbits, beginning treatment on the seventh day. We measured brain water content in the white matter of the sacrificed rabbits by the specific gravity method. We measured the length and width of the brain tumors of all the rabbits and estimated tumor volume. Systemic and topical dexamethasone administered from the third day produced statistically significant inhibition of tumor volume as well as a mean reduction in peritumoral brain edema in most tested sites. Systemic and topical dexamethasone treatment resulted in a statistically significant increase in survival relative to the untreated group. These results suggest that topical dexamethasone is efficacious in a brain tumor model and its administration to brain tumor beds constitutes a new therapeutic modality.

Administration, Topical↗
PubMed1992

High incidence of serious side effects of high-dose dexamethasone treatment in patients with epidural spinal cord compression.

Twenty-eight consecutive patients were given high-dose dexamethasone (96 mg i.v. loading dose, decreasing doses to zero in 14 days) and radiotherapy for epidural spinal cord compression due to malignant disease. There were eight events classified as side effects of the dexamethasone treatment. Four of these were considered as serious (one fatal ulcer with haemorrhage, one rectal bleeding and one gastrointestinal perforation from undetermined origins, and one perforation of the sigmoid colon) giving a total rate of serious side effects of 14.3 percent. Due to the high incidence of serious side effects of the high dexamethasone dose, the regimen was abandoned in favor of a standard dexamethasone dose of 16 mg daily reduced to zero in 14 days. There were three events classified as side effects, but none were considered as serious in 38 consecutive patients receiving this dose. The differences both in total number of side effects and number of serious side effects are statistically significant. There was no significant difference in the number of ambulant patients in the group that received the high dexamethasone dose. We conclude that the high dexamethasone dose in our experience gives an unacceptably high incidence of serious side effects and we have therefore abandoned the regimen in favour of a more standard dexamethasone dose.

Aged↗
PubMed1993

Effect of dexamethasone on insulin sensitivity, islet amyloid polypeptide and insulin secretion in humans.

The response of islet amyloid polypeptide and insulin and their molar ratios were investigated in eight healthy volunteers before and after treatment with dexamethasone by oral and frequently-sampled intravenous glucose tolerance tests. Following dexamethasone treatment the insulin sensitivity index decreased significantly from 6.5 +/- 1.3 to 4.1 +/- 1.0 (microU.ml-1).min-1, p < 0.05. The area under the curve representing above-basal levels of insulin during oral glucose tolerance test increased significantly following dexamethasone treatment from 48132 +/- 9736 to 82230 +/- 14846 pmol.l-1 x 3 h-1, p < 0.05, the area under the curve of islet amyloid polypeptide increased from 1308 +/- 183 to 2448 +/- 501 pmol.l-1 x 3 h-1, p < 0.05. The overall insulin/islet amyloid polypeptide molar ratios calculated from the area under the curve during the 3-h period of the oral glucose tolerance test was not significantly different before and after dexamethasone treatment (42 +/- 5 vs 40 +/- 4). During the oral glucose tolerance test the insulin/islet amyloid polypeptide ratio increased significantly from baseline to 30 min (p < 0.05), then declined towards initial values before and after dexamethasone treatment. In conclusion, dexamethasone induced a significant decrease in insulin sensitivity and a significant increase in insulin secretion during the oral glucose tolerance test. However, in contrast to previous animal experiments we did not find a change in the insulin/islet amyloid polypeptide ratio before and after dexamethasone treatment.

Adult↗
PubMed1989

Dexamethasone and corticosterone receptor sites. Differential topographic distribution in rat hippocampus revealed by high resolution autoradiography.

High resolution light microscopic autoradiography was used, together with regional surveys and combined acridine orange staining, to define in rat hippocampus cellular and subcellular sites of concentration and retention of 3H dexamethasone and to compare the topographic pattern of labeling with that of 3H corticosterone. Nuclear uptake of 3H dexamethasone in the hippocampus is demonstrated for the first time in vivo. With 3H dexamethasone, strongest nuclear radioactive labeling was observed in certain glial cells throughout the hippocampus, followed by strong nuclear labeling in most neurons in area CA1 and in the adjacent dorsolateral subiculum and weak nuclear labeling in granule cells of the dentate gyrus. Neurons in areas CA2, CA3, CA4, and in the dorsomedial subiculum and indusium griseum showed little or no nuclear labeling after 3H dexamethasone. With 3H corticosterone, strongest nuclear labeling was observed in neurons in area CA2 and in the dorsomedial subiculum and indusium griseum, followed by area CA1, then CA3 and CA4; the dentate gyrus contained scattered strongly labeled cells among cells with intermediate nuclear labeling. At the subcellular level, evidence for both nuclear and cytoplasmic accumulation of label was found. The results indicate that dexamethasone and corticosterone have both nuclear and cytoplasmic binding sites and that particular patterns of target cell distribution exist, characteristic for each agent. This suggests a differential regulation of cellular functions for the two compounds. Corticosterone nuclear binding appears to be more extensive and encompasses regions with dexamethasone binding. Whether in certain of these common regions corticosterone binds to the same receptor as dexamethasone, which seems possible, or to different receptors, remains to be clarified.

Animals↗
PubMed1993

Dexamethasone reduces tachykinin but not ACh airway hyperreactivity after O3.

We investigated whether dexamethasone pretreatment affected the acute increase in airway reactivity produced by high-level ozone exposure. Reactivity to intravenous IV substance P (SP), IV acetylcholine (ACh), or aerosolized capsaicin (CAP) before and 1 hr after ozone exposure (3 ppm for 2 hr) was determined by measuring specific airway resistance in anesthetized, spontaneously breathing guinea pigs, half of whom had been pretreated for 2 days pre-ozone with dexamethasone (2 mg/kg intramuscularly [IM] daily). The amount of IV SP, IV ACh, or inhaled capsaicin necessary to increase baseline specific airway resistance by 100% (ED200ACh or ED200SP) or 35% (ED135CAP) was determined by interpolation from dose-response curves. Compared to their pre-ozone status on the day of exposure, we found that dexamethasone-pretreated animals manifested significantly less of an increase in airway reactivity postozone to IV SP or inhaled CAP than did untreated animals. Changes in logEDs of the pretreated group were 0.18 +/- 0.03 (mean +/- SE) for SP and 2.20 +/- 0.11 for CAP compared to 0.27 +/- 0.04 and 3.38 +/- 0.34, respectively, for the untreated groups post-ozone (p < 0.05 and n = 4 for each). In contrast, dexamethasone pretreatment had no effect on IV ACh reactivity postozone: changes in logED200ACh were 0.27 +/- 0.08 and 0.28 +/- 0.04 for the pretreated and untreated groups, respectively (n = 4). In animals pretreated with captopril to block possible dexamethasone stimulation of angiotensin-converting enzyme synthesis that could influence tachykinin reactivity, we found that the corticosteroid effect on post-ozone SP reactivity was as marked as that seen in animals without captopril (n = 4). Because these reactivity studies were consistent with the possibility that dexamethasone may ameliorate ozone-induced, tachykinin hyperreactivity by stimulating airway neutral endopeptidase (NEP), we measured NEP activity by high-performance liquid chromatography (HPLC) of each tracheal homogenate made from other groups of animals. Homogenates from ozone-exposed, dexamethasone-pretreated animals demonstrated significantly greater NEP activity (81 +/- 24%) than that from ozone-exposed, untreated animals (p < 0.05, n = 5). We conclude that corticosteroid pretreatment reduces the acute increase in airway reactivity to exogenous and endogenous tachykinins caused by ozone. This reduction may be at least partly due to stimulation of airway NEP activity, perhaps most of which is nonmucosal in that ozone acutely inactivates mucosal NEP.

Acetylcholine↗
PubMed1995

The effects of dexamethasone on transcapillary transport in experimental brain tumors: II. Canine brain tumors.

We studied the effect of dexamethasone on transcapillary transport in ten Avian Sarcoma Virus (ASV)-induced canine brain tumors, before and one week after administration of dexamethasone, 2.5 mg/kg/day. A computed tomographic (CT) method was used to measure regional values of K1 (blood-to-tissue transfer constant), k2 (tissue-to-blood efflux constant), and Vp (tissue plasma vascular space) of meglumine iothalamate (Conray-60); the values were reconstructed for each 0.8 x 0.8 x 5 mm volume element of the CT data. For all tumors considered together, there was a decrease in the whole tumor K1 value of meglumine iothalamate from 26 +/- 2.2 (SE) before dexamethasone to 24 +/- 2.9 microliters/g/min after dexamethasone. Vp decreased from 7.2 +/- 0.7 to 6.7 +/- 0.9 ml/100 g, and the size of the tumor extracellular space (Ve) decreased from 0.30 to 0.26 ml/g. These changes were not statistically significant. However, when each tumor was used as its own control, K1 significantly decreased after dexamethasone in four tumors, significantly increased in two and was unchanged in four. These results suggest that decreased blood-to-tissue transport may be one mechanism underlying resolution of tumor associated cerebral edema in some brain tumors and that the effects of dexamethasone on blood-to-tissue transport in brain tumors are variable from one tumor to the next. Decreased 'permeability' may not be the sole mechanism by which dexamethasone reduces tumor-associated cerebral edema.

Animals↗
PubMedDate not supplied

Mechanism of the beneficial effect of dexamethasone on myocardial cell integrity in acure myocardial ischemia.

Dexamethasone (6 mg/kg) given intravenously to anesthetized cats exerted no significant hemodynamic effect on control open-chest cats or in cats subjected to acute myocardial ischemia by coronary artery ligature. However, dexamethasone normalized elevated S-T segments toward preischemic values, and prevented much of the increase in plasma CPK activity following coronary artery ligation. Moreover, dexamethasone prevented loss of CK activity within ischemic myocardial tissue five hours after the onset of ischemia. Dexamethasone also reduced the extent of ischemic damage as assessed by a nitro-blue tetrazolium staining technique, providing anatomic verification of the reduced ischemic damage. Moreover, dexamethasone prvented the swelling and vacuolization of myocardial lysosomes in the ischemic region, indicating a stabilization of lysosomal membranes within the heart. These data indicate that lysosomal disruption is an important consequence of myocardial ischemia and that early treatment with dexamethasone prevents the loss of myocardial lysosomal and cellular enzymes as reflected in normalization of the ECG and plasma CK activity of ischemic cats. In this way, dexamethasone may act to retard the spread of the developing infarct within the ischemic myocardium.

Acute Disease↗
PubMed1996

Inhibition of PAF-, LPS-, and cytokine-induced granulocyte accumulation in guinea pig lung by dexamethasone: evidence that inhibition of IL-5 release is responsible for the selective inhibition of eosinophilia by glucocorticoids in guinea-pigs.

The potency of dexamethasone has been determined as an inhibitor of intratracheally administered platelet activating factor- (PAF), or interleukin (IL)-5-induced eosinophilia, and of lipopolysaccharide-(LPS), tumour necrosis factor alpha-(TNF alpha) or cytokine-induced neutrophil chemoattractant- (CINC) induced neutrophilia in guinea-pig lungs. Dexamethasone was a potent inhibitor of PAF- induced eosinophil accumulation, but higher doses of dexamethasone were required to inhibit IL-5-induced eosinophilia. LPS-induced neutrophilia was less sensitive to the inhibitory effects of dexamethasone, than PAF-induced eosinophilia. Both LPS- and TNF alpha-induced neutrophilia were inhibited by the same doses of dexamethasone. In contrast, higher doses of dexamethasone were required to inhibit CINC-induced neutrophilia. Since data in the literature show that PAF-induced eosinophilia in guinea-pig lungs is dependent on the generation of IL-5, it is concluded that inhibition of this response, by dexamethasone, is due to inhibition of release of IL-5. Similarly, although data in the literature show that LPS-induced neutrophilia is dependent on the generation of TNF alpha, it is concluded that inhibition of this response, by glucocorticoids, is due to an action on an event which occurs after the release of TNF alpha, possibly through inhibition of chemokine release.

Analysis of Variance↗
PubMed1980

The effects of dexamethasone on metabolic activity of hepatocytes in primary monolayer culture.

The effects of dexamethasone on multiple metabolic functions of adult rat hepatocytes in monolayer culture were studied. Adult rat liver parenchymal cells were isolated by collagenase perfusion and cultured as a primary monolayer in HI/WO/BA, a serum free, completely defined, synthetic culture medium. Cells inoculated into the culture medium formed a monolayer within 24 hr. Electron microscopy showed that the cells in primary culture had a fine structure identical to liver parenchymal cells in vivo, including the observation of desmosomes and bile canaliculi in intercellular space. There was significant gluconeogenesis by the cells 24 hr postinoculation but it had decreased markedly by 48 hr. There was a marked induction of tyrosine aminotransferase (TAT) by dexamethasone, which was maintained for up to 72 hr postinoculation of cells. The transport of alpha-aminoisobutyric acid into the cells in monolayer culture was stimulated by dexamethasone and was dependent on the concentration of dexamethasone. Albumin synthesis and secretion by the cells was measured by a quantitative electroimmunoassay. Albumin production was shown to increase linearly over an incubation period of 24 to 48 hr postinoculation. Dexamethasone depressed the albumin synthesis. The effects of dexamethasone are slow, and at times require more than 6 hr to show variation from the control, indicating that dexamethasone is not a single controlling hormone. Possibly it functions in a cooperative and coordinating role in the regulation of cell metabolism.

Albumins↗
PubMed2003

Dexamethasone prevents postoperative nausea and vomiting more effectively in women with motion sickness.

PURPOSE: To evaluate the antiemetic effect of iv dexamethasone for preventing postoperative nausea and vomiting (PONV) in women with and without a history of motion sickness. METHODS: This randomized, double-blinded, placebo-controlled study was carried out in 168 female patients with (n = 84) and without (n = 84) a history of motion sickness undergoing gynecological laparoscopy. Patients received 8 mg dexamethasone or saline immediately before induction of anesthesia. Postoperatively patients were assessed for 24 hr for nausea, vomiting, and complete response (no vomiting, no need for rescue antiemetics). RESULTS: The complete response for patients with a history of motion sickness was 80.5% and 37.5% for recipients of dexamethasone and saline, respectively [P < 0.001; number needed-to-treat (NNT) = 2.3]; with corresponding incidences of 83.3% and 53.7% when there was no such history (P = 0.009; NNT = 3.4). Calculation of the efficacy of dexamethasone for the different subgroups shows that dexamethasone was 45.3% more effective in patients with motion sickness than in those without it. CONCLUSIONS: Prophylactic administration of dexamethasone is effective in reducing PONV in patients with and without a history of motion sickness. The results of this study were more favourable in patients with a history of motion sickness, demonstrating a higher effectiveness of dexamethasone for preventing PONV in this subgroup of patients.

Adult↗
PubMed2006

Epidural dexamethasone reduces postoperative pain and analgesic requirements.

PURPOSE: Epidural steroids may have potential advantages for providing postoperative analgesia. We therefore undertook a study to evaluate the efficacy of epidurally administered dexamethasone in reducing postoperative morphine requirements, as a measure of analgesia following laparoscopic cholecystectomy. METHODS: In a randomized, double-blind study, 94 patients undergoing laparoscopic cholecystectomy were randomly assigned to one of three groups. Group 1 (Control) patients received dexamethasone 5 mg iv with epidural injection of 0.25% bupivacaine 8 mL and normal saline 2 mL, Group 2 (D1) patients received normal saline 2 mL iv with epidural injection of 0.25% bupivacaine 8 mL and dexamethasone 5 mg in normal saline 2 mL, and Group 3 (D2) patients received normal saline 2 mL iv with epidural injection of dexamethasone 5 mg in normal saline 10 mL. After surgery, morphine 2-4 mg iv was administered as needed for analgesia. Postoperative morphine requirements, visual analogue scale (VAS) pain scores at rest and with effort, and time to first analgesic administration were recorded by a blinded observer. RESULTS: Total morphine consumption for the first 24 hr following surgery was lower in both epidural dexamethasone groups (D1, D2) compared to the control group (P < 0.05). The percentage reduction in morphine consumption in Group D1 was 53.9% and in Group D2 was 52.9% in the first 24 hr. Postoperatively at 12 hr, 18 hr and 24 hr, the VAS scores at rest and during effort were also lower in the epidural dexamethasone groups (D1, D2) compared to the control group (P < 0.05). The percentage reductions in VAS scores with effort at 12 hr, 18 hr and 24 hr in Group D1 were 50%, 52.9% and 50% respectively, and in Group D2 percentage reductions in pain scores with effort were 54.8%, 58.8% and 55.5% at corresponding sampling intervals. CONCLUSION: Preoperative epidural administration of dexamethasone 5 mg, with or without bupivacaine, reduces postoperative pain and morphine consumption following laparoscopic cholecystectomy.

Adult↗
PubMed1998

Dexamethasone-induced radioresistance occurring independent of human papilloma virus gene expression in cervical carcinoma cells.

BACKGROUND: Inactivation of p53 by binding to simian virus 40-T antigen (SV40-T) and human papilloma virus type 16 protein E6 (HPV 16 E6) in transfected human diploid fibroblasts causes enhanced radioresistance. The aim of this study was to investigate the role of HPV 18 E6 and E7 gene products with respect to radiosensitivity of two cervical carcinoma cell lines. MATERIALS AND METHODS: The two cervical carcinoma lines C4-1 and SW 756 were used in which treatment with dexamethasone allows to modulate expression levels of HPV 18 E6 and E7 genes: upregulation in C4-1, downregulation in SW 756. Effects of treatment with dexamethasone on plating efficiency and radiosensitivity were assessed using a clonogenic assay. RESULTS: Treatment with dexamethasone increased plating efficiency of the C4-1 cells, but did not affect plating efficiency of SW 756 cells. Treatment with dexamethasone induced enhanced radioresistance in both cell lines. Thus in C4-1 cells the observed changes in radioresistance correlate to the enhancement in expression of HPV 18 genes E6/E7, whereas in SW 756, a reduced expression correlates negatively with the enhanced radioresistance. CONCLUSIONS: In C4-1 and SW 756 cells, treatment with dexamethasone induces radioresistance, and changes in expression levels of HPV 18 genes E6 and E7 do not correlate with the changes in radiosensitivity. Dexamethasone-induced radioresistance has previously been observed in HeLa cells, another human cervical carcinoma cell line. This leads us to speculate that dexamethasone-induced radioresistance may be important in certain clinical situations, and that therefore, the phenomenon deserves further study.

Cell Division↗
PubMed1992

Inhibitory effect of dexamethasone on the oxytocin response to insulin-induced hypoglycemia in normal men.

Glucocorticoids are known to reduce both ACTH and arginine vasopressin responses to insulin-induced hypoglycemia in normal men. The present study was undertaken in order to establish whether glucocorticoids are capable of modifying the oxytocin (OT) response to hypoglycemia. For this purpose, 8 normal men (28-33 yr) were tested with insulin (0.15 IU/kg in an iv bolus) [insulin tolerance test (ITT)] with and without pretreatment with dexamethasone (2 or 4 mg in an iv bolus 10 min before insulin). Eight different subjects (29-35 yr) were tested with dexamethasone alone. The administration of dexamethasone (2 or 4 mg) alone changed neither ACTH nor OT concentrations in the plasma during the next hour. Insulin produced similar hypoglycemic responses, regardless of dexamethasone treatment. ACTH levels rose significantly in response to insulin-induced hypoglycemia, with a mean peak response at 45 min (p less than 0.01 vs baseline). Two and four mg dexamethasone produced similar significant reductions of the ACTH response to hypoglycemia (p less than 0.02 at 45 min, p less than 0.05 at 30 and 60 min vs ITT). In the ITT, OT levels rose significantly in response to hypoglycemia, with a mean peak response at 45 min (p less than 0.01 vs basal value). The pretreatment with 2 or 4 mg dexamethasone reduced in a similar manner the hypoglycemia-induced OT rise (p less than 0.05 at 30 and 45 min vs ITT). These findings show a partial inhibition by dexamethasone of the OT response to hypoglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1999

Insulin resistant subjects lack islet adaptation to short-term dexamethasone-induced reduction in insulin sensitivity.

AIMS/HYPOTHESIS: To establish whether islet compensation to deterioration of insulin action depends on inherent insulin sensitivity. METHODS: We examined insulin and glucagon secretion after i.v. arginine (5 g) at fasting, 14 and greater than 25 mmol/l glucose concentrations before and after lowering of insulin sensitivity by oral dexamethasone (3 mg twice daily for 2 1/2 days) in 10 women with normal glucose tolerance, aged 58 or 59 years. Five women had high insulin sensitivity as shown by euglycaemic, hyperinsulinaemic clamp (99 +/- 12 nmol glucose.kg body weight-1.min-1/pmol insulin.l-1; means +/- SD) whereas five women had low insulin sensitivity (34 +/- 15 nmol glucose.kg body weight-1.min-1/pmol insulin.l-1). RESULTS: Dexamethasone reduced insulin sensitivity in both groups. Fasting insulin concentration increased by dexamethasone in high insulin sensitivity (72 +/- 10 vs 49 +/- 9 pmol/l, p = 0.043) but not in low insulin sensitivity (148 +/- 63 vs 145 +/- 78 pmol/l) whereas the fasting glucose concentration increased in low insulin sensitivity (6.5 +/- 0.8 vs 5.8 +/- 0.6 mmol/l, p = 0.043) but not in high insulin sensitivity (5.3 +/- 0.8 vs 5.3 +/- 0.6 mmol/l). Fasting glucagon concentration was not changed. Plasma insulin concentrations after raising glucose to 14 and more than 25 mmol/l and the insulin response to arginine at more than 25 mmol/l glucose were increased by dexamethasone in high insulin sensitivity (p < 0.05) but not changed by dexamethasone in low insulin sensitivity. Furthermore, in high but not in low insulin sensitivity, dexamethasone reduced the glucagon response to arginine (p = 0.043). CONCLUSION/INTERPRETATION: The results show that adaptation in islets function to dexamethasone-induced short-term reduction in insulin sensitivity is lacking in subjects with low inherent insulin sensitivity.

Arginine↗
PubMed2004

Dexamethasone decreases neurological sequelae and caspase activity.

OBJECTIVE: To evaluate the use of dexamethasone in a model of meningitis-induced brain injury. Changes in neurobehavioral performance were the primary outcome variables. Changes in caspase activation and markers of neuronal injury were the secondary outcome variables. DESIGN: Randomized, prospective animal study. SETTING: University research laboratory. SUBJECTS: Male Wistar rats. INTERVENTIONS: Animals underwent a basilar cistern injection of either placebo or a suspension of Group B Streptococcus. Sixteen hours after inoculation, animals were randomized and received either dexamethasone or placebo in addition to antibiotics. Neurobehavioral performance and biological markers of brain injury were assessed at 3 days and 9 days after randomization. In a second experiment, caspase 1 and 3 were evaluated at 6 h, 24 h, and 72 h after dexamethasone administration. MEASUREMENTS AND MAIN RESULTS: Neurobehavioral performance at 3 days and 9 days was significantly improved in the dexamethasone group. Serum C-tau and cerebral edema were decreased after 3 days of dexamethasone treatment. Dexamethasone decreased Caspase 3 activation in meningitic animals. CONCLUSION: These findings demonstrate that dexamethasone decreases acute brain injury in a rat model of bacterial meningitis as measured by preservation of neurobehavioral performance.

Animals↗