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PubMed1998

Dexamethasone aggravates ischemia-induced neuronal damage by facilitating the onset of anoxic depolarization and the increase in the intracellular Ca2+ concentration in gerbil hippocampus.

The Ca2+ mobilization across the neuronal membrane is regarded as a crucial factor in the development of neuronal damage in ischemia. Because glucocorticoids have been reported to aggravate ischemic neuronal injury, the effects of dexamethasone on ischemia-induced membrane depolarization, histologic outcome, and changes in the intracellular Ca2+ concentration in the gerbil hippocampus were examined in vivo and in vitro. The effects of metyrapone, an inhibitor of glucocorticoid synthesis, were also evaluated. Changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 2.5 minutes were compared among animals pretreated with dexamethasone (3 microg, intracerebroventricularly), metyrapone (100 mg/kg, intraperitoneally), and saline. The histologic outcome was evaluated 7 days after ischemia by assessing the delayed neuronal death in the hippocampal CA1 pyramidal cells of these animals. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effect of dexamethasone (120 microg/L in the medium) on the cytosolic Ca2+ accumulation was examined. The effect in a Ca2+-free ischemialike condition was also investigated. Preischemic administration of dexamethasone reduced the onset latency of ischemia-induced membrane depolarization by 22%, and aggravated neuronal damage in vivo. In contrast, pretreatment with metyrapone improved the histologic outcome. The onset time of the increase in the intracellular concentration of Ca2+ provoked by in vitro hypoxia was advanced in dexamethasone-treated slices. The Ca2+-free in vitro hypoxia reduced the elevation compared with that in the Ca2+-containing condition. Treatment with dexamethasone facilitated the increase on both the initiation and the extent in the Ca2+-free condition. Aggravation of ischemic neuronal injury by endogenous or exogenous glucocorticoids is thus thought to be caused by the advanced onset times of both the ischemia-induced direct-current potential shift and the increase in the intracellular Ca2+ concentration.

Animals↗
PubMed1998

Neurotransmitter and amino acid analysis and ultrastructural observations of fetal brain cortex transplantation to adult rat brain under the effect of dexamethasone.

OBJECTIVE: To conduct an investigation of fetal cortical tissue graft survival using transmission electron microscopy and analyzing neurotransmitters and amino acids and their function, with special reference to the effect of dexamethasone. METHODS: Transplantation of fetal cortical brain tissue to 100 adult Wistar albino rats weighing 170 to 220 g was performed. The rats were divided into three groups. Only transplantation of fetal cortical brain tissue was performed in the first group (n=36). In the second group (n=48), dexamethasone was administered in addition to fetal cortical tissue transplantation. The third group (n=16) was used as the surgical control group. The rats were allowed to live for 6 weeks and were then decapitated. The grafts were examined by electron microscopy. Additionally, quantitative analyses of the neurotransmitters and amino acids of the grafts were conducted using high-pressure liquid chromatography. RESULTS: Electron microscopic observations revealed that the grafts were still surviving at the end of the 6th week in both groups. However, in the group that received dexamethasone, neurons and their organelles were better developed than in the group that did not receive dexamethasone. Concommitantly, results of quantitative analysis in the dexamethasone group revealed statistically extremely significant higher amino acid values for glutamic acid, aspartic acid, beta-alanine, and lysine and significantly higher values for gamma-aminobutyric acid, glutamine, glycine, and serine when compared to the nondexamethasone group. CONCLUSION: Dexamethasone is effective in increasing the survival and in developing the ultrastructural and functional outcome of transplanted neurons in fetal grafts.

Amino Acids↗
PubMed1989

Dexamethasone treatment for bacterial meningitis in children and adults.

Four hundred twenty-nine patients with bacterial meningitis were assigned on a nonselective alternating basis into one of two therapeutic regimens. Patients in Group I received dexamethasone in addition to standard antibacterial chemotherapy of ampicillin and chloramphenicol whereas those in Group II received antibacterial chemotherapy alone. Dexamethasone was given intramuscularly (8 mg to children younger than 12 years and 12 mg to adults every 12 hours for 3 days). Both treatment groups were comparable with regard to age, sex, duration of symptoms and state of consciousness at the time of hospitalization. A significant reduction in the case fatality rate (P less than 0.01) was observed in patients with pneumococcal meningitis receiving dexamethasone; only 7 of 52 patients died compared with 22 of 54 patients not receiving dexamethasone. A reduction in the overall neurologic sequelae (hearing impairment and paresis) was observed in patients receiving dexamethasone. This reduction was significant only in patients with Streptococcus pneumoniae meningitis; none of the 45 surviving patients receiving steroids had hearing loss whereas 4 of 32 patients not receiving dexamethasone had severe hearing loss (P less than 0.05). No significant difference was observed between the two groups with regard to time for patients to become afebrile or to regain consciousness or in the mean admission and 24- to 36-hour cerebrospinal fluid leukocyte count, glucose or protein content.

Adult↗
PubMed2004

Low-dose dexamethasone ameliorates circulatory failure and renal dysfunction in conscious rats with endotoxemia.

Corticosteroids have long been proposed as a therapeutic adjuvant in septic renal dysfunction because of their anti-inflammatory properties and favorable results from animal experiments. However, some reports suggested the potential for harm associated with the administration of early high-dose corticosteroids in patients with severe sepsis and septic shock. Thus, we examined the effects of low-dose dexamethasone (0.01 and 0.1 mg/kg) on hemodynamics and renal function in conscious rats with endotoxemia. Intravenous injection of rats with endotoxin (E. coli lipopolysaccharide, LPS, 1 mg/kg) caused hypotension, vascular hyporeactivity, and tachycardia as well as renal dysfunction. Circulatory failure and renal dysfunction caused by LPS were significantly attenuated in the dexamethasone 0.1 mg/kg-treated group. The nitric oxide (NO) production in plasma and renal tissue and the iNOS protein expression in the kidney were suppressed by cotreatment of LPS rats with dexamethasone, 0.1 mg/kg. Light microscopy showed that 0.1 mg/kg dexamethasone reduced marked infiltration of neutrophils in renal tissues from LPS rats. Moreover, the survival rate at 18 h was significantly increased in the dexamethasone 0.1 mg/kg-treated group when compared with the LPS group. These results suggest that the beneficial effects of low-dose dexamethasone (0.1 mg/kg) in conscious rats with endotoxic shock are associated with amelioration of circulatory failure and renal dysfunction, and this is attributed to inhibition of NO production.

Animals↗
PubMed2005

Dexamethasone and recovery of contractile tension after a muscle injury.

Muscle strains, frequently the result of a lengthening contraction, sometimes are treated with corticosteroids. We tested whether an injection of dexamethasone administered soon after muscle injury would minimize inflammation and facilitate the recovery of contractile tension. We applied one eccentric contraction on the tibialis anterior of 76 rats, which were randomly assigned to one of three groups: sham-injured plus dexamethasone, injured plus vehicle, and injured plus dexamethasone. Electrophysiology, histology, and reverse transcription-polymerase chain reaction were used to study the relation between contractile tension, inflammation, and the expression of inflammatory molecules. The single eccentric contraction led to a reversible muscle injury characterized initially by reduced contractile tension and inflammation. The dexamethasone injection reduced the expression of interleukin-1beta and transforming growth factor-beta1 compared with injured vehicle-injected controls and led to a transient improvement of contractile tension 3 days after the injury. No adverse effects were seen for as much as 3 weeks after the dexamethasone injection. The data indicate that one dose of dexamethasone administered soon after muscle strain may facilitate recovery of contractile tension without causing major adverse consequences in this experimental model.

Animals↗
PubMed2007

Role of tumor necrosis factor-alpha, interleukin-8, and dexamethasone in the focal adhesion kinase expression by human nucleus pulposus cells.

STUDY DESIGN: Human nucleus pulposus cells from intervertebral disc specimens were cultured to study the effects of tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 on the focal adhesion kinase (FAK) expression by these cells. The effect of co-stimulation with dexamethasone on the FAK expression by nucleus pulposus cells was also studied. OBJECTIVES: To evaluate the possible role of activated FAK expressed by the human nucleus pulposus cells and its correlation with inflammatory cytokines (TNF-alpha, IL-8) and dexamethasone. SUMMARY OF BACKGROUND DATA: There have been no reported studies showing the correlation between the activated FAK expression by human nucleus pulposus cells with inflammatory cytokines and dexamethasone. METHODS: The FAK expression in cultured human nucleus pulposus cells was studied, and Western blot and immunofluorescence analysis were performed to assess its relation to TNF-alpha, IL-8, and dexamethasone. RESULTS: Treatments of TNF-alpha and IL-8 up-regulated the activated FAK expression. Dexamethasone attenuated the cytokine-induced FAK expression. The effects of inflammatory cytokines on the FAK expression were found to be concentration dependent, with greater correlation shown by IL-8 than TNF-alpha. CONCLUSION: TNF-alpha and IL-8 stimulation up-regulated the FAK expression of human nucleus pulposus cells, and the coadministration of dexamethasone attenuated it.

Cells, Cultured↗
PubMed2003

Dexamethasone reduces postoperative troponin levels in children undergoing cardiopulmonary bypass.

OBJECTIVE: We previously demonstrated that dexamethasone treatment before cardiopulmonary bypass in children reduces the postoperative systemic inflammatory response. The purpose of this study was to test the hypothesis that dexamethasone administration before cardiopulmonary bypass in children correlates with a lesser degree of myocardial injury as measured by a decrease in cardiac troponin I release. DESIGN: A prospective, randomized, double-blind study. SETTING: The cardiac surgery operating room and intensive care unit of a pediatric referral hospital. SUBJECTS: Twenty-eight patients who underwent open-heart surgery for congenital heart defects. INTERVENTIONS: Patients received either placebo (group I, n = 13) or dexamethasone, 1 mg/kg iv (group II, n = 15), 1 hr before initiation of cardiopulmonary bypass. Plasma cardiac troponin I samples were obtained at three time points: immediately before study agent (sample 1), 10 mins after protamine sulfate administration after cardiopulmonary bypass (sample 2), and 24 hrs postoperatively (sample 3). MEASUREMENTS AND MAIN RESULTS: Mean cardiac troponin I levels (+/-sd) were significantly lower at sample time 3 in group II (dexamethasone; 33.4 +/- 20.0 ng/mL) vs. group I (control; 86.9 +/- 81.1) (p =.04). CONCLUSION: Dexamethasone administration before cardiopulmonary bypass in children resulted in a significant decrease in cardiac troponin I levels at 24 hrs postoperatively. We postulate that this may represent a decrease in myocardial injury, and, thus, a possible cardioprotective effect produced by dexamethasone.

Analysis of Variance↗
PubMed2003

Preoperative dexamethasone improves surgical outcome after laparoscopic cholecystectomy: a randomized double-blind placebo-controlled trial.

OBJECTIVE: To determine the effects of preoperative dexamethasone on surgical outcome after laparoscopic cholecystectomy (LC). SUMMARY BACKGROUND DATA: Pain and fatigue are dominating symptoms after LC and may prolong convalescence. METHODS: In a double-blind, placebo-controlled study, 88 patients were randomized to intravenous dexamethasone (8 mg) or placebo 90 minutes before LC. Patients received a similar standardized anesthetic, surgical, and multimodal analgesic treatment. All patients were recommended 2 days postoperative duration of convalescence. The primary endpoints were fatigue and pain. Preoperatively and at several times during the first 24 postoperative hours, we measured C-reactive protein (CRP) and pulmonary function, pain scores, nausea, and number of vomiting episodes were registered. Analgesic and antiemetic requirements were recorded. Also, on a daily basis, patients reported scores of fatigue and pain before and during the first postoperative week and the dates for resumption of work and recreational activities. RESULTS: Eight patients were excluded from the study, leaving 40 patients in each study group for analysis. There were no apparent side effects of the study drug. Dexamethasone significantly reduced postoperative levels of CRP (P = 0.01), fatigue (P = 0.01), overall pain, and incisional pain during the first 24 postoperative hours (P < 0.05) and total requirements of opioids (P < 0.05). In addition, cumulated overall and visceral pain scores during the first postoperative week were significantly reduced (P < 0.05). Dexamethasone also reduced nausea and vomiting on the day of operation (P < 0.05). Resumption of recreational activities was significantly faster in the dexamethasone group versus placebo group (median 1 day versus 2 days) (P < 0.05). CONCLUSION: Preoperative dexamethasone (8 mg) reduced pain, fatigue, nausea and vomiting, and duration of convalescence in patients undergoing noncomplicated LC, when compared with placebo, and is recommended for routine use.

Adult↗
PubMed1983

Effects of dexamethasone on erythroid colony and burst formation from human fetal liver and adult marrow.

Dexamethasone, a prototypic synthetic glucocorticoid, was added to cultures of human fetal liver and adult marrow cells to assess its effects on erythroid colony and burst formation. Dexamethasone decreased the number of fetal liver erythroid colonies and bursts formed in the presence of erythropoietin, and also decreased the number of cells per colony. The amount and type of haemoglobin produced per cell were unaffected by adding dexamethasone to the cultures. Dexamethasone inhibited the incorporation of 3H-thymidine into DNA in fetal liver cells stimulated with erythropoietin, supporting the hypothesis that dexamethasone inhibits the proliferation but not the differentiation of fetal liver CFU-E and BFU-E. In contrast, addition of dexamethasone to adult bone marrow cultures had a variable effect on erythroid colony and burst formation.

Adult↗
PubMed1994

Selective enhancement of an A type potassium current by dexamethasone in a corticotroph cell line.

Perforated patch recording was used to examine the effect of the synthetic steroid dexamethasone on the whole cell potassium (K+) current, in the mouse corticotroph tumour cell line AtT20/D16-16. In 15 out of 52 control cells (29%) there was a rapidly-activating, rapidly-inactivating K+ current of the A type, the amplitude of which was strongly dependent on the holding potential in use prior to its activation by depolarising voltage pulses, and which was blocked by 1 mM 4-aminopyridine (4-AP, n = 5). The effect of dexamethasone (100 nM, 2 h, 37 degrees C) was that the A current increased in prevalence (24 out of 31 cells, 77%), lost its dependence on holding potential (over the range studied), and as a result became significantly larger than in controls, for certain voltage steps (peak A current density was 18.5 +/- 2.4 pA/pF (n = 12) for control cells and 26.3 +/- 3.9 pA/pF (n = 18) for dexamethasone treated cells, for a step to +30 mV from -60 mV, values are mean +/- SEM). All cells exhibited a slowly-activating, sustained K+ current, which was unaffected by changes in the holding potential, unaffected by 4-AP and consisted of at least 3 components: one blocked by 30 mM tetraethylammonium(TEA) or 100 nM charybdotoxin (CTX); a second blocked by 100 nM apamin; and a third not blocked by TEA, CTX, apamin, clofilium (100 nM) or niflumic acid (0.1 mM). Dexamethasone produced no change in the slowly-activating, sustained current nor in any of its individual components. The effect of dexamethasone on the A current was completely blocked by 0.1 mM puromycin, a protein synthesis blocker, while puromycin alone did not affect the size or frequency of the A current, nor alter the slowly-activating, sustained current. Secretion studies using 4-AP confirmed that the A current has a role in stimulated adrenocorticotrophic hormone (ACTH) secretion. In summary, AtT20 cells contain at least four types of K+ current: an A current and 3 currents contributing to the slowly-activating current. Selective enhancement of the A current by dexamethasone, shown here to require synthesis of new protein, is one of the mechanisms whereby glucocorticoids exert inhibitory control on ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1998

Nausea and vomiting after dexamethasone versus droperidol following outpatient laparoscopy with a propofol-based general anesthetic.

BACKGROUND: The purpose of this randomized, double-blinded study was to compare the incidence and severity of postoperative nausea and vomiting (PONV) after dexamethasone versus droperidol following gynecologic laparoscopy, a group at high risk for developing PONV. METHODS: Ninety-five patients who underwent a propofol-based general anesthetic received either dexamethasone 0.17 mg/kg i.v., or droperidol 0.02 mg/kg i.v., just prior to abdominal incision. Nausea, retching, vomiting, degree of sedation, and discharge times were assessed in the Post Anesthesia Care Unit (PACU), and the Ambulatory Care Unit (ACU). Following hospital discharge (24 h), the patients were contacted by telephone to assess any further complications. RESULTS: PONV in the PACU (14.6% vs. 14.9%) and ACU (8.3% vs. 14.9%) was as common after dexamethasone as after droperidol. PONV following hospital discharge was, however, less common after dexamethasone than after droperidol (4.2% vs. 17.0%, P = 0.041). Postoperatively, no complications of therapy were detected. CONCLUSIONS: We conclude that PONV is similar with dexamethasone and droperidol, but dexamethasone may have a longer duration of action in patients undergoing gynecologic laparoscopy.

Adolescent↗
PubMed1996

Direct activating effects of dexamethasone on glycogen metabolizing enzymes in primary cultured rat hepatocytes.

The direct effects of dexamethasone on glycogen synthase and phosphorylase and glycogen content have been investigated in primary cultured rat hepatocytes. Dexamethasone induced the transient translocation of glycogen synthase from the soluble to the 10000xg pelletable fraction and the activation of this enzyme, although more significant, longer-standing activation was achieved in the pelletable fraction. Neither total glycogen synthase content nor glycogen synthase mRNA levels were modified. Dexamethasone also caused the sustained activation (up to 6h) of glycogen phosphorylase, which was not accompanied by an increase in its mRNA level. Glycogen cell content and the incorporation of (14C) glucose into glycogen decreased after dexamethasone treatment. The data show that dexamethasone, unlike other glycogenolytic hormones, at concentrations of 10 nM or higher, stimulate hepatocyte glycogenolysis without inducing the inverse coupling of synthase and phosphorylase. The co-existence of active forms of both glycogen synthase and phosphorylase promoted by dexamethasone leads to a situation that is analogous to that of the fasted liver.

Animals↗
PubMed1997

Dexamethasone increases expression of 5-lipoxygenase and its activating protein in human monocytes and THP-1 cells.

The aim of this study was to assess the effect of dexamethasone on 5-lipoxygenase pathway expression in human peripheral blood monocytes and the acute monocytic leukemia cell line, THP-1. Cells were conditioned over a period of days with dexamethasone, at concentrations relevant in vivo, to study the effect of the glucocorticoid on calcium-ionophore-stimulated 5-lipoxygenase product and arachidonic acid release. The effect of dexamethasone on levels of immunoreactive protein and steady-state messenger RNA encoding for 5-lipoxygenase and its activating protein (5-LAP) was also assessed. Dexamethasone increased the stimulated release of 5-lipoxygenase products from both monocytes and THP-1 cells in a dose-dependent fashion. The increase in product generation was not due to changes in the availability of arachidonic acid. However, immunoreactive protein and steady-state messenger RNA encoding for 5-lipoxygenase and 5-LAP were increased by conditioning with dexamethasone. There was no apparent effect of the glucocorticoid on LTA4-hydrolase-immunoreactive protein levels or specific activity. We conclude that dexamethasone increases 5-lipoxygenase pathway expression in both monocytes and in THP-1 cells. This effect is due, at least in part, to increases in immunoreactive protein and steady-state messenger RNA encoding for 5-lipoxygenase and 5-LAP. These results suggest a role for glucocorticoids in the regulation of 5-lipoxygenase pathway expression in mononuclear phagocytes.

5-Lipoxygenase-Activating Proteins↗
PubMed1997

Metalloelastase expression in a mouse macrophage cell line--regulation by 4beta-phorbol 12-myristate 13-acetate, lipopolysaccharide and dexamethasone.

The regulation of the expression of mouse macrophage elastase (MME) was investigated using the murine tumor cell line P388D1. The effects of three factors were studied: a phorbol ester (4beta-phorbol 12-myristate 13-acetate, PMA), an endotoxin (lipopolysaccharide, LPS) and a corticosteroid (dexamethasone). Both in situ hybridization and northern blot analysis showed that P388D1 cells constitutively express the MME gene. Quantification of the MME mRNA by northern blot analysis showed that only PMA and dexamethasone significantly regulate MME gene expression in a time-dependent and dose-dependent manner. After PMA treatment, the MME mRNA level was maximal between 4 h and 9 h (medium-term response), and the mean amplitude of the response to a concentration of 100 nM was 2.5-fold (P<0.01). LPS did not induce any significant change in MME mRNA level even when 1% serum was added to the cultures. Following dexamethasone treatment, the MME mRNA level was minimal between 21 h and 33 h (long-term response), and the mean amplitude of the response to a concentration of 100 nM was 0.49-fold (P < 0.05). Using actinomycin D, it appeared that the inhibition of RNA synthesis reduces the ulterior stimulating effect of PMA from 184% to 121%, and that MME mRNA has a half-life longer than 8 h, which is not diminished by dexamethasone. These results strongly suggest that the two factors modify MME mRNA level by stimulating (PMA) or inhibiting (dexamethasone) the transcription of the gene, rather than by modifying the transcript stability. Analysis of the cell-conditioned media by elastin zymography showed the MME as a lysis band in the 22-kDa region, the intensity of which varied with the treatments. The MME secretion is stimulated by PMA, inhibited by dexamethasone and does not show any variation after LPS treatment.

Animals↗
PubMed2007

Effects of dexamethasone on mRNA abundance of nuclear receptors and hepatic nuclear receptor target genes in neonatal calves.

Hepatic nuclear receptors (NR), particularly constitutive androstane receptor (CAR) and pregnane X receptor (PXR), are involved in the coordinated transcriptional control of genes that encode proteins involved in the metabolism and detoxification of xeno- and endobiotics. A broad spectrum of metabolic processes are mediated by NR acting in concert with ligands such as glucocorticoids. This study examined the role of dexamethasone on hepatic mRNA expression of CAR, PXR and several NR target genes. Twenty-eight male calves were allotted to one of four treatment groups in a 2 x 2 arrangement of treatments: feed source (colostrum or milk-based formula) and glucocorticoid administration (twice daily intramuscular dexamethasone). Liver biopsies were obtained at 5 days of age. Real-time reverse transcription polymerase chain reaction was used to quantify mRNA abundances. No effects of feed source on mRNA abundances were observed. For the NR examined, mRNA abundance of both CAR and PXR in dexamethasone-treated calves was lower (p < 0.05) by 39% and 40%, respectively, than in control calves. Abundance of NR target genes exhibited a mixed response. SULT1A1 mRNA abundance was 39% higher (p < 0.05) in dexamethasone-treated calves compared with control calves. mRNA abundance of CYP2C8 tended also to be higher (+44%; p = 0.053) after dexamethasone treatment. No significant treatment effects (p > 0.10) were observed for mRNA abundances of CYP3A4, CYP2E1, SULT2A1, UGT1A1 or cytochrome P450 reductase (CPR). In conclusion, an enhanced glucocorticoid status, induced by pharmacological amounts of dexamethasone, had differential and in part unexpected effects on NR and NR target systems in 5-day-old calves. Part of the unexpected responses may be due the immaturity of NR and NR receptor target systems.

Age Factors↗
PubMedDate not supplied

Dexamethasone-induced changes in endometrial growth and inducible nitric oxide synthase during decidualization in rats.

1. The present study investigated the time-dependent inhibitory responses of endometrial growth and inducible nitric oxide synthase (iNOS) to dexamethasone during deciduoma development that was surgically induced on day 4 of pseudopregnancy (PG). 2. Groups of rats (n = 6) were subcutaneously injected with dexamethasone (1.5 mg/rat per day) for 3 days (PG days 1-3, 4-6, 7-9, 10-12 and 12-15). Rats in each group were killed on the last injection day. 3. Dexamethasone produced comparable temporal inhibitory changes in endometrial growth (wet weight, protein and DNA concentrations; P<0.0001) and in iNOS activity (130 kDa protein band), which peaked after PG days 4-6 and 7-9 pretreatments. 4. Endometrial matrix metalloproteinases (72 and 92 kDa) activity profiles displayed maximal reductions (36 and 53%, respectively) following PG days 4-6 pretreatment. Serum progesterone levels were equally (P<0.0001) but asynchronously inhibited by dexamethasone on PG days 9 and 12. 5. Dexamethasone inhibition of endometrial growth and in situ iNOS was most pronounced during decidual development (PG days 4-9). Minor reductions in these endometrial parameters occurred before deciduoma induction (PG days 1-3) and during deciduoma regression (PG days 10-15). 6. These results indicate that, in the endometrium, the iNOS/endogenous nitric oxide system may be linked to the biochemical and metabolic mechanisms responsible for the developmental responsiveness of the deciduoma to dexamethasone exposure. These time-dependent changes in endometrial growth and iNOS apparently were not mediated by progesterone.

Animals↗
PubMed1991

The use of dexamethasone in full-term infants with severe respiratory failure and pulmonary barotrauma.

Eight full-term infants (mean gestation 39.9 weeks [range 37-42] and mean birthweight 3642 g [range 3060-4200]) with severe respiratory failure (median oxygenation index 28 [range 16-65] and median arterial/alveolar PO2 ratio (a/APO2) 0.094 [range 0.038-0.165]) and pulmonary barotrauma were treated with Dexamethasone, 0.5 mg/kg per day, from the median age of 5 days (range 3-22). Six of the eight (75%) infants survived. They were weaned from mechanical ventilation and extubated a median of 2.5 days after commencing treatment with Dexamethasone. Two infants died and one of them suffered recurrent pneumothoraces. There was a significant improvement in oxygenation in the seven infants who survived the 72 h period of observation. Their median oxygenation index was 24 when Dexamethasone was commenced compared with 8 after 12 h (P less than 0.05) and 10 after 36 h (P less than 0.025). Their a/APO2 ratio was 0.095 when Dexamethasone was commenced compared with 0.289 after 12 h (P less than 0.05) and 0.207 after 36 h (P less than 0.025). There was a significant increase in the infants' arterial mean blood pressure associated with Dexamethasone therapy and one infant developed Staphylococcus aureus septicaemia. In this uncontrolled study of eight full-term infants with severe respiratory failure and pulmonary barotrauma, the use of Dexamethasone was associated with significant improvement in oxygenation and rapid weaning from mechanical ventilation.

Barotrauma↗
PubMed2004

Additive effects of dexamethasone in nebulized salbutamol or L-epinephrine treated infants with acute bronchiolitis.

BACKGROUND: Although it is the most common lower respiratory infection of infancy, the optimal treatment for acute bronchiolitis is still controversial. The aim of this study was to compare the early and late effects of nebulized L-epinephrine (EPI) and intramuscular dexamethasone (DEX) combination therapy with nebulized salbutamol (SAL) and dexamethasone combination and bronchodilators alone in outpatients with acute bronchiolitis. METHODS: A total of 69 infants aged 2-21 months who were admitted to the Pediatrics Department of the Faculty of Medicine, Mersin University, with acute bronchiolitis were included in a randomized, placebo-controlled, prospective trial study. Patients were assigned to receive either nebulized L-epinephrine (3 mg) or salbutamol (0.15 mg/kg) and 15 min later, either dexamethasone 0.6 mg/kg or placebo (PLA), intramuscularly, in a double-blind randomized fashion. The study groups were: epinephrine + dexamethasone group (group 1, n=23), salbutamol + dexamethasone group (group 2, n=23), epinephrine + placebo group (group 3, n=11), and salbutamol + placebo group (group 4, n=12). The outcome measures were heart rate, respiratory rate and Respiratory Distress Assessment Instrument (RDAI) score determined at 30, 60, 90 and 120 min, 24 h, and 5 days after the first therapy. Patients were then followed-up during the subsequent 2 months for the prevalance of respiratory complaints regarding bronchial hyperreactivity. RESULTS: There were no significant differences between the outcome variables of the four groups within the first 120 min and at 24 hours, or between the rates of requirement of a second dose of the same bronchodilator. However, fifth day RDAI score values of both DEX groups were significantly lower than that of SAL + PLA group (P=0.000 and P=0.01, respectively). The fifth day score value of group 1 was also significantly better than that value of EPI + PLA group but not different from group 2. CONCLUSIONS: A single dose of intramuscular dexamethasone added to nebulized L-epinephrine, or salbutamol therapies resulted in better outcome measures than bronchodilators alone in the late phase (fifth day) of mild to moderate degree bronchiolitis attack. However, effects of EPI + DEX combination was not different from SAL + DEX combination.

Acute Disease↗