Injection Of Hydrocortisone Research Articles

Synergistic Effect Between Ouabain and Glucocorticoids for the Induction of Thymic Atrophy

The present report shows that thymocyte death, induced by glucocorticoids, may be modulated in vivo by ouabain. Young, ten days old, mice injected with 140 mg/kg sodium succcinate of hydrocortisone (HC) intraperitonially (i.p.) displayed, 24 h after the injection, a decrease in thymus size and cellular content, an effect that was magnified when ouabain (OUA) 0.56 mg/kg, i.p. was given 1 h prior to the HC injection. Ouabain per se was not capable of producing these changes. Both HC and the combination OUA plus HC induced the death of immature double positive lymphocytes (CD4+CD8+) whereas CD69+ cells survived both treatments. An increase in annexin positive cells and a decrease in mitochondrial membrane potential, assessed by cytofluorimetry, using the fluorescent dye DiOC6, was observed in thymocytes from HC treated animals indicating apoptosis of these cells. Furthermore, a synergistic effect between OUA and HC was also observed using this parameter. The synergy observed in the thymus of animals treated with glucocorticoids and OUA might occur under stress, when both hormones are released, or in situations when ouabain is administered exogenously in a moment of the circadian cycle when glucocorticoid levels are elevated. However the impact of this effect on the immune response is still unknown.

Cortisol and parathyroid hormone-related peptide are reciprocally modulated by negative feedback

In previous in vitro studies, we have shown that the N-terminal region of parathyroid hormone-related protein (PTHrP) can stimulate cortisol production in sea bream, Sparus auratus, interrenal tissue, possibly through a paracrine action. In the current study, the systemic interaction between cortisol and PTHrP was studied in vivo. Sustained elevated blood cortisol levels, induced either by cortisol injection or confinement stress, suppressed circulating PTHrP 6 and 24-fold, respectively, by comparison to control fish. Dexamethasone treatment reduced cortisol levels, prevented the decrease of plasma PTHrP observed in confined fish and raised plasma PTHrP levels in non-confined fish. In contrast, a single injection of (1–34) PTHrP caused a short-term (within 30 min and up to 2.5 h) decrease in plasma cortisol. The antagonistic effects between PTHrP and cortisol were substantiated by an overall (data pooled from all experiments) highly significant negative correlation ( r 0 = −0.745, p < 0.001, n = 115) between the plasma levels of the two hormones. Although the underlying mechanism of the interaction still has to be determined, the high levels of PTHrP in circulation and the existence of systemic regulation favour the hypothesis that in fish PTHrP may act as an endocrine factor, although the gland that produces it still remains to be identified.

Cortisol promotes survival and regeneration of axotomised retinal ganglion cells and enhances effects of aurintricarboxylic acid

Neuroprotection is essential for repair processes after a traumatic insult in the central nervous system. We have demonstrated previously significant neuroprotective properties of the anti-apoptotic drug aurintricarboxylic acid in the model of axotomised retinal ganglion cells. Glucocorticoids are widely used to treat injuries of the nervous system. Due to the anti-inflammatory and microglia-inhibiting properties of glucocorticoids, we studied the neuroprotective effects of intravitreally administered cortisol after an optic nerve cut. Ninety-eight adult Sprague-Dawley rats were used in this study. The optic nerve was cut intra-orbitally. Either vehicle or compound solution was injected intravitreally. Fluorescent dye was put onto the optic nerve stump to label retinal ganglion cells retrogradely. Retinal whole mounts were prepared 2 weeks after axotomy, and surviving retinal ganglion cells were counted. Two weeks after axotomy, up to 50+/-7% of all retinal ganglion cells survived if cortisol was injected into the eye compared with 17+/-5% survival if only vehicle solution was injected. The neuroprotective effects of aurintricarboxylic acid (43+/-5% survival) could be further enhanced if combined with cortisol (up to 61+/-5% survival). Regeneration of cut retinal ganglion cell axons into a peripheral nerve graft could also be enhanced by an intravitreal injection of cortisol (169+/-42 regenerating retinal ganglion cells per mm2 vs. 73+/-12 cells per mm2 after vehicle injection). The increase was not as high as with aurintricarboxylic acid (192+/-40 cells per mm2), although more retinal ganglion cells survived with cortisol. This indicates that neuronal survival alone is not sufficient for subsequent axonal regeneration. Nevertheless, regeneration could be markedly increased if aurintricarboxylic acid and cortisol were combined (308+/-72 cells per mm2). Whereas aurintricarboxylic acid seems to act directly on lesioned retinal ganglion cells, cortisol seems to act on the glial environment, as indicated by microglial cell morphology and enhanced glial fibrillary acidic protein expression. The results show that both neuroprotection and regeneration can be enhanced by the combination of two simple compounds acting on different sites.

Expression of glucocorticoid receptor in the intestine of a euryhaline teleost, the Mozambique tilapia ( Oreochromis mossambicus): Effect of seawater exposure and cortisol treatment

Cortisol plays an important role in controlling intestinal water and ion transport in teleosts possibly through glucocorticoid receptor (GR) and/or mineralocorticoid receptor. To better understand the role of GR in the teleost intestine, in a euryhaline tilapia, Oreochromis mossambicus, we examined (1) the intestinal localizations of GR; (2) the effects of environmental salinity challenge and cortisol treatment on GR mRNA expression. The mRNA abundance of GR in the posterior intestinal region of tilapia was found to be higher than that in the anterior and middle intestine. In the posterior intestine, GR appears to be localized in the mucosal layer. GR mRNA levels in the posterior intestine were elevated after exposure of freshwater fish to seawater for 7 days following an increase in plasma cortisol. Similarly, cortisol implantation in freshwater tilapia for 7 days elevated the intestinal GR mRNA. These results indicate that seawater acclimation is accompanied by upregulation of GR mRNA abundance in intestinal tissue, possibly as a consequence of the elevation of cortisol levels. In contrast, a single intraperitoneal injection of cortisol into freshwater tilapia decreased intestinal GR mRNA. This downregulation of the GR mRNA by cortisol suggests a dual mode of autoregulation of GR expression by cortisol.

Alterations in cortisol negative feedback inhibition as examined using the ACTH response to cortisol administration in PTSD

Studies using the dexamethasone suppression test (DST) have demonstrated an enhanced negative feedback inhibition at the pituitary in PTSD, but have not provided information about central feedback effects, since dexamethasone (DEX) does not penetrate the brain well. The authors therefore examined the change in ACTH and cortisol before and after cortisol administration, which acts at central feedback sites in addition to peripheral targets. Blood was obtained from 31 male veterans (18 with PTSD) before, and 8, 40 and 95 min following injection of 17.5 mg cortisol and placebo. A greater decline in ACTH was observed after cortisol injection in PTSD. Central as well as peripheral negative feedback inhibition may be altered in PTSD.

Central Nervous System (CNS) Relapse in Adult Patients with Acute Lymphoblastic Leukemia (ALL): Frequency and Prognosis in 467 Patients without Cranial Irradiation for CNS Prophylaxis.

Background. Recurrence of ALL in CNS in adults is considered a poor prognostic feature but few studies have analyzed this issue. The objective of this study was to analyze the frequency, prognosis and predictive factors of CNS involvement and recurrence in adult patients with ALL treated with 4 PETHEMA protocols not including cranial irradiation for CNS prophylaxis.Methods. From June 1989 to December 2003, 467 adult patients (≥ 15-years-old) diagnosed with ALL were treated with one of the four consecutive protocols of PETHEMA group: ALL-89 (standard and high risk, n=108), ALL-93 (high risk, n=222), ALL-96 (standard risk, n=84), and ALL-97 (Burkitt's leukemia, n=53). CNS prophylaxis consisted of intrathecal (IT) injection of methotrexate (12 mg), cytarabine (30 mg) and hydrocortisone (20 mg), for 12–14 courses, together with high-dose systemic methotrexate and cytarabine during the early intensification phase. Cranial or craniospinal irradiation was not used in any case.Results. The median (SD) age was 33 (16) years and 272 (58%) were males. ALL type according to the FAB classification was: L1 28%, L2 61%, L3 11%. Immunological subtypes were: early-pre-B 15%, common 45%, pre-B 5%, mature B 11% and T 24%. CNS involvement at diagnosis was observed in 18 (3.9%) patients. Predictive factors for CNS involvement at diagnosis were: L3/mature B ALL (p<0.0001) and testicular involvement (p=0.006). Overall, complete remission (CR) was achieved in 381 (81%) of the patients, of whom 159 (42%) relapsed: 137 (36%) in bone marrow (BM) and 22 (5.8%) in CNS (14 isolated and 8 combined CNS and BM). The median (range) CR duration prior to CNS recurrence was 1.06 yr (95%CI0.11–2.01) for isolated CNS relapse, 0.6 yr (95%CI o.30–0.89) for combined relapse and 0.93 (95%CI 0.78–1.07) for BM relapse (p=0.76). No correlation was found between initial CNS involvement and CNS relapse. An initial LDH value > 1,000 U/L was the only factor associated with higher risk of CNS relapse (p<0.001). Treatment of CNS relapse consisted of systemic and IT therapy in the 22 cases (cranial irradiation was added to one) and CR was attained in 7 (32%) out of 22 of these patients. Stem cell transplantation was performed in 4 patients and 3 patients developed a second CNS recurrence. The median overall survival (OS) after recurrence was 0.7 yr for isolated CNS relapse, 0.13 yr for combined relapse and 0.41 yr for BM relapse (p=0.11).Conclusions. The frequency of CNS relapse in adult ALL patients receiving IT and systemic therapy for CNS prophylaxis is similar to that observed in protocols including cranial irradiation. An initial LDH value > 1,000 U/L was the only factor associated with higher risk of CNS relapse. Adult patients with CNS recurrence have a poor prognosis, although it is not different from that observed in BM relapses.

Effects of intraperitoneal injection of cortisol on non‐specific immune functions of Ctenopharyngodon idella

After grass carps Ctenopharyngodon idellus were injected with cortisol, with (CBC) and without (C) a cocoa butter carrier, the effects of both slowly and rapidly acting exogenous cortisol on their non‐specific immune functions were investigated. On the one hand, after injection with CBC, the cortisol concentration and lysozyme activity in fish serum were enhanced and were sustained at high levels for a long period (30 days). The killing activity in the serum declined with time, and phagocytosis of head kidney macrophages diminished significantly (P &lt; 0·05 or P &lt; 0·01). The leukocrit values in the high dose group (31·8 mg cortisol fish−1) increased over time, however, with the maximum average being 5·6% at day 30. The spleen mass index in the high dose group was 0·93 × 10−3 after 30 days, notably lower (P &lt; 0·05) than that in the control group. In addition, a decrease in resistance to Aeromonas hydrophila infection in cortisol‐treated fish was shown, with the final cumulative mortalities being 54·5 and 66·7% in the low and high dose groups, respectively. On the other hand, there was a decrease in both serum cortisol concentration and lysozyme activity of the experimental fish within 2 weeks after injection with C, where plasma bactericidal activities in the high dose group (31·8 mg cortisol fish−1) were remarkably lower (P &lt; 0·01) than those in the control group at each sampling, but were increased slightly over time. The results of which were different from those in the CBC trial. Phagocytic activity of head kidney macrophages and spleen mass index decreased significantly (P &lt; 0·05), while there were increases in leukocrit value and cumulative mortality due to A. hydrophila. The results of which were similar to those in the CBC trial. This study indicated that the injection of cortisol depressed the non‐specific immune functions of the grass carp and increased its susceptibility to disease.

Gene expression profiling of gilthead sea bream during early development and detection of stress-related genes by the application of cDNA microarray technology

Large-scale gene expression studies were performed for one of the main European aquaculture species, the gilthead sea bream Sparus auratus L. For this purpose, a cDNA microarray containing 10,176 clones from a cDNA library of mixed embryonic and larval stages was constructed. In addition to its importance for aquaculture, the taxonomic position and the relatively small genome size of sea bream makes it a prospective model for evolutionary biology and comparative genomics. However, so far, no large-scale analysis of gene expression exists for this species. In the present study, gene expression was analyzed in gilthead sea bream during early development, a significant period in the determination of quantitative traits and therefore of considerable interest for aquaculture. Synexpression groups expressed primarily early and late in development were determined and were composed of both known and novel genes. Furthermore, it was possible to identify stress response genes induced by cortisol injections using the cDNA microarray generated. The creation of gene expression profiles for sea bream by microarray hybridization will accelerate identification of candidate genes involved in multifactorial traits and certain regulatory pathways and will also contribute to a better understanding of the genetic background of fish physiology, which may help to improve aquaculture practices.

Effects of Wenshen Jianpi Recipe on chronic wound healing in rats

To study the effects of Wenshen Jianpi Recipe (WSJPR, a traditional Chinese medicine for warming kidney and invigorating spleen) on chronic wound healing and the mechanism. Ninety-six SD rats were randomly divided into 4 groups, with 24 rats in each group, and back wound was made in the rats. For rats in 3 of the 4 groups, hydrocortisone injection was administered to induce chronic wound. Rats in 2 of the 3 groups were treated with WSJPR and Xinpukang Granules (XPKG) respectively, and the rats in the other group were untreated. The rats in the fourth group were taken as control. The wound healing time and the width of new epidermis were observed, and the histomorphological changes and cell cycle of the granulation tissue, and the protein expressions of epidermal growth factor (EGF), transforming growth factor-beta(1) (TGF-beta(1)) and fibronectin (FN) in the granulation tissue were tested with immunohistochemical technique and flow cytometry. The wound healing time of the WSJPR-treated and XPKG-treated groups was (17.0+/-1.9) and (18.8+/-1.9) d respectively, much shorter than that of the untreated and control groups (P<0.05). On the 14th experiment day, the width of new epidermis of the WSJPR-treated and XPKG-treated groups was (3.73+/-0.19) and (3.21+/-0.15) mm respectively, much wider than that of the untreated and control groups (P<0.05). The numbers of angiogenesis, fibroblasts and cells in the S phase in WSJPR-treated and XPKG-treated groups were much higher than those in the untreated and control groups (P<0.05). Compared with the untreated and control groups, the protein expressions of EGF, TGF-beta(1) and FN in WSJPR-treated and XPKG-treated groups were higher (P<0.05). WSJPR can enhance the wound healing. It was likely through accelerating the cell proliferation and up-regulating the expressions of EGF, TGF-beta(1) and FN.

Effects of cortisol and cocaine on plasma prolactin and growth hormone levels in cocaine-dependent volunteers

In rodents, corticosterone (cortisol in humans) facilitates cocaine self-administration purportedly via enhancement of dopaminergic activity in the brain. This study sought to assess central dopaminergic effects of cortisol in humans and to compare them to those of cocaine. Twelve cocaine-dependent individuals received an intravenous bolus of cortisol (0.5 and 0.2 mg/kg; n=6 for each dose) and cocaine (0.2 mg/kg) in a double-blind randomized placebo-controlled and counterbalanced fashion. Their plasma was assayed over the next 120 min for prolactin and growth hormone (GH), which are two neuroendocrine indices of dopaminergic function. Cortisol injections produced significant increases in GH, while cocaine resulted in significant decreases in prolactin. Placebo administration was associated with gradual declines in prolactin, but the levels at the 90- and 120-min time points were significantly lower after cocaine than after placebo infusion. These different neuroendocrine response profiles point to important differences between dopaminergic effects of cortisol and cocaine.

Experimental study on observation of hemorheologic parameters of hydrocortisone caused Shen-Yang deficiency in rat models

Objective: To explore the relationship between Shen deficiency and blood stasis.Methods: Using consecutive intramuscular injection of hydrocortisone to build Shen-yang deficiency model rats, and detect their hemorheological and biochemical parameters.Results: Comparison between the model group and control group showed that the in vitro thrombus significantly lengthened in the model group (P<0.05), the dry weight increased (P<0.01), hematocrit and whole blood viscosity under high sheared change lowered (P<0.05), blood glucose elevated (P<0.01), and RBC infiltration index, aggregation index increased (P close to 0.05).Conclusion: Under the condition of Shen-yang deficiency, although blood does not show such properties of blood stasis as being “viscous, concentrated, coagulated and aggregated”, partial change of hemorheology occurs, and it is liable to form thrombus, which proves that the Shen deficiency status is accompanied with the tendency of blood stasis.

Juvenile recurrent parotitis: a new method of diagnosis and treatment.

Juvenile recurrent parotitis (JRP) is a nonobstructive, nonsuppurative parotid inflammation in young children. Causative factors, such as local autoimmune manifestation, allergy, infection, and genetic inheritance, have been suggested, but none of them has been proved to date. Until now, treatment of JRP was divided into conservative observation and antibiotic treatment, and no preventive therapy was available. Twenty-six cases symptomatic JRP in children were diagnosed and treated with a combined endoscopic approach. Sialography and sialoendoscopy were performed bilaterally in all children. The treatment modality was composed of lavage, ductal dilation, and hydrocortisone injection. Sialography showed multiple sialectasis in the affected gland and in the contralateral one as well. Dilations and strictures were noticed in the main duct, and kinks could be identified in 31% of the glands. The main endoscopic finding was a white appearance of the ductal layer without the healthy blood vessel coverage. Recurrence of the symptoms occurred in only 2 (8%) children. The endoscopic technique provides the possibility of a correct diagnosis and treatment. In this article, we present a new treatment modality of irrigation and dilation under direct vision by endoscopically guided miniature surgical instruments.

Plasma cortisol levels in acute asthma.

The study was undertaken with the aim to determine correlation between the initial plasma cortisol level and severity of asthma attack and the response to standard treatment for acute exacerbation of bronchial asthma in pediatric age group. The study was performed in 33 asthmatic patients between 5-12 years of age, presenting to pediatric emergency with acute exacerbation of bronchial asthma. None of the patients included in the present study was on steroids. Venous blood sample for determination of plasma cortisol level was taken and patients were nebulized with salbutamol every 20 minutes, up to 1 hour. The patients who failed to respond even after three nebulizations were labeled as nonresponders and repeat venous blood sample for plasma cortisol estimation was taken before giving injection hydrocortisone. In responders sample was taken 1 hour after last nebulization. The mean plasma cortisol value at the time of admission in responders (12.42 +/- 1.9 microg/dl) was not found to be significantly different from that in nonresponders (13.1 +/- 2.74 microg/dl). Children with severe attack of asthma had significantly higher plasma cortisol levels both at the time of admission (p=0.03) and at the end of study (p=0.001), as compared to patients with moderate attack. The mean percentage change in plasma cortisol levels in nonresponders was an increase of 80.65 +/- 60.64%, whereas, in responders it decreased by 16.49 +/- 21.7% and this difference was statistically significant (p<0.05). The hypothalamo pituitary adrenal axis functions normally in asthmatic patients, producing a rise in cortisol levels corresponding to degree of stress; and from initial cortisol level alone, it cannot be predicted, whether a patient will respond to beta-2 agonist (salbutamol) nebulization alone or will require exogenous corticosteroids.

Pathway-specific response to cortisol in the metabolism of catfish

Cortisol produced biochemical pathway-specific effects on metabolic enzymes and other macromolecules in the freshwater catfish, Clarias batrachus. Injection of cortisol increased 1.6-fold activity of citrate synthase (CS) in brain, liver and skeletal muscle of the fish over vehicle-injected control, while administration of metyrapone (a cortisol synthesis inhibitor) reduced CS activity by 52%. Cortisol treatment of metyrapone-treated fish induced CS activity by approximately 2.5-fold, which was blocked after administration of actinomycin D or cycloheximide. This shows de novo synthesis of CS to enhance aerobic capacity of fish. In contrast the activities of glucose-6-phosphate dehydrogenase (G6-PDH) and lactate dehydrogenase (LDH) increased in response to metyrapone and decreased after administration of cortisol in all the three tissues. The cortisol-mediated decrease in G6-PDH and LDH activities reflects reduction in biosynthetic and anaerobic capacity of fish. Administration of metyrapone significantly increased RNA/DNA ratio and protein but cortisol decreased these macromolecular contents in brain, liver and skeletal muscle. It shows cortisol-induced decrease in protein synthesis capacity of fish. The present study suggests that cortisol-induces catabolic and aerobic but inhibits anabolic and anaerobic processes in freshwater catfish. The cortisol-dependent metabolic responses may also be associated with the permissive effect of cortisol on other hormone(s) in fish.

Modest protection of early hydrocortisone treatment in a rat model of volume-controlled haemorrhage.

Major insults may trigger generalized inflammatory responses that contribute to progressive multiple organ dysfunction. The present study was performed to test the potential of early hydrocortisone treatment to influence these responses as well as organ function following an episode of rapid and profound blood loss. In isoflurane anaesthesia, 35 spontaneously breathing male Sprague-Dawley rats were bled 2.5 ml 100 g-1 body weight over 10 min. Immediately following withdrawal of blood, one group (n = 17) was given 2 mg of hydrocortisone, and the other (n = 18) had the same amount of normal saline. Seventy-five minutes after initiation of bleeding, two-thirds of the blood was retransfused, together with a new injection of hydrocortisone or saline. Thereafter the rats were observed for 2 h. Key mediators of systemic inflammation and plasma markers of organ function and integrity were measured. Internal organs were weighed and scored for visible pathology. Leukocyte infiltration of the liver was counted in a light microscope. Hydrocortisone reduced the plasma levels of IL-6 (P < 0.05); non-significant reductions of TNF-alpha (P = 0.12) and IL-10 (P = 0.44) were noted. The synthesis of reactive oxygen species in peritoneal cells was unaffected. Relative organ weights and organ injury scores tended to be reduced, but only wet organ weight for the lungs reached statistical significance. Leukocyte infiltration of the liver was equal in both groups. Plasma levels of ALT, AST, alpha-GST and creatinine did not differ significantly between groups. Two of the hydrocortisone treated rats died compared with four controls. Early treatment with hydrocortisone had a limited organ protective effect in this model of controlled haemorrhagic shock. Although a general tendency for better outcome in the hydrocortisone group was noted, clear-cut and significant advantages of the treatment were not obtained.

Dual mode of cortisol action on GH/IGF-I/IGF binding proteins in the tilapia, Oreochromis mossambicus.

Glucocorticoids are known to impede somatic growth in a wide range of vertebrates. In order to clarify the mechanisms through which they may act in an advanced teleost fish, we examined the effects of cortisol administration on the growth hormone (GH)/insulin-like growth factor-I (IGF-I)/IGF-binding protein (IGFBP) system in the tilapia (Oreochromis mossambicus). In a short-term experiment, fish were injected intraperitoneally with cortisol (2 or 10 microg/g), and killed at 2, 4, 8 and 24 h after the injection. In a longer-term experiment, fish were killed 24 and 48 h after cortisol injection (2, 10 and 50 microg/g). Cortisol at doses of 2 and 10 microg/g significantly increased IGFBPs of four different sizes (24, 28, 30, and 32 kDa) in the plasma within 2 h without altering plasma levels of IGF-I or GH. On the other hand, cortisol at doses of 10 and 50 microg/g significantly reduced plasma IGF-I levels after 24 and 48 h. IGF-I mRNA levels in the liver were also significantly reduced by cortisol at doses of 10 and 50 microg/g after 48 h, suggesting that a decrease in plasma IGF-I levels is mediated through the attenuation of IGF-I gene expression in the liver. In contrast, no significant change was observed in plasma or pituitary contents of GH at any time point examined, which would appear to indicate that cortisol reduces IGF sensitivity to GH (GH-resistance). These results clearly indicate that cortisol induces a rapid increase in plasma IGFBPs and a more delayed decrease in IGF-I production. The dual mode of cortisol action may contribute to the inhibitory influence of cortisol on somatic growth in teleosts.

Hypothalamo-pituitary-adrenal function in patients with depressive disorders is correlated with baseline cytokine levels, but not with cytokine responses to hydrocortisone

Dysfunction of the hyopthalamo-pituitary adrenal (HPA) system is frequently found in major depression. In addition, signs of non-specific inflammatory system activation have been reported. However, very little is known about interactions between the HPA and immune systems in depressive patients. To assess HPA system function, we performed a combined dexamethasone suppression and corticotropin-releasing hormone stimulation (DEX/CRH) test in 14 depressive patients. Moreover, baseline nocturnal plasma levels of the inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor (TNF)-α were measured. In addition, the system was challenged with an intraveneous pulsatile injection of hydrocortisone (1 mg/kg body weight in total) and again cytokine levels were measured across one night. Baseline TNF-α levels were negatively correlated with the amount of ACTH released upon CRH stimulation during the DEX/CRH test. Acute hydrocortisone administration suppressed TNF-α and IL-6 levels independently of baseline HPA system activity. We conclude that chronic HPA system overactivity in depressed patients might compromise the production of inflammatory cytokines under baseline conditions. However, the responsivity of the cytokine production to acutely administered glucocorticoids does not seem to correlate with the state of the HPA system.

The effect of high dose of cortisol on glucose-6-phosphatase and fructose-1,6-bisphosphatase activity, and glucose and fructose-2,6-bisphosphate concentration in carp tissues ( Cyprinus carpio L.)

The effect of a high dose of cortisol (200 mg kg −1 body mass) on juvenile carp was investigated. The activity of glucose-6-phosphatase in liver and of fructose-1,6-bisphosphatase in liver, kidney and muscle, the serum glucose and fructose-2,6-bisphosphate concentration as well as the serum concentration of the injected hormone were measured after 24, 72 and 216 h after intraperitoneal cortisol injection. The activities of fructose-1,6-bisphosphatase in liver and kidney and glucose-6-phosphatase in liver were elevated in comparison with the control, while the fructose-1,6-bisphosphatase activity in the muscle tissue was unchanged. After cortisol injection, the serum glucose level was nearly two times higher after 24 and 72 h and was still 50% higher after 216 h compared with controls. In contrast, the liver fructose-2,6-bisphosphate concentration was unchanged after 24 h. More than two times higher fructose-2,6-bisphosphate concentration was observed in liver after 72 h and it was still elevated after 216 h after the cortisol injection.

Interactive effects of cortisol treatment and ambient seawater challenge on gill Na+,K+-ATPase and CFTR expression in two strains of Atlantic salmon smolts

Abstract During peak smoltification, the interactive effects of cortisol and ambient seawater challenge were compared in two strains of Atlantic salmon ( Salmo salar ) smolts: a domesticated strain, AquaGen and a native River Imsa strain. Tissue and blood samples were taken from untreated fish on 20 May. Fish were then transferred to experimental tanks, allowed to recover for 24 h and cortisol (50 mg kg body mass −1 ), dissolved in vegetable oil, or vegetable oil alone (sham) was implanted. Samples were taken 5 days post implantation. Fish were then exposed to 24 h ambient seawater challenge (FW–SW) or freshwater to freshwater replacement (FW–FW) and sampled as before. Sham implantation had no significant impact on any of the measured parameters. Cortisol implantation significantly elevated plasma cortisol in FW–FW Imsa smolts, while no effect was observed in FW–SW Imsa smolts. Cortisol implantation had no effect on the plasma cortisol levels of AquaGen smolts regardless of FW–SW challenge. Increased plasma cortisol corresponded with significantly higher plasma glucose levels in FW–FW Imsa smolts. Plasma Na + and Cl − levels were not affected by cortisol implantation but were significantly increased in FW–SW smolts of both strains. Gill Na + ,K + -ATPase activity increased in response to cortisol implantation in only FW–FW smolts but not FW–SW smolts. Gill Na + ,K + -ATPase α-subunit mRNA levels were not affected by strain, cortisol injection or transfer protocol, while both CFTR I and CFTR II mRNA levels were significantly higher in AquaGen versus Imsa smolts regardless of treatment. CFTR I mRNA was elevated following cortisol implantation in FW–FW smolts from both strains suggesting CFTR I expression is under the control of cortisol. These findings also suggest that plasma cortisol levels are regulated differently between strains and that cortisol implantation and ambient FW–SW challenge interact, interfering with the individual effects of each of these factors.

Differential effects of maternal betamethasone and cortisol on lung maturation and growth in fetal sheep

Objectives: We asked whether maternal or fetal cortisol treatments induced fetal lung maturation and growth restriction compared with betamethasone and whether medroxyprogesterone (MPA) influenced lung maturation. Study Design: Pregnant sheep were randomized to receive MPA or saline solution at 100 days of gestation. At 117 days of pregnancy, ewes were randomized to receive maternal or fetal treatments with 0.5 mg/kg betamethasone, four injections of hydrocortisone given over 4.5 hours or saline solution. Body weight and lung maturation were evaluated at 125 days. Results: Maternal betamethasone decreased in birth weight by 16% and induced lung maturation. Fetal cortisol or betamethasone induced only lung maturation. Maternal cortisol caused neither growth restriction nor lung maturation. MPA did not alter lung function in control lambs or in betamethasone-treated preterm lambs. Conclusions: Maternal cortisol treatments had no apparent effects on the fetus, suggesting that growth restriction caused by betamethasone may result from unidentified effects on the maternal-placental unit. (Am J Obstet Gynecol 2003;188:22-8.)