Plasma Cortisone Concentrations Research Articles

Effects of Xuebijing on hypothalamus-pituitary-adrenal axis in early stage of septic rats

To explore the levels of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisone (CORT) and ultrastructural abnormalities in hypothalamus, pituitary, adrenal specimens and potential effects of Xuebijing injection in septic rats. Sepsis was induced in adult male Sprague-Dawley rats by cecal ligation and puncture (CLP). A total of 40 rats were randomly divided into control group (n = 10), sham-operated group (n = 10), saline treatment group (NS, 4 ml/kg, n = 10), Xuebijing injection treatment group (XBJ, 4 ml/kg, n = 10). The histological abnormalities associated with sepsis were examined in hypothalamus, pituitary and adrenals. Radioimmunoassay (RIA) was used to detect the levels of CRH in hypothalamic tissue and the plasma levels of ACTH and CORT. Compared with normal control or sham group, the levels of CRH in hypothalamus tissue of CLP group and plasma levels of ACTH and CORT increased in early stage of sepsis. In NS group, the plasma CORT concentration ((30.66 ± 1.55) ng/ml) was significantly higher than that in normal control group ((7.63 ± 0.56) ng/ml, P < 0.01) and sham group ((11.85 ± 0.87) ng/ml, P < 0.01). In XBJ group, the plasma CORT concentration ((22.13 ± 1.49) ng/ml) was significantly lower than that in NS group (P < 0.01). There was no significant difference between normal control and sham groups (P > 0.05). In NS group, the plasma concentration of ATCH ((26.26 ± 1.63) pg/ml) was significantly higher than that in normal control group ((8.84 ± 1.39) pg/ml, P < 0.01) and sham group ((11.43 ± 0.47) pg/ml, P < 0.01). In XBJ group, the plasma concentration of ATCH ((22.13 ± 1.49) ng/ml) was significantly lower than that in NS group (P < 0.01). No significant difference existed between normal control and sham groups (P > 0.05). In NS group, the level of CRH in hypothalamus tissue ((101.92 ± 6.61) ng/ml) was significantly higher than that in normal control group ((61.65 ± 6.05) ng/ml, P < 0.05) and sham group ((66.65 ± 4.04) ng/ml, P < 0.05). In XBJ group, the concentration of CRH in hypothalamus tissue ((84.90 ± 2.54) ng/ml) was significantly lower than that in NS group (P < 0.05). There was no significant difference between normal control and sham groups (P > 0.05). The ultrastructures of hypothalamus, pituitary and adrenal changed. In CLP group, the ultrastructure of hypothalamus was as follows: rough endoplasmic reticulum expanded. There were degranulation and Golgi complex swelling. A large number of endocrine granules could be seen in ATCH cells in pituitary and a depletion of adrenal lipid droplets. Xuebijing injection can lessen the excessive activated status of hypothalamic-pituitary-adrenal axis.

The Contribution of Visceral Adipose Tissue to Splanchnic Cortisol Production in Healthy Humans

Cortisol is regenerated from cortisone by 11beta-hydroxysteroid dehydrogenase type 1 (11HSD1), amplifying glucocorticoid action in adipose tissue and liver. 11HSD1 inhibitors are being developed for type 2 diabetes and may be most effective in obesity, where adipose 11HSD1 is increased. However, the magnitude of regeneration of cortisol in different tissues in humans is unknown, hindering understanding of the pathophysiological and therapeutic importance of 11HSD1. In eight healthy men, we infused 9,11,12,12-(2)H4-cortisol and measured tracer enrichment in the hepatic vein as an indicator of total splanchnic cortisol generation. Oral cortisone (25 mg) was then given to measure first-pass hepatic cortisol generation. In steady state, splanchnic cortisol production was 45 +/- 11 nmol/min when arterialized plasma cortisone concentration was 92 +/- 7 nmol/l. Extrapolation from hepatic cortisol generation after oral cortisone suggested that, at steady state, the liver contributes 15.2 nmol/min and extrahepatic splanchnic tissue contributes 29.8 nmol/min to the total splanchnic cortisol production. We conclude that tissues draining into the portal vein, including visceral adipose tissue, contribute substantially to the regeneration of cortisol. Thus, in addition to free fatty acids and adipokines, the portal vein delivers cortisol to the liver, and inhibition of 11HSD1 in visceral adipose tissue may indeed be valuable in ameliorating insulin resistance in obesity.

Síndrome de exceso aparente de mineralocorticoides por déficit de 11 ß hidroxiesteroide deshidrogenasa.: Estudios clínicos y genéticos en una familia chilena afectada seguida por 19 años

An 11-year old girl was seen in 1981 with hypokalemia, low renin, low aldosterone, and severe hypertension. A medical adrenalectomy with dexamethasone and aminoglutethimide, and the blockade of mineralocorticoid receptors with spironolactone improved her condition, but the blockade of glucocorticoid receptors with RU-486 worsened it. An aldosterone infusion induced no changes. A sister was born in 1982 with similar findings. Both patients had an impaired ability to convert cortisol to cortisone after an oral load of 200 mg cortisol. In urine, an elevated ratio for metabolites of cortisol to metabolites of cortisone was found. These data suggested a defect in the activity of renal 11 beta-hydroxysteroid dehydrogenase. Both parents were asymptomatic, phenotypically normal and non-consanguineous. Their urinary metabolites of cortisol and cortisone were normal before and after stimulation with ACTH. However, the mother reached a peak plasma cortisone concentration 3 SD below the mean reached by normal subjects after an oral 200-mg cortisol load, a fact that suggests that this test could be used to detect heterozygotes. The genetic studies revealed a homozygous mutation on exon 3 of the HSD11K gene, which by substituting TGC for CGC changes Arg 213 for Cys and induces a loss of 84% of the enzymatic activity in transfected cells. Both unrelated parents had the same heterozygous mutation. Both patients have been treated with dexamethasone but have also required spironolactone. The older sister has also required high doses of nifedipine to lower her blood pressure. After 19 years of follow-up, the older sister has become normotensive and normokalemic under therapy, and reached a final height of 140 cm at age 17. The younger sister has increased her mean blood pressure at a rate of 1 mm Hg per year, in spite of treatment. Her final height is 143.5 cm.

Radioimmunoassay of cortisone in the adult Atlantic salmon, Salmo salar L

A radioimmunoassay (RIA) was developed to measure cortisone in Atlantic salmon plasma. Diatomaceous earth microcolumn chromatography was used to separate the cortisone from other steroids. The RIA method following chromatography was validated by analyzing each of six samples of blood by double isotope derivative assay (DIDA) and RIA. The RIA gave significantly lower plasma cortisone concentrations ( P < 0.05) than the DIDA: the correlation coefficient was 0.84. Accuracy of the RIA was also demonstrated by addition of radioinert cortisone and measurement of increasing volumes of plasma. Specificity of the antisera was very good. Sensitivity of the RIA was 11 pg/RIA tube or 0.025 μg cortisone/dl plasma corrected for recovery and fraction assayed. Plasma cortisone concentrations in adult Atlantic salmon ranged from 2 to 26 μg/dl. The mean plasma cortisone concentration of salmon in fresh water was not significantly different from that in sea water. The mean cortisone/cortisol ratio in both adult and juvenile Atlantic salmon was between 1.40 and 1.92 indicating that cortisone and not cortisol may be the principal corticosteroid in Atlantic salmon.

Feto-maternal production and transfer of cortisol in the rhesus ( [formula omitted]>)

Four pregnant rhesus monkeys cnd their fetuses. were infused constantly with 14C-cortisol and 3H-cortisol. Steady state plasma specific activities for 14C and 3H-cortisol were obtained after 80 to 90 minutes in both mother and fetus. These data and the rates of infusion of radioactivity were used to calculate the following parameters for both mother and fetus: 1) metabolic clearance rates, 2) production rates, 3) mean adrenal secretory rates, 4) transfer rates from mother to fetus and fetus to mother cnd, 5) the fraction of cortisol in each vascular compartment derived from the maternal and fetal edrenals. Plasma cortisone concentrations, as well as the fraction of cortisone derived from fetal and maternal cortisol were determined. Tetrahydrocortisol and tetrahydrocortisone concentrations were calculated. Mean cortisol secretory rates for the maternal and fetal adrenals were 60.0±11.8 and 1.82±0.42 mg/day. Fifty-eight % of the cortisol in the fetal compartment was of maternal origin. During transfer across the placenta to the fetus, cortisol was largely converted to cortisone. In fetal plasma 76% of the cortisone was of maternal origin. Cortisone concentrations in fetal plasma were higher than those of cortisol.

Plasma cortisone concentration as measured by radioimmunoassay.

A radioimmunoassay for measurement of cortisone in plasma has been developed utilizing rabbit anti-sera against a cortisone-bovine serum albumin complex. To insure specificity thin layer chromatography was used because unchromatographed samples resulted in 10–20% higher values than the chromatographed, even though the cross reactivity with cortisol was only 0.68% and with corticosterone 1.15%. The sensitivity of the assay varies 50–79 pg with recovery of cortisone added to plasma found to be 94.2 ± 5.8 (sd). The mean morning plasma level of cortisone in young men was 2.6 μg/100 ml ± 0.5 (sd) and in women 1.96 ± 0.54. Evening levels decreased in relation to cortisol concentration. Pregnant women had elevation of cortisone levels comparable to that of cortisol. After dexamethasone suppression plasma cortisone levels decreased but following ACTH and usually during acute stress there were no significant changes noted. In patients with severe liver disease cortisone concentration tended to be lower than normal...