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PubMed1997

Additional value of measurement of urinary cortisone and unconjugated cortisol metabolites in assessing the activity of 11 beta-hydroxysteroid dehydrogenase in vivo.

OBJECTIVE: It has been shown recently that 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) is expressed as at least 2 isozymes. In the liver, 11 beta-HSD1 converts cortisone to cortisol; in the kidney, 11 beta-HSD2 converts cortisol to cortisone. Conventional assessment of 11 beta-HSD activity in vivo has relied on gas chromatographic measurement of the ratios of conjugated cortisol and cortisone metabolites. However, these do not permit distinction between the tissue-specific activities of the enzymes and do not reflect all forms of 11 beta-HSD deficiency. In this report, we have assessed the usefulness of measuring unconjugated cortisol metabolites and free cortisol and cortisone in urine as indices of renal 11 beta-HSD activity in man. DESIGN: Six healthy male subjects established in sodium balance were given either glycyrrhetinic acid (170 mg t.d.s., to inhibit 11 beta-HSD2), carbenoxolone (100 mg t.d.s., to inhibit both 11 beta-HSD1 and 11 beta- HSD2) or both inhibitors in combination. MEASUREMENTS: Urinary electrolytes were measured and the concentrations of total and unconjugated urinary cortisol and its metabolites were determined by gas chromatography mass spectrometry. RESULTS: Glycyrrhetinic acid and carbenoxolone inhibited renal 11 beta-HSD2 to a similar degree, as judged by similar sodium retention. As previously reported, conventional measurement of ratios of total cortisol to cortisone metabolites were influenced to a greater extent by glycyrrhetinic acid (100-200% increase in ratio from baseline) than by carbenoxolone (< 30% increase). However, the effect of carbenoxolone was readily detected by measurement of urinary unconjugated cortisol/cortisone (130-480% increase of ratio from baseline) and also by measurement of ratios of unconjugated cortisol metabolites (60-130% increase). CONCLUSIONS: Measurement of free cortisol and cortisone in urine provides the most sensitive index of renal 11 beta-HSD activity. Measurement of total and conjugated urinary steroids is insensitive in circumstances where 11 beta-HSD activity in liver or elsewhere may be abnormal.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2000

[Fear of cortisone: in pulmonary rehabilitation it is less than expected. Results of a patient survey].

BACKGROUND: The treatment of diseases of the upper and lower respiratory tracts can't be imagined without corticoids, applied systemically of locally. In specialist literature one can find indications of a certain reservation towards this kind of medication on the part of many patients. Sometimes, this reservation is so strong that it can be referred to as a regular fear of cortison. Bad compliance and with it, frequently, a deterioration of the symptoms, are inevitable consequences. The aim of the study was to find out how distinct the fear of cortison is with patients in pneumological rehabilitation and wether there are any relations with other spheres of attitude. METHOD: Patients with COPD and asthma with inhalative and/or systemic corticoid medication received an extensive questionnaire during their rehabilitation as in-patients for four weeks. 102 questionnaires were evaluated. RESULTS: The statements of the patients indicated high compliance regarding corticoid medication. As to the fear of such preparation, only 5/102 (4.9%) of those questioned produced results which suggest strong fear of cortison. Fear of cortison is, among other things, slightly related to general psychic-stress and a general negative attitude towards medicine. There is a negative correlation between compliance at the taking of medicine and fear of cortison. CONCLUSIONS: Contrary to statements in specialist literature of wide-spread reservations and fear towards cortison, we have found out that these play only a minor part, at least with the mostly elderly clientele of pneumological rehabilitation. Different explanations are discussed.

Adult↗
PubMed1979

The role of cortisone acetate in liver RNA synthesis of gamma-irradiated rats.

The possible role of induced endogenous glucocorticoid levels stimulated by ionizing radiation and their subsequent effect on rat-liver RNA was investigated in adrenalectomized rats using an intraperitoneal injection of cortisone acetate immediately prior to exposure to gamma-radiation (1800 rad). Adrenalectomized rats were divided into four groups: (1) control rats, (2) irradiated rats, (3) nonirradiated rats treated with cortisone acetate (10 mg/rat), and (4) irradiated rats which received cortisone acetate immediately before irradiation. Newly synthesized RNA was measured by an intraperitoneal injection of 8 muCi (6-14C) orotic acid either immediately after irradiation or 40 min prior to killing. All the rats were killed 6 hours post-irradiation. The results of these investigations indicate that (1) newly synthesized (40 min labelling) RNA increased in irradiated adrenal-intact rats, but not in adrenalectomized animals; (2) cortisone acetate by itself stimulated RNA synthesis whether the radioactive precursor was administered 6 hours of 40 min prior to killing; and (3) irradiation of adrenalectomized rats pre-treated with cortisone acetate induced more RNA synthesis than did cortisone alone. The results of this study support the suggestion that ionizing radiation may induce rat-liver RNA synthesis, at least in part, via stimulated adrenal secretion of glucocorticoids.

Adrenal Glands↗
PubMed1952

Induction of arterial hypertension in normal and adrenalectomized rats given cortisone acetate.

1. Marked hypertension was induced in adrenalectomized rats on a sodium-restricted intake by the administration of cortisone acetate; on a similar regimen, adrenalectomized rats receiving DCA failed to become hypertensive. 2. The incorporation of a liberal amount of sodium in the diet of adrenalectomized rats receiving cortisone acetate resulted in a lesser degree of hypertension; whereas on a similar regimen, DCA-injected animals became strikingly hypertensive, as has been previously reported. 3. The presence of hypertension in the cortisone acetate-treated rats was not associated with histological evidence of renal damage or serum electrolyte disturbance, such as was observed in hypertensive animals receiving DCA. 4. The hypertension in sodium-restricted normal rats receiving cortisone acetate was less striking than in similarly treated adrenalectomized animals. On a liberal sodium intake similar degrees of hypertension were noted in both intact and adrenalectomized groups. 5. To approximate the loss of weight which occurred in cortisone acetate-injected rats, it was necessary to curtail the food intake of partially fasted control groups to 50 to 75 per cent of the amount consumed by the animals receiving the steroid. 6. The serum cholesterol levels of the cortisone acetate-injected rats were consistently and strikingly elevated as contrasted with normal, partially fasted, or DCA-treated animals.

Animals↗
PubMed2003

Cortisol and cortisone in human follicular fluid and serum and the outcome of IVF treatment.

BACKGROUND: The glucocorticoid status of ovarian follicular fluid has been linked to oocyte quality. The aim of this study was to examine whether the concentrations of cortisone and cortisol and their calculated ratios in the follicular fluid and serum samples are predictive of IVF outcome. METHODS: In the prospective study of 387 patients (420 treatment cycles) undergoing IVF treatment the concentrations of cortisone and cortisol were measured with specific assays, and their calculated ratios in the follicular fluid and serum samples obtained after ovarian stimulation and induced ovulation were determined. RESULTS: In 75 patients, treatment resulted in clinical pregnancy and was associated with significantly lower follicular cortisone (24+/-12 versus 29+/-16 nmol/l, P<0.002) and higher cortisol/cortisone ratio (7.24+/-2.22 versus 6.45+/-2.17 nmol/l, P<0.007). In addition, the ratios of serum cortisone and cortisol to follicular cortisone and cortisol were significantly higher in those women who became pregnant. CONCLUSIONS: We propose that the follicular fluid glucocorticoid concentration resulting from the conditions in the circulation and the course of the intrafollicular cortisol-cortisone interconversion appear to play a role in the outcome of IVF.

Adult↗
PubMed1999

Relationship between left ventricular mass index and 24-h urinary free cortisol and cortisone in essential arterial hypertension.

OBJECTIVE: Besides arterial blood pressure, nonhemodynamic factors are known to induce cardiac hypertrophy. In Cushing's syndrome, severe ventricular hypertrophy has been linked not only to increased aortic pressure, but also to elevated plasma cortisol. The aim of this study was to examine the relationship between the cortisol/cortisone levels and left ventricular mass index (LVMI) in essential arterial hypertension with and without echocardiographic left ventricular hypertrophy (LVH). DESIGN: Eighteen untreated Caucasian patients (nine men, nine women, mean age 48+/-6 years) with essential hypertension (163+/-26/100+/-14 mm Hg) were enrolled. An age-matched control group of 13 subjects (seven men, six women) with normotension (121+/-9/79+/-7 mm Hg) were enrolled also. Left ventricular dimensions were echocardiographically assessed and cortisol production evaluated by 24-h urinary free cortisol and cortisone concentrations. RESULTS: LVMI averaged 115+/-31 g/m2 and 24-h urinary free cortisol and cortisone were 23+/-14 microg per 24 h and 31+/-18 microg per 24 h. Prevalence of echocardiographic LVH was 56%. LVMI correlated significantly with 24-h urinary free cortisol (r = 0.61, P = 0.007) and cortisone (r = 0.60, P = 0.009). Patients with echocardiographic LVH were characterized by higher daytime ambulatory blood pressure, LVMI (particularly the posterior wall), and 24-h urinary cortisol, while office blood pressure, septal: posterior wall ratio and 24-h urinary cortisone were comparable in all patients. In control individuals, LVMI averaged 91+/-18 g/m2 and 24-h urinary free cortisol and cortisone, respectively, were 34.7+/-6.6 microg per 24 h and 64.3+/-10.8 microg per 24 h (P<0.05 versus patients). Neither LVMI nor the contributing ventricular dimensions showed significant correlation with 24-h urinary free cortisol or cortisone in the control group. CONCLUSIONS: Our data provide evidence for a significant relationship between LVMI and cortisol production independently of arterial blood pressure in untreated mild to moderate hypertension.

Adult↗
PubMed1984

Plasma cortisol delivery from oral cortisol and cortisone acetate: relative bioavailability.

Plasma cortisol levels were measured before and for 6 h after the intravenous injection of 50 mg cortisol as sodium succinate and oral administration of 50 mg cortisol and 50 mg cortisone acetate in 10 subjects with primary or secondary adrenal failure and in two normal volunteers. Peak cortisol levels of 1518 +/- 190 nmol 1(-1) (mean +/- s.e. mean) and 739 +/- 74 nmol 1(-1) were found 1.46 +/- 0.25 and 1.79 +/- 0.16 h after oral cortisol and cortisone acetate respectively. The relative bioavailability of oral cortisol and cortisone acetate varied widely (cortisol 26-91%, mean 54 +/- 6.9%, cortisone acetate 21-95%, mean 44 +/- 6.5%) but despite this wide variation there was, in individual subjects, a highly significant correlation between the bioavailability of the two steroids (r = 0.870, P less than 0.001). This suggests that the wide interindividual variations in plasma cortisol levels seen after oral cortisone acetate are not related to variations in bioconversion of cortisone.

Administration, Oral↗
PubMed1978

Procoagulant activity of peritoneal leukocytes: effects of cortisone and endotoxin.

Procoagulant activity of peritoneal leukocytes from rabbits given cortisone acetate, endotoxin, and both materials was measured in studies designed to test the hypothesis that cortisone acetate prepares rabbits for the generalized Shwartzman reaction by enhancing leukocyte procoagulant activity. Two types of peritoneal leukocyte suspensions were examined: mixed granulocyte-macrophage suspensions and macrophage suspensions. In both types, procoagulant activity could be accounted for by the number of macrophages in the suspensions. Cortisone alone did not affect the procoagulant activity, whereas endotoxin increased the procoagulant activity. Suspensions from animals given both cortisone and endotoxin varied in activity depending upon cell composition. Granulocyte-macrophage suspensions had less apparent procoagulant activity than suspensions with endotoxin alone. In contrast, macrophage suspensions--particularly sonicated suspensions--had greater procoagulant activity than those with endotoxin alone. The ability of cortisone acetate to increase macrophage procoagulant activity after endotoxin could represent one mechanism whereby cortisone acetate prepares rabbits for the generalized Shwartzman reaction after endotoxin.

Animals↗
PubMed1977

Increase in the severity of allergic-type bronchospasm in sensitized and challenged cats treated with cortisone.

The feline model of immediate hypersensitivity to intraperitoneal ovalbumin sensitization, followed 65 days later by intravenous challenge, was used in this study to determine the effect of cortisone acetate administration on the severity of allergic bronchospasm. Cortisone acetate given intramuscularly prior to, during and immediately after sensitization increased the severity of the allergic response. Comparison of the respiratory, blood pressure and heart rate responses in cortisone-treated animals with nontreated controls indicated a significantly increased challenge reaction among the treated group. Of 7 cats receiving cortisone treatment, 5 died during the 30-min challenge monitoring period. None of the nontreated control group died. It is hypothesized that cortisone treatment impaired the activity of the cortisone-sensitive thymus-derived (T) cells.

Animals↗
PubMed1973

Effects of 1,25-dihydroxycholecalciferol on intestinal calcium transport in cortisone-treated rats.

The administration of glucocorticoids may decrease intestinal calcium absorption in vivo and the active transport of calcium in rat duodenum in vitro. It has been suggested that this apparent "anti-vitamin D-like" effect of steroid hormones may be related to alterations in vitamin D metabolism. In order to test this hypothesis, vitamin D-deficient control and cortisone-treated rats were given an intraperitoneal injection of 5.5 IU of 1,25-dihydroxycholecalciferol (1,25-DHCC), the probable end-organ active vitamin D metabolite in the intestine, and 16 h later studies of duodenal calcium transport were performed in modified Ussing chambers. In the vitamin D-deficient state, cortisone administration was associated with a diminution in J(MS), J(Net), and the flux ratio (J(MS)/J(SM)). While the magnitude of the increases in J(MS) and J(Net) that resulted from 1,25-DHCC treatment were approximately the same in control and cortisone-treated animals, 1,25-DHCC failed to restore these parameters to "normal levels" in the steroid-treated rats. Furthermore, contrary to the results obtained in the saline-treated controls, 1,25-DHCC failed to reduce J(SM) in the duodenum from cortisone-treated rats. The cortisone-related defect in calcium transport was due to alterations in both unidirectional calcium fluxes (decrease in J(MS) and increase in J(SM)), such that the J(Net) and the flux ratio (J(MS)/J(SM)) were only approximately 50% of the levels achieved in vitamin D-deficient control animals repleted with the same dose of 1,25-DHCC. The administration of 1,25-DHCC was accompanied by a marked increase in the serum calcium levels of control rats, but there was no such response in the cortisone-treated group. The results support the concept that under the conditions of these experiments in the rat the apparent antagonism between glucocorticoids and vitamin D may be due to steroid hormone-related alterations in end organ function that are independent of any direct interaction between the hormone and the vitamin and that cannot be reversed by the vitamin.

Animals↗
PubMed1997

Urinary free cortisol and cortisone determined by high performance liquid chromatography in the diagnosis of Cushing's syndrome.

To determine the efficacy of cortisol and its metabolite, cortisone, measured simultaneously by high performance liquid chromatography (HPLC) in the diagnosis of Cushing's syndrome, we retrospectively reviewed the histories of 29 surgically proven Cushing's syndrome patients (20 Cushing's disease, 5 ectopic ACTH syndrome, and 4 adrenal Cushing's syndrome) and 6 patients with exogenous Cushing's syndrome. These 35 patients had urinary free cortisol determined by both HPLC and competitive binding methods. The efficacy of the HPLC assay using cortisol alone was equivalent to that of the competitive binding assay; 22 of 29 (76%) patients had increased cortisol. Cortisone also aided in the diagnosis; 25 of 29 (86%) had increased cortisone. Twenty-seven of the 29 (93%) patients had either both cortisone and cortisol (n = 19) or at least 1 of the 2 (n = 8) increased. All 6 patients with exogenous Cushing's syndrome had suppressed urinary free cortisol, cortisone, and the presence of prednisone and prednisolone. In the competitive binding assay, all exogenous Cushing's patients had falsely increased cortisol results. In conclusion, urinary free cortisol plus cortisone determined simultaneously by HPLC added a new dimension to the diagnosis of Cushing's syndrome. It should be considered when exogenous Cushing's syndrome is suspected or when only one urinary cortisol test is allowed to be ordered.

ACTH Syndrome, Ectopic↗
PubMed1991

Modulation of immunoreactive epidermal growth factor levels in the submandibular gland, pancreas, liver, kidney and gastrointestinal tract of suckling rats by cortisone and tri-iodothyronine.

Suckling rats exhibit age-dependent differences in epidermal growth factor (EGF) levels in several organs. The present studies evaluated the effects of two hormones known for their maturative effect on suckling rats, cortisone and tri-iodothyronine (T3), on immunoreactive EGF levels in specific organs. Suckling rats were administered cortisone (5 mg/100 g body weight per day) or T3 (50 micrograms/100 g body weight per day) on days 8, 9, 10 and 11 after birth, and killed on day 12. Submandibular glands, kidneys, pancreas, liver and gastrointestinal tract mucosa and lumen were assayed for immunoreactive EGF by a species-specific radioimmunoassay. Low levels of EGF in the submandibular glands were increased slightly by both T3 and cortisone treatment. Cortisone evoked a tenfold increase in EGF in the pancreas, but had no effect on levels in the kidney or liver. In contrast, T3 evoked a sixfold increase in the EGF level in the kidney, but had no effect on levels in the pancreas or liver. Hormonal administration had no effect on EGF levels in the stomach. Within the intestinal tract, cortisone had no effect on the luminal EGF content of the duodenum, jejunum or ileum, but caused a decrease in the midjejunum. T3 evoked a decrease in the luminal EGF content of the ileum. The effect of cortisone on mucosal EGF content varied between regions; an increase was seen in the duodenum with a decrease in the midjejunum and ileum. T3 administration resulted in a significant decrease in EGF only in the mucosa of the ileum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Validation of a high-throughput liquid chromatography-tandem mass spectrometry method for urinary cortisol and cortisone.

BACKGROUND: Urinary free cortisol and cortisone measurements are useful in evaluation of Cushing syndrome, apparent mineralocorticoid excess, congenital adrenal hyperplasia, and adrenal insufficiency. To reduce analytical interference, improve accuracy, and shorten the analysis time, we developed a liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for urinary cortisol and cortisone. METHODS: We added 190 pmol (70 ng) of stable isotope cortisol-9,11,12,12-d(4) to 0.5 mL of urine as an internal standard before extraction. The urine was extracted with 4.5 mL of methylene chloride, washed, and dried, and 10 microL of the reconstituted extract was injected onto a reversed-phase C(18) column and analyzed using a tandem mass spectrometer operating in the positive mode. RESULTS: Multiple calibration curves for urinary cortisol and cortisone exhibited consistent linearity and reproducibility in the range 7-828 nmol/L (0.25-30 microg/dL). Interassay CVs were 7.3-16% for mean concentrations of 6-726 nmol/L (0.2-26.3 microg/dL) for cortisol and cortisone. The detection limit was 6 nmol/L (0.2 microg/dL). Recovery of cortisol and cortisone added to urine was 97-123%. The regression equation for the LC-MS/MS (y) and HPLC (x) method for cortisol was: y = 1.11x + 0.03 microg cortisol/24 h (r(2) = 0.992; n = 99). The regression equation for the LC-MS/MS (y) and immunoassay (x) methods for cortisol was: y = 0.66x - 12.1 microg cortisol/24 h (r(2) = 0.67; n = 99). CONCLUSION: The sensitivity and specificity of the LC-MS/MS method for urinary free cortisol and cortisone offer advantages over routine immunoassays or chromatographic methods because of elimination of drug interferences, high throughput, and short chromatographic run time.

Chromatography, Liquid↗
PubMed1987

Inhibitory effects of heparin plus cortisone acetate on endothelial cell growth both in cultures and in tumor masses.

A combination of heparin and cortisone acetate significantly inhibited both embryonic angiogenesis and the tumor growth of Lewis lung carcinoma (3LL) transplanted into C57BL/6 mice, although each of these agents used alone affected neither angiogenesis nor tumor growth. On the other hand, this combination neither decreased the number of metastatic foci in the lung nor prolonged the survival time of mice with 3LL. All tumor-bearing mice died of hemothorax due to pulmonary metastases. Cortisone acetate by itself increased metastasis, and addition of heparin did not affect accelerated metastasis. Because an antiangiogenic activity appears independent of metastasis acceleration by cortisone acetate, the use of steroids other than cortisone acetate having no metastasis-promotion effect should be required for an antiangiogenic tumor therapy in the presence of heparin. Heparin plus cortisone acetate prevented the DNA synthesis of cultured vascular endothelial cells but not that of cultured 3LL cells. Additionally, oral administration of this combination decreased the [3H]thymidine labeling of endothelial cells of tumor blood vessels prior to the suppression of tumor growth. The specific inhibition of the growth of endothelial cells by heparin plus cortisone acetate was revealed in both the in vitro and the in vivo tests.

Animals↗
PubMed1989

Decreased yield of Pneumocystis carinii from cortisonized rats.

Thirty-five male Sprague-Dawley rats were divided into 3 groups, including 1 control and 2 experimental groups, in order to compare the efficacy of using cortisone acetate alone or in addition to intranasal inoculation of Pneumocystis carinii organisms for the purpose of inducing acute P. carinii pneumonia. The presence of P. carinii was monitored in nasal secretions on a weekly basis and in lungs at autopsy. Titers of IgG antibody were also monitored by enzyme-linked immunosorbent assay. No rat receiving cortisone acetate injections alone and only 2 of the rats receiving both cortisone and intranasal inoculation of P. carinii organisms showed Pneumocystis organisms in the lungs. However, Pneumocystis cysts did appear in the nasal secretions of 3 of the 5 control rats, all 8 rats receiving cortisone acetate injections only, and 12 of 18 rats receiving both cortisone acetate injections and an intranasal inoculum. IgG titers of both cortisonized groups remained less than 1:4 throughout the course of the experiment. The titer of the control group increased from negative to 13 (geometric mean).

Animals↗
PubMed1982

Influence of cortisone on amoeboid microglia and microglial cells in the corpus callosum in postnatal rats.

Amoeboid microglia and typical microglial cells in the corpus callosum of rats were studied following a subcutaneous injection of cortisone at birth. The rats were killed 2, 5, 10 and 20 days after the injection. The most striking change in the corpus callosum was the great reduction in the number of amoeboid microglial cells as shown by the silver carbonate stain of Rio-Hortega. The change was sustained throughout the period studied. Ramified and typical microglial cells which do not normally appear until between the fifth and tenth postnatal day, were observed on the second postnatal day after the cortisone administration. Cell enumeration in semithin sections showed that the proportion of amoboid microglial cells was reduced to 50% of their normal value soon (2 days) after the cortisone injection. This proportion was further decreased and the cells were absent from the fifth postnatal day onwards. Typical microglial cells were developed prematurely and they constituted more than 2% of the total glial population 2 days after the cortisone injection. Another striking change noted in the semithin section was the increase in the compactness of the axons in the corpus callosum in the experimental animals. Electron microscopic observations were in general agreement with the light microscopy. The amoeboid microglial cells appeared less active; they contained small Golgi apparatus, accumulations of lipid droplets and sparse lysosomes. The cell outline was regular. The reduction in the number of amoeboid microglia after the cortisone injection was explained by the fact that the drug suppressed the production of their precursor cells, i.e. circulating monocytes, Moreover, it was suggested that cortisone probably interfered with the phagocytic activity of the amoeboid microglial cells which would normally undergo structural changes to become the quiescent microglia which were observed in the early postnatal animals.

Animals↗
PubMed1982

The effects of cortisone on fecundity, number, and distribution of adult Trichinella spiralis and on trichinous enteritis in the host.

The effects of cortisone on fecundity, distribution, and numbers of adult Trichinella spiralis and on enteritis in the host were compared in mice receiving different numbers of larvae. As the amount of cortisone given to mice was increased enteritis decreased, and fecundity of adult worms increased. Injection of mice with cortisone caused retention of a greater percentage of adult worms in the anterior regions of the host small bowel than in uninjected mice. By day 11 PI, when adult worms in cortisone-injected mice were more widely distributed along the host small intestine, fecundity of adult worms isolated from mice receiving more worms (500, 1,000, or 2,000 worms) attained levels previously seen only in worms from mice infected with 250 T. spiralis. The extended longevity of adult worms in cortisone-injected mice was accompanied by a severe reduction in fecundity after day 11 PI. Addition of cortisone to the culture medium at concentrations above 0.1 mg% was accompanied by a reduction in fecundity of adult worms.

Animals↗
PubMed1981

The effects of cortisone therapy on lung macrophage host defense function and glucose metabolism.

The administration of high-dose glucocorticoid therapy in the treatment of lung inflammatory and immune diseases often results in an increased susceptibility to pulmonary infections. The effects of cortisone therapy on the phagocytic function and glucose metabolism of alveolar macrophages (AM) were evaluated in guinea pigs treated for 7 days with 100 mg/kg of cortisone acetate. AM were harvested 24 hours following the final daily drug treatment by lung lavage techniques. Cortisone treatment produced a profound leukocytosis, lymphocytopenia, and monocytopenia in the peripheral blood while decreasing by greater than 40% the number of AM obtainable by lung washings. Macrophage phagocytosis, as assessed by the in vitro uptake of radiolabeled heat-killed Pseudomonas aeruginosa by monolayers of lung macrophages, was depressed in AM harvested from cortisone-treated animals. In addition, cortisone therapy also inhibited the stimulation in glucose oxidation normally associated with macrophage phagocytosis as well as depressing the membrane transport of 2-deoxyglucose. These results demonstrate that high-dose cortisone therapy can impair both functional and metabolic activities of the phagocytic defense mechanism of the lower respiratory tract.

Animals↗