SEARCH · PubMed Health

Results for “CORTISONE/effects”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

PubMed1957

The influence of cortisone on experimental viral infection. IV. Negation of interference as the mechanism by which cortisone induces increased virus yields.

The interference with viral synthesis which is induced by large quantities of non-infective influenza B virus is inhibited or negated with small quantities of cortisone and other C-21 steroids. The specificity of this effect is attested by the inactivity of 11-alpha hydroxy epimers of highly active compounds. Maximal activity in negation of interference is associated with the presence of oxygen at the C-11 position of the steroid molecule. In view of the demonstration that negation of interference can occur, it is concluded that the phenomenon of multiplicity reactivation of non-infective virus is not primarily influenced by cortisone. Rather, it is suggested that the reactivation phenomenon is unmasked by cortisone through its inhibiting effect on the autointerference intrinsic in multiplicity infection. If it is accepted that influenza virus infections in ovo are self-limited in part by viral autointerference, present evidence is consistent with the view that negation of this autointerference is the mechanism by which cortisone induces definitively increased yields of virus.

Cortisone↗

PubMed1957

The influence of cortisone on experimental viral infection. V. Inhibition of influenza virus synthesis.

Cortisone is a highly potent inhibitor of influenza virus synthesis in the chick embryo, inducing manifest inhibition in doses of 0.1 to 1.0 microg/egg. Inhibition of viral synthesis is only temporarily manifest. As infection continues, the negation by cortisone of the self-limiting effects of viral autointerference obscures the coincident cortisone effect on synthesis. The inhibitory effect of cortisone may be induced late in the course of viral multiplication, after conclusion of the latent period. It is proposed that inhibition of viral synthesis with cortisone is a corollary of the steroid's inhibitory effects on growth and protein synthesis of the infected host. The role of adrenal corticoids in the regulation of infection with obligate intracellular parasites deserves continued investigation.

Animals↗

PubMed1951

The influence of cortisone on primate malaria.

Studies have been made of the effects of cortisone on the course of primary and developed infections with P. cynomolgi in the rhesus monkey. This investigation has shown that repetitive admmistration of the hormone in daily doses of 10 mg. per kg. during the primary attack produced striking intensification of the peripheral blood infection during the postcrisis phases of the disease. Similar administration of 10 or 50 mg. per kg. doses of the hormone during the chronic or latent stages of the infection provoked recrudescences of remarkable severity. In both early and late infections the responses induced by cortisone treatment corresponded closely to the reactions to splenectomy. Collateral studies have shown that the doses of cortisone which produced the reactions described above also evoked a lymphopenia, marked reductions in the sizes of the axillary and inguinal lymph nodes and spleen, and striking histological changes in the latter organ. These changes involved severe regression or exhaustion of lymphoid elements in both splenic nodules and pulp with almost complete obliteration of proliferative activities involved in the production of macrophages from lymphocytes. Indications are that the resulting reduction in supply of macrophages, rather than inhibition of phagocytic activity per se, was responsible for the intensification of the disease produced by cortisone.

Animals↗

PubMed1952

Alteration of experimental poliomyelitis infection in the Syrian hamster with the aid of cortisone.

Cortisone produces a significant enhancement of infection with MEF1 and Lansing strains of poliomyelitis virus in the Syrian hamster. The enhancement manifests itself in increased severity of symptoms, shortening of the incubation period, marked reduction in survival time and a high mortality rate. The effect of cortisone is protracted, the duration depending on the dose used. There is a reciprocal relationship between the dose of cortisone and the amount of virus, the larger the dose of the hormone, the smaller the amount of virus being necessary to produce the infection. An amount of virus of low infectivity causes amarked disease with a high mortality rate in hamsters receiving a single injection of 3 mg. of cortisone, while a dose as small as 2 mg. gives a highly fatal disease with a stronger concentration of the virus. There is a 2 log increase in the concentration of the virus in cortisone-treated hamsters. Hamsters from various sources seem to respond differently to the enhancing effect of cortisone, one breed showing no enhancement of the infection with the Lansing strain. Hormones other than cortisone, i.e., DCA, progesterone, diethylstilbestrol, and fast and slow acting ACTH injected repeatedly fail to modify the poliomyelitis infection in the hamster.

Animals↗

PubMed1952

The emergence of pseudotuberculosis in rats given cortisone.

The emergence of a severe infection in albino rats during cortisone administration is reported. Evidence is present that the causative agent of the disease was Corynebacterium pseudotuberculosis murium, a microbial species not demonstrably a part of the usual bacterial flora of the host. It has been possible to reproduce the disease in rats by a relatively large infecting inoculum of this strain of Corynebacterium, but the susceptibility of normal rats to infection has been found to be low. The disease occurred in 41 of 50 rats given cortisone and in 28 of 30 instances in which isolation of the etiologic agent was attempted, this strain of Corynebacterium was recovered. The disease was characterized by widespread necrotizing lesions, with multiple coalescent lesions occurring in the lungs, and similar, though smaller lesions of the pericardium, pleurae, liver, and kidneys. In its gross appearance the pulmonary disease was similar to that of a disseminated, far advanced tuberculous process. The histologic appearance of the lesions, however, was sufficiently distinctive so that they could be readily differentiated from the lesions characteristically produced by Mycobacterium tuberculosis. Moreover, the host-parasite relationship established by the experimental infection with avian tubercle bacilli, was not markedly altered by the factors which led to the emergence of the pseudotuberculosis. In contrast to the high frequency of pseudotuberculosis in rats given cortisone, no instance of this disease has been encountered in a similar group of animals given large quantities of corticotropin.

Animals↗

PubMed1952

The effect of cortisone on the Shwartzman reaction; the production of lesions resembling the dermal and generalized Shwartzman reactions by a single injection of bacterial toxin in cortisone-treated rabbits.

1. Cortisone, in a dose of 25 mg. daily and with a pretreatment period of 3 days, in rabbits weighing 1 to 1.5 kilos, did not inhibit the dermal Shwartzman reaction produced by meningococcal or S. marcescens toxin. 2. In cortisone-treated rabbits, a single intradermal injection of toxin produced a primary reaction of hemorrhage and necrosis in the skin at the injected site. This lesion resembled the Shwartzman reaction in its gross and histological appearance. 3. Like the Shwartzman reaction, the primary hemorrhagic reaction in cortisone-treated rabbits was prevented by nitrogen mustard, and the preventive effect of nitrogen mustard was partly eliminated when the femoral marrow was protected against the latter agent. 4. A single intravenous injection of meningococcal or S. marcescens toxin, in cortisone-treated rabbits, was followed by bilateral cortical necrosis of the kidneys in the majority of instances. The renal lesions, as well as hemorrhages in the lungs, spleen, liver, and gastrointestinal tract, resembled the lesions of the generalized Shwartzman reaction. Histologically, the glomerular capillaries in both types appeared to be occluded by homogeneous, eosinophilic material which showed a strongly positive Schiff reaction. 5. The renal lesion following a single injection of toxin in cortisone-treated animals, and that following two intravenous injections in the generalized Shwartzman reaction, were both completely prevented by nitrogen mustard. This effect of nitrogen mustard was inhibited when the femoral marrow was protected against the latter agent. 6. The injection of S. marcescens toxin into the skin of normal rabbits did not cause systemic symptoms, nor was it possible to provoke the generalized Shwartzman reaction by this route. In cortisone-treated rabbits, a similar intradermal injection was regularly followed by the development of bilateral cortical necrosis of the kidneys, indicating that absorption of toxin from the skin occurred in these animals. 7. Possible mechanisms to account for the observations are discussed. The authors are obliged to Professor James R. Dawson for many helpful suggestions during the course of this investigation.

Animals↗

PubMed1952

The effects of cholesterol dosage, cortisone, and DCA on total serum cholesterol, lipoproteins, and atherosclerosis in the rabbit.

The effects of cholesterol dosage, cortisone, and desoxycorticosterone acetate on total serum cholesterol, lipoproteins, and atherosclerosis were studied over a period of 112 days in thirty-two rabbits. Cholesterol was administered by feeding the rabbits diets containing 0.063, 0.25, and 1.0 per cent cholesterol At intervals measurements were made of total serum cholesterol and of low density lipid and lipoprotein components of three classes, S(f), 5-9, S(f) 10-15, and S(f) 16-30. All three classes of lipoproteins increased with cholesterol feeding. The total serum cholesterol concentration was linearly related to both the quantity of cholesterol consumed and its concentration in the diet. Lipoprotein and total serum cholesterol concentrations were significantly and equally well correlated with the severity of atherosclerosis. Cortisone administration in the normal rabbit increased the concentrations of total cholesterol and of lipoprotein components of the S(f) 10-15 and S(f) 16-30 classes, but did not produce atherosclerosis. Cortisone treatment in cholesterol-fed rabbits did not significantly affect the levels of serum lipoproteins, cholesterol concentration, or atherosclerosis produced by a 1.0 per cent cholesterol diet alone. Values for total cholesterol and S(f) 5-9 class of lipoproteins in DCA-treated animals were lower than those in controls but the degree of atherosclerosis was not significantly less.

Animals↗

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↗

PubMed1952

The inhibition by cortisone of the cytotoxic activity of PPD on tuberculin-hypersensitive cells in tissue culture.

Using the roller tube method of tissue culture, it has been shown that cortisone and compound F inhibit the cytotoxic action of PPD upon macrophages from the splenic tissue of tuberculous guinea pigs. Pretreatment of the cells for 24 hours with hormones before exposure to PPD was found to be essential. Estrone and desoxycorticosterone glucoside had no protective activity. Certain advantages of the tissue culture method in studies of tuberculin hypersensitivity and possible mechanisms and implications of this protective action of cortisone are discussed.

Animals↗

PubMed1953

The mechanism of action of cortisone in experimental hypersensitivity. II. Hypersensitivity of the serum sickness type.

Cortisone markedly suppressed the cardiovascular and renal lesions of serum sickness type hypersensitivity which ordinarily develop following the intravenous injection of bovine albumin. The inhibitory effect of cortisone on the allergic granulomatous lesions of the spleen was less striking; the lesions were less extensive, but the percentage of animals affected was unchanged. Cortisone in the dosage employed had no effect on the elimination of antigen following its intravenous administration or on the appearance of circulating antibody. These findings indicate that inhibition of the lesions of serum sickness by cortisone does not depend on the suppression of antibody production. Therefore, it is inferred that cortisone somehow protects the animal from the damaging effects of antigen-antibody union.

Animals↗

PubMed1953

The effect of tuberculin and cortisone singly and in combination on explanted tissues of guinea pigs, mice and rabbits.

Tuberculin (P.P.D.) and cortisone acetate, singly and in combination, were added to explanted splenic tissue derived from guinea pigs, mice, and rabbits, and buffy coats obtained from rabbits. These tissues came from normal animals or from animals which had been infected with the tubercle bacillus or immunized with killed tubercle bacilli. 5 microg./ml. of tuberculin or 0.5 microg./ml. of cortisone was the largest concentration of the respective reagents which was tolerated by cultured cells from normal animals. From the results with all tissues studied it would appear that P.P.D. selectively damaged only the growing cells of splenic tissues from sensitive guinea pigs and to a lesser degree the migrating cells of buffy coats obtained from sensitive rabbits. Cortisone appeared to have increased toxicity for only explanted splenic cells from tuberculin-sensitive guinea pigs. The specific effect of P.P.D. on tissues from tuberculin-sensitive animals was not modified by cortisone under the conditions of these experiments. Thus these data furnished no evidence that cortisone had any direct effect on the response of the sensitive cells to P.P.D.

Allergens↗

PubMed1954

The effect of adrenal steroids, corticotropin, and growth hormone on resistance to experimental infections.

Cortisone acetate, hydrocortisone, and hydrocortisone acetate depress the resistance of mice to pneumococcal and influenza viral infections, although hydrocortisone acetate is somewhat less effective than the free alcohol, when given subcutaneously. Pituitary adrenocorticotropin, even in highly purified form and in oil and beeswax, does not significantly alter the resistance of mice to these experimental infections, even when given in doses which may cause profound eosinopenia, lymphopenia, and weight loss, and which are at the limit of tolerance of the animals. Corticosterone depresses resistance to pneumococcal infections significantly, but fails to alter resistance to influenza viral infections. The findings suggest that murine adrenals may produce one of the known adrenal steroids such as corticosterone along with another steroid, or may produce a steroid other than cortisone, hydrocortisone, or corticosterone. When resistance is decreased by adrenal steroids, survival time is invariably shortened, and the effect of the steroid hormones is frequently demonstrable within the 1st day after infection with pneumococci, making it unlikely that the depression of resistance that is seen is primarily due to depression of antibody formation. A single dose of 5 mg. of cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward. Growth hormone (somatotropic hormone) in highly purified form, and in the doses used, did not overcome the weight loss induced by cortisone, but the animals treated with growth hormone and cortisone regained their lost weight more rapidly than those receiving cortisone alone. Growth hormone alone caused a slight increase in the rate of gain in weight over controls. Growth hormone alone did not increase resistance to infection, and did not increase the survival time, in mice infected with either pneumococci or influenza virus. Growth hormone in various dosages failed to overcome the effect of cortisone in depressing resistance to these infections. Cortisone, hydrocortisone, corticosterone, and corticotropin did not alter significantly the titers of influenza virus attained in the murine lungs during the first 2 days after infection, but cortisone and hydrocortisone markedly delayed the rate at which virus titers declined during the subsequent 6 days. Corticosterone and corticotropin delayed the rate at which the titers declined but slightly, and growth hormone had no apparent effect, as compared with controls. Growth hormone did not overcome the effect of cortisone and hydrocortisone on viral titers. No detectable antibody was found as late as 6 days after infection, in controls or in hormone-treated animals.

Adrenal Cortex↗

PubMed1954

The effect of cortisone on the serum lipids and on the development of experimental cholesterol atherosclerosis in the rabbit.

An experiment was performed to determine the effect of cortisone on the serum lipids and on the development of experimental cholesterol atherosclerosis in the rabbit. Litter mate rabbits of the same sex were employed; both sexes were represented in the experiment. The report is based upon four experimental groups comprising (1) 12 rabbits fed cholesterol and treated with cortisone vehicle; (2) 12 rabbits fed cholesterol and treated daily with cortisone; (3) 11 rabbits treated with cortisone; and (4) 7 rabbits that received cortisone vehicle. It was observed that: (1) There was less aortic atherosclerosis in the cholesterol-fed cortisone-treated rabbits as judged by both morphological and chemical means than in the rabbits fed cholesterol without cortisone treatment. (2) Cortisone depressed appreciably the hypercholesterolemia resulting from the feeding of cholesterol to rabbits. (3) Cortisone treatment caused a moderate hypercholesterolemia in normal rabbits. (4) Cortisone caused a moderate increase in serum lipid phosphorus equal to that produced by cholesterol feeding alone. (5) The combination of cholesterol feeding and cortisone did not result in a higher phospholipidemia than either one of these agents alone. (6) Cortisone caused a great increase in serum-neutral fat; it was not apparent whether cholesterol feeding affected the neutral fat lipemia due to cortisone treatment alone. (7) The total cholesterol to lipid phosphorus ratio was about normal in the rabbits that received cortisone only. It was doubled in the animals receiving both cholesterol and cortisone, and it was increased about four times in those that received only cholesterol. The significance of the alterations in the serum lipids induced by cortisone is discussed in relation to the inhibition of the development of aortic atherosclerosis that occurred in the cholesterol-fed rabbits treated with cortisone.

Animals↗

PubMed1954

Effects of cortisone on regenerating rat liver.

The effects of continuous administration of cortisone on the metabolism of regenerating rat liver have been studied. Whereas the restoration of the weight of the liver after partial hepatectomy was not markedly affected by cortisone, the multiplication of cells was reduced to a significant degree after the first 2 days of regeneration. Liver restoration in terms of nucleic acids was similarly inhibited by cortisone. The results are consistent with the interpretation that the inhibition of cell multiplication in this system is dependent on and keeps pace with the inhibition of nucleic acid synthesis by this drug. At almost any time after hepatectomy, the nucleic acid content of the liver cells was the same in treated and in untreated animals. In ancillary studies, it was shown that cortisone caused the cells of regenerating liver to be increased in size and weight through the increased infiltration of lipids. Changes in water, protein, and carbohydrate content of the liver cells did not contribute to this increase in the weight of the cells. Since all animals were treated with cortisone for 5 days before hepatectomy, data were also obtained on the effect of this agent on the resting liver. This course of treatment brought about a significant decrease in the number of cells per unit wet weight and in the water content of the livers. The nucleic acid content of the cells at hepatectomy, on the other hand, was unchanged.

Animals↗

PubMed1951