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PubMed1955

Effects of cortisone on rat liver mitochondria.

Experiments were designed to determine the effects of parenteral administration of cortisone on mitochondrial numbers of rat liver cells. Observations were made in three ways: (1) after osmic acid fixation and appropriate stain, (2) by phase microscopy on intact cells, (3) by actual enumeration of mitochondria and nuclei to provide data on mitochondria per cell. The results of the experiments indicate that the mitochondria per cell are significantly reduced under the conditions used. Each experimental approach provided similar data, and each tended to support the results obtained from the others.

Animals↗
PubMed1956

Alterations in biochemical composition and ribonucleic acid metabolism induced in rat liver by cortisone.

An investigation of the effect of cortisone administration upon the chemical composition of intracellular particulates of rat liver has been made. Livers were homogenized in 0.25 M sucrose solutions and submitted to differential centrifugation. Five fractions were prepared: mitochondria (Mit), microsomes (Mi), ultracentrifugable (U), non-sedimentable (S), and nuclear (Nuc). Measurement was made of total and polymerized RNA, nitrogen, lipide P, and uptake of P(32) by the RNA of each fraction. The following observations were made:- Cortisone administration caused a fall in concentration in all measured constituents except glycogen. On a per liver basis, however, total liver RNA was unchanged in amount; nitrogen content of Mi fell and that of S increased; the lipide P of Mit and Mi also decreased. The biochemical composition of a statistical mitochondrion was significantly altered; in contrast, the microsomal fraction decreased in amount, but the relationship between the chemical constituents was unchanged. When polymerized RNA was sought by a process involving precipitation from ethanol at 20 degrees C., none was found in the Mit of cortisone livers and the amount in Mi was much less than found in the normal. When, however, precipitation was conducted at 4 degrees C., yields of polymerized RNA in all fractions after cortisone were equal to or greater than those found in the normal. Furthermore, incubation of mixtures of homogenates from normal and cortisone livers resulted in loss of warm precipitable RNA. These data strongly suggest the presence of an enzyme in cortisone livers which upon incubation with normal livers made preparation of polymerized RNA virtually impossible by use of the warm method. This agent, thought to operate in vivo and in vitro, was not present in significant amounts in normal livers, since incubation in this instance had no effect upon the amount of polymerized RNA. Mit from cortisone livers obtained by the cold technique had a significantly decreased rate of incorporation of P(32) even though the yield of RNA from this fraction was increased. To reconcile these observations, it was proposed that under the influence of cortisone a variant of normal RNA is synthesized or normal RNA is converted to this variant. This "new" RNA has new solubility properties, a new rate of incorporation of P(32), and conceivably it cannot act as a template for normal protein synthesis.

Animals↗
PubMed1956

The effect of cortisone on DNA content of rat hepatocytes.

Rats were treated with cortisone, x-radiation, and both agents in combination, and the effect noted on the DNA content of hepatocytes. Nuclei were enumerated both in whole liver homogenates and following isolation. The incorporation of P(32) into DNA was also studied in relation to these agents. The following observations were made:- 1.The DNA content of nuclei fell both during cortisone administration and following x-radiation. In the former instance, the fall was progressive with continuing administration of hormone; in the latter instance, there was a return to normal 5 days after radiation. 2. Cortisone administration to x-radiated rats caused a fall in DNA/nucleus and prevented the return to normal at 5 days. 3. There was no evidence that the effects of cortisone and x-rays were additive in reducing DNA/nucleus. 4. These data indicate an alteration in DNA/nucleus, but simple changes in ploidy cannot be excluded. Either explanation requires that the agents used affect the DNA of non-regenerating nuclei. 5. Cortisone interfered with the incorporation of P(32) into the DNA of regenerating liver. Only a small effect on DNA synthesis in resting liver was observed with cortisone or x-radiation. 6. DNA content of nuclei returned to normal 5 days after x-radiation and 3 days after discontinuance of cortisone. Slight increase in the incorporation of P(32) by DNA was observed during recovery phases. 7. The hypothesis is proposed that the apparent losses and increases in DNA/nucleus were due to depolymerization and repolymerization of DNA. Following x-radiation and/or cortisone administration, it is proposed that some DNA is depolymerized and becomes cold acid-soluble and dissociated from organized chromatin. Later, conditions are such that this degraded DNA is repolymerized. 8. These data might be interpreted to indicate that a portion of the DNA is not essential to cell integrity; alternatively, there may be two or more species of DNA, one of which is more readily affected by the agents investigated in the present report.

Animals↗
PubMed1959

Cytophotometric study of deoxyribonucleic acid in cortisone-treated rat hepatocytes.

Rats were treated by intramuscular injection with cortisone acetate, 25 mg./day for 5 days. Small pieces of liver obtained from treated and normal animals were squashed on a microscope slide so as to obtain many areas only a single cell in thickness. After Feulgen staining to demonstrate DNA, optical density was measured using a projection technique. In both the normal and treated animals the nuclei were easily segregated in three ploidy classes, diploid, tetraploid, and octaploid, depending upon Feulgen intensity. In all three classes, the absorbence of nuclei from cortisone-treated animals was approximately 20 per cent lower than the normal. These data were interpreted to indicate that a change in DNA content had been induced by cortisone administration. These findings are comparable to data obtained from similar animals using chemical methods for the determination of DNA.

Animals↗
PubMed1955

The effects of drugs upon a graded cough response obtained in sensitized guinea pigs exposed to aerosol of specific antigen.

A technique is described for measuring objectively and quantitatively the reaction of sensitized guinea pigs when exposed to an aerosol of specific antigen. The principle involves registration by semi-automatic means of the number of coughs produced in animals passively sensitized with known amounts of antibody. The number of coughs is shown to be linearly related to log dose of antibody within a limited range and a dose-response curve is presented. The cough produced by this procedure is not inhibited by the antitussive drugs, codeine and propadrine, but can be inhibited by anti-allergic agents, such as cortisone and an antihistaminic drug. It is also inhibited by narcotine. The last is the only compound so far tested which suppresses both the cough produced by this procedure and that produced by a simple irritant. The action of cortisone and the antihistaminic drug, pyrilamine, is shown to be synergistic. A small dose of pyrilamine in animals pretreated with cortisone gives a degree of inhibition which cannot be obtained by increasing the dose of pyrilamine in animals not treated with cortisone.

Aerosols↗
PubMed1955

Studies on the antipyretic action of cortisone in pyrogen-induced fever.

The mode of action of cortisone as an antipyretic has been studied in rabbits challenged with intravenous injections of bacterial pyrogens. The fever induced by pyromen or dextran was found to be markedly suppressed when cortisone was administered in liberal amounts (25 mg. twice daily) for 3 days prior to the challenge. Although the cortisone effectively blocked the febrile response to both pyrogens, it failed to influence the transient but marked leucopenia which characteristically precedes the onset of fever. The antipyretic action of the drug also was shown to bear no relation to the activity of the serum factor recently demonstrated by Farr, Grant, and others to be involved in the production of pyrogen-induced fever. In preliminary experiments with typhoid vaccine as the inciting pyrogen, the presence of serum factor activity in normal blood and its absence in the blood of pyrogen-tolerant rabbits was confirmed. Subsequently the blood of rabbits treated with antipyretically effective doses of cortisone was shown to contain just as much serum factor activity as that of normal rabbits. In addition, previous incubation of the pyrogen with serum factor failed to influence the antipyretic effect of the drug. It is concluded from these findings that in suppressing pyrogen fever, cortisone acts neither upon the leucopenic reaction nor upon the fever-accelerating factor of the serum. By exclusion it would appear that the drug must influence some later stage of the fever-producing process. The mechanisms involved in the later stages of the response to exogenous pyrogen remain undefined, and the need for determining whether they are related to the prefebrile leucopenia is emphasized.

Animals↗
PubMed1955

Reactivation of non-infective virus in a cortisone-injected host.

The administration of cortisone to chick embryos inoculated with large quantities of inactive influenza B virus results in a rate of viral increase greater than is concommittantly observed with inocula of comparable infectivity which are devoid of inactive particles. Thus, more than a mere negation of autointerference is effected. It is concluded that in the presence of cortisone reactivation has occurred of non-infective virus to a state in which it can participate in viral synthesis. Cortisone-induced viral reactivation is dependent upon a high partide/cell ratio and is thus analogous to the previously described phenomenon of "multiplicity reactivation." Cortisone does not influence either homologous or heterologous viral interference unless reactivation of the inactive interfering virus occurs. Virus reactivable with cortisone possesses both interfering and enzymatic properties. Reactivation of virus with cortisone cannot be effected in vitro but is mediated by the host cell. Two hypotheses concerning the action of cortisone are presented.

Animals↗
PubMed1955

Studies on the pathogenesis of acute inflammation. II. The action of cortisone on the inflammatory response to thermal injury.

The anti-inflammatory action of cortisone upon the acute cellular response to thermal injury has been systematically studied in the rabbit ear chamber. The hormone has been shown to suppress the reaction of acute inflammation in its earliest recognizable phase; i.e., that involving vasodilatation and the adherence of leucocytes to the vascular endothelium. Evidence has been presented that the anti-inflammatory effect of the hormone cannot be explained on the basis of its vasoconstrictive properties alone. The experimental observations support the hypothesis that cortisone exerts a direct protective action upon endothelial cells and leucocytes, and that in so doing, it renders them refractory to the tissue products which initiate inflammation.

Animals↗
PubMed1955

Factors influencing host-virus interactions. I. A comparison of viral multiplication and histopathology in infant, adult, and cortisone-treated adult mice infected with the Conn. -5 strain of Coxsackie virus.

A study was made of the pathogenesis of infection due to the Conn.-5 strain of Coxsackie virus in 4 to 5 day old infant mice, untreated adult mice, and adult mice treated with cortisone. The quantitative distribution of virus and the evolution of lesions in different tissues were followed for the first 7 days of the infection. Virus dissemination was prompt and widespread via the blood in all groups. In 4 to 5 day old infant mice viral multiplication and cellular injury occurred in many organs and tissues, while in untreated adult mice these processes were largely limited to the pancreas, even though infecting virus appeared to be equally available to other tissues from the blood. Treatment of adult mice with a single injection of 2.5 mg. cortisone resulted in viral multiplication and tissue damage in several sites in addition to the pancreas, the most marked occurring in the liver and heart. In a consideration of possible mechanisms involved, it was thought unlikely that the differences in the course of the disease in the three groups could be attributed solely to differences in the specific immune response. It is suggested that developmental changes in cells and tissues, perhaps related to cellular metabolism and alterable by cortisone administration, are the major factors determining the location and extent of viral multiplication and tissue injury in this infection in mice.

Animals↗
PubMed1956

Studies on serum proteolytic enzyme inhibition; effect of tissue destruction, cortisone acetate, and splenectomy on the serum trypsin inhibitor.

Serial studies of the serum levels of trypsin inhibitor have been performed on monkeys following injection of turpentine-falba, total body irradiation, thermal injury, splenectomy, administration of cortisone acetate and egg albumin. Following the injection of turpentine-falba mixture there was a prompt elevation in the trypsin inhibitor power of the serum. A similar response accompanied the administration of cortisone acetate. The response to cortisone was not inhibited by removal of the spleen. Animals premedicated with cortisone acetate for 3 and 4 weeks showed no statistically significant change in the level of the serum inhibitor following injection of the turpentine-falba. Total body irradiation and immunization with egg albumin were accompanied by a very slight rise in the inhibitory power of the serum despite a prompt and extensive drop in the total white blood cell count in the irradiated animals, and development of precipitins in all of the immunized animals. The significance of these findings is discussed.

Animals↗
PubMed1956

Reversible collapse of rabbit ears after intravenous papain, and prevention of recovery by cortisone.

A substance has been demonstrated in solutions of crude papain, which, when injected intravenously into 1 kilo rabbits, in amounts less than 5 mg., results in complete collapse of both ears. The phenomenon becomes visible 4 hours after injection, and is complete within 24 hours. 3 or 4 days after papain, the ears gradually reassume their normal form. Ear collapse is associated with depletion of the ear cartilage matrix, and the disappearance of basophilia from the matrix. Similar changes occur in all other cartilage tissues, including bones, joints, larynx, trachea, and bronchi. At the time when the ears are restored to normal shape, the basophilic matrix reappears in cartilage. Repeated injections of papain, over a period of 2 or 3 weeks, bring about immunity to the phenomenon of ear collapse. When the arterial circulation to one ear is occluded for 15 minutes at the time of injection of papain, this ear is protected against collapse. The effect of crude papain could not be reproduced by crystalline papain protease or crystalline papain lysozyme, which together comprise a considerable portion of the dry weight of papain. The nature of the responsible factor has not been determined, and the possibility that chymopapain may be implicated is currently under study. Cortisone prevents the return of papain-collapsed ears to their normal shape and rigidity. Possibly this reflects a capacity of cortisone to impede the synthesis or deposition of sulfated mucopolysaccharides in tissues.

Animals↗
PubMed1957

The influence of cortisone on experimental viral infection. IIL Effects on certain dynamics of influenza virus increase.

The administration of cortisone to chicken embryos infected with influenza B virus results in (a) an initial inhibition of viral synthesis and (b) an eventual increase in the final yield of virus attained. Increased yields of virus are attained regardless of the number of viral particles in the infecting inoculum or the proportion of particles which are infective. Changes in the distribution ratios of allantoic fluid and intramembrane virus are effected by cortisone only as the secondary result of reduction in viral synthesis. The manifest effect of cortisone on influenza A virus increase is inhibitory unless inocula containing relatively high proportions of inactive viral particles are used.

Animals↗