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At least 55 records · Page 3Linked to original sources
PubMed1955

Studies on the pathogenesis of acute inflammation. I. The inflammatory reaction to thermal injury as observed in the rabbit ear chamber.

A special adaptation of the rabbit ear chamber has been devised to study in vivo, under high magnification, the acute inflammatory reaction to thermal injury. Systematic observations of the cellular response have led to the following conclusions. 1. Contrary to the commonly accepted view, vasodilatation does not always precede the adherence of leucocytes to vascular endothelium. 2. The fact that leucocytes often adhere to one another as well as to the endothelium indicates that the increased adhesiveness characteristic of the early stages of inflammation is not limited to the surfaces of the endothelial cells. 3. The sharing of erythrocytes and platelets in this increased stickiness suggests that a "plasma factor" is involved. There is indirect but as yet inconclusive evidence that the plasma factor may concern the clotting mechanism of the blood. 4. The adherence of leucocytes to the endothelium is usually first noted on the side of the vessel closest to the site of injury. This previously undescribed phenomenon of "unilateral sticking" is in keeping with the concept that the vascular reaction is caused by products of cellular damage which diffuse to the vessel from the site of injury. 5. Leucocytes always become adherent to the endothelium before penetrating the vessel wall. They often migrate about for some time on the endothelial surface before undergoing diapedesis. 6. Although no definite stomata are at any time visible in the endothelium, penetrating leucocytes may leave behind temporary defects through which other leucocytes and even erythrocytes may pass. 7. The diapedesis of leucocytes appears to depend primarily upon cellular motility. It may occur in static vessels where there is presumably little if any hydrostatic pressure. 8. The diapedesis of erythrocytes, on the other hand, is a passive process depending upon intravascular pressure. Its occurrence is greatly exaggerated in areas in which intravascular pressure becomes elevated. Such elevations occur as the result of proximal arteriolar dilatation and distal occlusion of vessels. 9. Once they have reached the extravascular tissues the leucocytes move about more or less at random, apparently uninfluenced by any compelling chemotactic force. Their resultant migration, however, is toward the site of injury around which they eventually tend to congregate. 10. The histiocytes normally present in the connective tissue appear to play no role in the type of acute inflammatory reaction produced in these experiments.

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↗
PubMed1961

Studies on the pathogenesis of staphylococcal infection. II. The effect of non-specific inflammation.

Studies have been described in which the effect of early and late or established inflammation, upon staphylococcus infection of rabbit skin has been evaluated. Inflammation was produced in skin by thermal, chemical, bacterial and immunological injury, and it was found that the area of inflammation was more susceptible to staphylococcus infection than was normal skin if the bacteria were injected within 2 to 3 days after the injury. When staphylococci were injected into an area of inflammation of over 3 days' duration, there appeared to be an increase in local resistance to infection. The way in which inflammation was produced seemed to have a little influence upon the effects observed. This influence of non-specific inflammation upon staphylococcus infection was compared with the influence of specific bacterial hypersensitivity, which also is associated with an increase in infectivity of the microorganism in sensitized animals. It was concluded that specific bacterial hypersensitivity probably increases susceptibility to infection with the staphylococcus in the same way as non-specific inflammation. The general significance of non-specific inflammation upon infection is also discussed.

Animals↗
PubMed1961

Studies of acute phase protein. I. An immunohistochemical method for the localization of Cx-reactive protein in rabbits. Association with necrosis in local inflammatory lesions.

A method is presented for the immunohistochemical localization of Cx-reactive protein in rabbits, based on the use of a defined antiserum and rigorous fixation techniques requisite for this antigen. In animals in which inflammatory lesions and CxRP response were induced by intramuscular injection of typhoid vaccine, Cx-reactive protein was localized only in the area of local inflammation within muscle fibers showing morphologic evidence of necrotic change. Within such altered fibers, CxRP was observed in peripheral segments of myofiber or in subsarcolemmal sarcoplasm, in scattered deposits in sarcoplasm, and in vacuolar inclusions. No CxRP was found at any time in polymorphonuclear or mononuclear cells in the inflammatory lesion, nor in contralateral muscle, regional or distal lymph nodes, liver, spleen, thymus, heart, or kidney, except as traces in lumens of vessels or interstitium. CxRP was first detected in necrotic myofibers at the inflammatory site after a latent period of 8 to 10 hours following injection of the inflammatory stimulus and could be demonstrated in these sites for the 48 hours of the experiment. It could not be observed at the inflammatory site before appearance in the blood. Identical histologic localization in necrotic myofibers at the site of the local lesions was found following induction of granulocytopenia with nitrogen mustard. These findings are consistent with the hypothesis that CxRP is formed locally at the site of inflammation from tissue elements undergoing necrotic change. Alternatively, secondary deposition from the blood at the inflammatory site cannot be excluded, but is considered less likely in view of the failure to obtain evidence of a cellular localization of CxRP in other organs.

Acute-Phase Proteins↗
PubMed1962

On the relation of necrosis and inflammation to denaturation of proteins.

Necrosis of the skin was produced by the injection of measured quantities of electrolytes and of amino compounds into the dermis, and the relative ability of these substances to produce it was determined. Inflammation characterized by edema and accumulation of leucocytes accompanied necrosis. The ability of electrolytes to produce necrosis was found to increase with the valence of their basic ion, and in this respect was in accord with their ability to denature proteins. The quantity of different electrolytes needed to produce necrosis varied in the same order as the molar concentration of these electrolytes, that is isotonic with liver or kidney cells. Necrosis caused by amino compounds occurred with similar relation to the isotonicity of liver cells. In this as in other relations the cells acted as osmometers. The foregoing relations indicate that denaturation of proteins, necrosis of living tissue, and osmotic activity of liver or kidney cells are determined by molecular weight, valence, and ion-dissociation of electrolytes, that is, by the factors that determine the colligative properties of electrolytes. Agents such as turpentine, mustard, or croton oil and some halogen substitution compounds of methyl that are insoluble in water and soluble in lipoids have produced skin necrosis and inflammation.

Amino Acids↗
PubMed1951

The effect of adrenocorticotropic hormone on inflammation due to tuberculin hypersensitivity and turpentine and on circulating antibody levels.

The treatment with adrenocorticotropic hormone of guinea pigs sensitized with heat-killed tubercle bacilli caused suppression of their skin reactivity to tuberculin. Similar animals treated with saline did not show this change. Normal guinea pigs treated with adrenocorticotropic hormone showed suppression of inflammation, but not necrosis, produced by intracutaneous oil of turpentine. There was slight, but probably not significant, diminution of inflammation during saline administration. Tuberculin complement-fixing antibody titers were not altered by either adrenocorticotropic hormone or saline administration. Adrenocorticotropic hormone produced marked eosinopenia and lymphopenia in guinea pigs.

Adrenocorticotropic Hormone↗
PubMed1959

Antiphlogistic activity of iproniazid.

Iproniazid was found to inhibit formalin-induced oedema of the foot, dextran-induced oedema and cotton-pellet-induced granulomatous tissue in the rat. The presence of the adrenals was essential for the antiphlogistic activity. The antiphlogistic action was not accompanied by any antipyretic effect. Inhibition of formalin-induced oedema was also observed with phenylbutazone and with salicylamide.

Animals↗
PubMed1961

Some inhibitors of histamine-induced and formaldehyde-induced inflammation in mice.

The swelling and capillary hyperpermeability of the mouse foot in response to an injection of formaldehyde, and the increased capillary permeability to an intradermal injection of histamine, have been investigated. Cortisone, mepyramine and sodium salicylate were effective in reducing histamine-induced inflammation, sodium salicylate being less active in the adrenalectomized animal. In formaldehyde-induced inflammation, however, cortisone was ineffective whereas sodium salicylate was effective in the intact mouse, but not in the adrenalectomized animal. Certain aryloxypropionates and anti-esterases were also active in reducing the severity of the formaldehyde-induced inflammation.

Analgesics↗
PubMed1962

A study of possible mediators of inflammatory reactions in the mouse foot.

A number of compounds have been studied for their ability to antagonize the inflammatory reaction produced by injections of formaldehyde and 5-hydroxytryptamine in the mouse foot. An attempt has been made to elucidate the ways in which certain hydroxybenzoates, pyrazolones, sympathomimetic amines, flavone and flavanone glycosides, local anaesthetics, antihistamines and anti-5-hydroxytryptamine substances produce their anti-inflammatory effect.

Anesthetics, Local↗