Anaphylactoid Inflammation Research Articles

Sensitization by insulin of the anaphylactoid inflammation in rats.

The possible mode of action of insulin, in terms of its sensitizing effect on dextran-induced anaphylactoid reaction was studied. In normal rats, the sensitizing effect was inhibited by actinomycin D and cycloheximide 1 h after the administration of the drugs. 24 h after actinomycin D or cycloheximide, the inflammatory response was considerably reduced. The inhibition could not be reversed by insulin. In contrast, insulin restored the decreased susceptibility of diabetic animals to dextran. This effect was not influenced by actinomycin D and cycloheximide. None of the drugs used influenced the blood-sugar-lowering activity of insulin. Cyclophosphamide, parallel to the profound lymphopenia produced, prevented the sensitizing effect of the hormone. Viable lymphoid cells prepared from young normal rats completely restored the suppressed insulin response. Liver cells had no such an effect. Lymph node cells incubated in the presence of insulin released a factor(s), capable of increasing dextran edema, to the incubation medium. Pretreatment with actinomycin D and cycloheximide of the lymphocyte-donor rats interfered with the ability of insulin to produce the pro-inflammatory factor(s). The possible significance of the findings is discussed.

Effect of various nucleic acid and protein synthesis inhibitors on the insulin-induced sensitization of anaphylactoid inflammation in rats

Effect of various nucleic acid and protein synthesis inhibitors on the insulin-induced sensitization of anaphylactoid inflammation in rats

Effect of various nucleic acid and protein synthesis inhibitors on anaphylactoid inflammation in rats

The effects of several nucleic acid and protein synthesis inhibitors (NAPSI) on dextran anaphylactoid inflammation, and on foot oedema evoked by compound 48/80 and serotonin (5-HT) were investigated in rats. Pretreatment with actinomycin D, mannomustine, 6-mercaptopurine (6-MP), emetine and chloramphenicol inhibited the inflammatory response induced by dextran and compound 48/80, but did not influence the response to 5-HT. A marked anit-inflammatory action of actinomycin D, mannomustine and emetine was present within 30 hr of giving the first dose, while the anti-inflammatory effect of 6-MP and chloramphenicol developed only after 12 days pretreatment. Intrapedal injection of an extract (0.1 ml) prepared freshly from the shock-organ of normal rats significantly antagonized the anti-inflammatory effect of the treatment with NAPSI in acute experiments. The authors suggest that pretreatment with NAPSI interferes with the de novo synthesis of the enzyme(s) which play a role in the release of those substances mediating the inflammatory reaction. The anti-inflammatory activity of these drugs can be attributed to the decreased level of enzyme(s) participating in the early vascular phase of the acute inflammation.

Suppression of inflammation and histidine decarboxylase by protein synthesis inhibitors.

ARTICLESSuppression of inflammation and histidine decarboxylase by protein synthesis inhibitorsRW Schayer, and MA ReillyRW Schayer, and MA ReillyPublished Online:01 Aug 1968https://doi.org/10.1152/ajplegacy.1968.215.2.472MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByInterleukin‐1 and histamine are essential for inducing nickel allergy in mice18 August 2019 | Clinical & Experimental Allergy, Vol. 49, No. 10Alicyclic Hydrocarbons17 August 2012Radiometric Methods of Enzyme Assay31 October 2006Alicyclic Hydrocarbons16 April 2001Induction by interleukin-1 (IL-1) of the mRNA of histidine decarboxylase, the histamine-forming enzyme, in the lung of mice in vivo and the effect of actinomycin DBiochemical Pharmacology, Vol. 53, No. 9Induced histidine decarboxylase in endotoxic shock: Identification of the enzyme in rat liver and influence of its inhibitors on survival parametersAgents and Actions, Vol. 18, No. 1-2Simultaneous induction of histidine and ornithine decarboxylases and changes in their product amines following the injection of escherichia coli lipopolysaccharide into miceBiochemical Pharmacology, Vol. 31, No. 8Comparison of the anti-inflammatory effects of dexamethasone, indomethacin and BW755C on carrageenin-induced pleurisy in ratsEuropean Journal of Pharmacology, Vol. 77, No. 4Metabolism and Excretion of HistamineRabbit aortic endothelial and medial histamine synthesis following short-term cholesterol feedingExperimental and Molecular Pathology, Vol. 23, No. 3Histamine and its metabolism in mammals part II: Catabolism of histamine and histamine liberationAgents and Actions, Vol. 5, No. 3Rabbit aortic histamine synthesis following short-term cholesterol feedingAtherosclerosis, Vol. 21, No. 2Histamine and microcirculationLife Sciences, Vol. 15, No. 3The histaminase activity of guinea-pig's plasma during experimental inflammation I. The enzyme activityAgents and Actions, Vol. 4, No. 2Effects of shearing stress on aortic histamine synthesisExperimental and Molecular Pathology, Vol. 20, No. 1Evaluation for Immunosuppressive and Antiallergic ActivityStudies on the mechanism of activation and deactivation of histidine decarboxylaseEuropean Journal of Pharmacology, Vol. 20, No. 3Histamine: Entering physiologyExperientia, Vol. 28, No. 9Effect of glucocorticoids on histamine metabolism in mice19 July 2012 | British Journal of Pharmacology, Vol. 45, No. 3Possible modes of action of ACTH and glucocorticoids in allergic diseasesClinical <html_ent glyph="@amp;" ascii="&"/> Experimental Allergy, Vol. 2, No. 1HISTAMINE FORMATION IN RAT BRAIN IN VIVO: EFFECTS OF HISTIDINE LOADS 2Journal of Neurochemistry, Vol. 19, No. 3The regulation of gastric histidine decarboxylase activity: I. Effect of pyridoxine deficiencyLife Sciences, Vol. 10, No. 21Effect of various nucleic acid and protein synthesis inhibitors on the insulin-induced sensitization of anaphylactoid inflammation in ratsLife Sciences, Vol. 10, No. 6In vivo studies on histamine catabolism and its inhibition19 July 2012 | British Journal of Pharmacology, Vol. 38, No. 3Enhancement of inflammation and histamine formation by actinomycin D19 July 2012 | British Journal of Pharmacology, Vol. 37, No. 2HISTIDINE DECARBOXYLASE AND ITS INHIBITIONAnnals of the New York Academy of Sciences, Vol. 166, No. 1 Vitamin B6 inChapter 19. Non-steroidal Anti-inflammatory AgentsFurther studies on the histidine-histamine relationship in vivo: effects of endotoxin and of histidine decarboxylase inhibitors19 July 2012 | British Journal of Pharmacology, Vol. 34, No. 3 More from this issue > Volume 215Issue 2August 1968Pages 472-476 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.215.2.472PubMed4298917History Published online 1 August 1968 Published in print 1 August 1968 Metrics

Allergic and anaphylactoid inflammation.

<h3>To the Editor:—</h3> The first reports on allergic phenomena uniformly stressed that sensitization produces a state without protection (anaphylaxis) against minimal amounts of the antigen. Testing procedures for the detection of allergies are only reliable when carried out with minimal amounts of the allergen. This rule is of utmost importance when testing with anaphylactoid substances. Intracutaneous or epicutaneous applications of such substances in higher amounts might easily produce anaphylactoid inflammation which is indistinguishable from true allergic inflammation. In "Allergy to Dermatologic Agents" (<b>198</b>:517, 1966), it was claimed that patch tests for neomycin allergy should be performed with 20% to 40% solutions. Even though the exact amount of solution for the testing procedure is not mentioned, one might assume that an amount of 50 to 200 mg of neomycin is applied on skin areas with greatly enhanced penetration. Studying the table in the paper, one finds the number of "allergic"

Catecholamine-induced Mast Cell Discharge with Anaphylactoid Purpura

It was observed almost thirty years ago that, following an intravenous or interaperitoneal injection of egg white, rats develop an acute swelling of the “acral regions” particularly the paws, snout, ears and tail. Histologically, the affected parts exhibit an acute serous inflammation similar to that seen in certain anaphylactic reactions, but since the egg-white-induced changes occur after the first injection (without previous sensitization) the response was named “anaphylactoid inflammation” (1).

EFFECTS OF INFLAMMATION ON PROTEINS AND ENZYMES IN RAT PLASMA

The effects of anaphylactoid inflammation in rats on the limb volume, hematocrit, and plasma proteins, and on the activities of plasmin, antiplasmin, and esterase of the plasma were studied. The hyperemia and edema of the limbs and other extremities which occurred following the injection of dextran were found to be accompanied by a transient hemoconcentration and a prolonged depression in the concentration of plasma proteins (both albumin and globulin fractions). The specific activity of plasma esterase was increased and that of antiplasmin was decreased during inflammation compared with control animals. No consistent or significant change was observed in the specific activity of plasmin.

Prevention by stress and cortisol of gastric ulcers normally produced by 48/80.

SummaryExperiments on rats indicate that gastric ulcers produced by various stressors (as part of alarm reaction) differ qualitatively from those induced by histamine liberator 48/80. The latter lesions as well as. the anaphylactoid inflammation and shock produced by 48/80 can actually be prevented by stressors or Cortisol, although these same agents are, in themselves, capable of producing the alarm-reaction type of gastric erosion.

EFFECTS OF INFLAMMATION ON PROTEINS AND ENZYMES IN RAT PLASMA

The effects of anaphylactoid inflammation in rats on the limb volume, hematocrit, and plasma proteins, and on the activities of plasmin, antiplasmin, and esterase of the plasma were studied. The hyperemia and edema of the limbs and other extremities which occurred following the injection of dextran were found to be accompanied by a transient hemoconcentration and a prolonged depression in the concentration of plasma proteins (both albumin and globulin fractions). The specific activity of plasma esterase was increased and that of antiplasmin was decreased during inflammation compared with control animals. No consistent or significant change was observed in the specific activity of plasmin.

Glucagon, insulin and anaphylactoid inflammation.

Glucagon, insulin and anaphylactoid inflammation.

Sensitization by insulin to dextran anaphylactoid inflammation in spinal rats.

Insulin sensitizes normal rats considerably to the ‘anaphylactoid’ inflammation produced by the administration of dextran. This sensitization manifests itself to the same extent in the spinal rats. Therefore, the sensitization takes place despite the interruption of the spinal nervous pathways and despite the stress.

An experimental model illustrating the pathogenesis of the diseases of adaptation.

WHEN the pituitary-adrenocortical axis is activated during the general adaptation syndrome, various types of inflammatory responses are suppressed. This had been demonstrated first for the so-called histamine appendicitis (1, 2), several varieties of acute inflammatory lung edema (3, 4) and the anaphylactoid inflammation caused by egg-white in the rat (5, 6). It undoubtedly holds true also for many other experimental and clinical instances of inflammation. However, subsequently it was noted that—at least under certain “conditioning” circumstances—systemic stress can also facilitate the production of inflammatory lesions (e.g., nephritis and myocarditis after exposure to cold). The adrenals were thought to play an important part in both these responses, since adrenalectomy prevented the inhibition, as well as the stimulation of inflammation by systemic stress (7). Later, when pure adrenal corticoids became available, it was observed that some, the so-called mineralo-corticoids (e.g., desoxycorticosterone) ...

Anaphylactoid inflammatory responses to preparations of duodenal intrinsic factor and of gastric nucin.

Experiments on rats showed that intravenously administered, partially purified, preparations of duodenal intrinsic factor and of gastric mucin are capable of producing a typical anaphylactoid inflammation in the rat.

Influence of inoculation site upon the course of the “anaphylactoid reaction” to dextran

The so-called “anaphylactoid reaction” is an acute serous inflammation limited to certain “shock organs,” namely, the paws, ears, snout, and the clitoris or penis. It is readily elicited by the intravenous, intraperitoneal or intrapleural injection of small doses of dextran. Small amounts of dextran, injected subcutaneously into such susceptible regions as the front or hind paws and the snout, produce not only a very marked topical inflammation but also a pronounced response in distant “shock organs.” In fact, under these conditions, even the hypersensitive regions, remote from the injection site, react more markedly than if the same amount is directly injected into the blood. Administration of comparable quantities of dextran into the subcutaneous tissue anywhere in the immediate vicinity, but just outside a “shock organ,” does not evoke either a local or a distant anaphylactoid response. In the event of direct intravenous administration of dextran, a maximal response is obtained at a relatively low dosage level; as the dose is raised above this, activity declines. It is not yet evident why dextran, injected directly into a region where it can produce topical anaphylactoid inflammation, also elicits a similar response at a distance, but certain possible pathogenic mechanisms have been considered.