Lack of involvement of leukotriene and platelet activating factor in passive cutaneous anaphylaxis in rats

Taira, Masafumi; Kohno, Shigekatsu; Yamamura, Hideki; Ohata, Katsuya

doi:10.1007/bf01968100

Cited by 17 publications

(6 citation statements)

References 14 publications

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“…In other words, the drug must affect any event prior to the vascular permeability in the PCA. As previously reported, the time courses of histamineand serotonin-induced cutaneous vascular permeability, and PCA are almost identical [3]: they are completed within 10 min, suggesting that the time required from antigen-antibody reaction to histamine and serotonin release from the mast cell is quite short. In addition to this, no rapid inhibition of histamine-and serotonin-induced cutaneous vascular permeability by the oral administration of l-ephedrine in the present experiments further strongly suggested that the rapid inhibition of PCA by oral l-ephedrine is exerted through the mechanism that the drug affects a reaction prior to the absorption from the gastrointestinal tract.…”

Section: Discussionsupporting

confidence: 54%

“…PCA results from the increased vascular permeability by anaphylactically released histamine and serotonin from mast cells [3]. Therefore, drugs suppressing any step from the antigen-antibody reaction to the vascular permeability results in the inhibition of the reaction.…”

Section: Discussionmentioning

confidence: 99%

“…Conditions for preparation and antigen challenge of the actively sensitised skin fragments were as described elsewhere [3]. In brief, on day 14 after the first immunisation, following sacrifice of the animal, the shaved dorsal skin was removed and cut into pieces of approximately 1 ¥ 1 ¥ 1 mm in size with a razor blade.…”

Section: Anaphylaxis Of the Skin Fragmentsmentioning

confidence: 99%

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Immediate inhibition by oral l -ephedrine of passive cutaneous anaphylaxis of rats: indirect inhibition of anaphylactic chemical mediator release from the mast cell

Shibata¹,

Minami²,

Hirata³

et al. 2000

Inflammation Research

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These results were strongly indicative that the prompt suppression of the PCA by oral l-ephedrine was not exerted following the drug was absorbed from the gastrointestinal tract. Thus, the result may be from an indirect inhibition of chemical mediator release, possibly through an unidentified stimulation of the nervous system, but not from the inhibition of chemical mediator release by the direct interaction of drug to mast cells and not from the decreased vascular permeability.

show abstract

Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Anaphylaxis Of the Skin Fragmentsmentioning

confidence: 99%

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Immediate inhibition by oral l -ephedrine of passive cutaneous anaphylaxis of rats: indirect inhibition of anaphylactic chemical mediator release from the mast cell

Shibata¹,

Minami²,

Hirata³

et al. 2000

Inflammation Research

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“…Mast cells release chemical mediators such as histamine and serotonin, which in turn increase vascular permeability and plasma exudation from the nearby microvasculature in the passive cutaneous anaphylactic reaction and in compound 48/80 challenge (Saria et al 1983(Saria et al , 1984. Since indomethacin has no effect on the plasma exudation in response to compound 48/80 and in the passive cutaneous anaphylactic reaction (Taira et al 1988;Wang et al 1994), the inhibition by PP1D1 of the edematous responses caused by polymyxin B, compound 48/80 and anaphylaxis was not mainly through inhibition of the prostaglandin pathway. Indeed, in the in vitro screening test, PP1D1 inhibited compound 48/80-induced rat peritoneal mast cell degranulation with an ICs0 value of about 1.5 gM (Lien JC, Huang L J, Wang JP, Teng CM, Lee KH, Kuo SC, unpublished observations).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of hind-paw edema and cutaneous vascular plasma extravasation by 2-chloro-3-methoxycarbonylpropionamido-1,4-naphthoquinone (PP1D1) in mice

Wang

Chen

Kuo

1996

Naunyn-Schmiedeberg's Arch Pharmacol

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2-Chloro-3-methoxycarbonylpropionamido-1,4-naphthoquinone (PP1D1) produced a dose-dependent inhibition of the polymyxin B-induced hind-paw edema in normal as well as in adrenalectomized mice. A comparable inhibitory profile was observed in mice to which PP1D1 was injected i.p. or applied orally. Unlike dexamethasone, PP1D1 had no effect on the liver glycogen content in fasting adrenalectomized mice. Ear edema caused by passive cutaneous anaphylactic reaction, or by subcutaneous injection of compound 48/80, histamine, serotonin, bradykinin or substance P was reduced by PP1D1 in a dose-dependent manner. In addition, topical application of PP1D1 suppressed the capsaicin- and arachidonic acid-induced ear edema. In compound 48/80-pretreated mice, the tissue histamine content was greatly reduced. Under these conditions, PP1D1 reduced the bradykinin- and substance P-induced ear edema to a significantly greater extent than diphenhydramine plus methysergide. These results suggest that the inhibitory effect of PP1D1 on the edematous response is due to the protection of the microvasculature from mediator challenge.

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“…Vasocortin inhibits the early phase of car rageenin paw edema, and antiflammin, a nonapeptide fragment of lipocortin with inhibitory activity for phos pholipase A2 in vitro, inhibits the late phase in rats. In spite of these reports, however, roles of these proteins in the anti-inflammatory or anti-allergic action of GC have not yet been established, and lipocortin is consi dered not to play important roles in the inhibition of PCA by GC in mice and rats (35,36).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms for Glucocorticoid Inhibition of Immediate Hypersensitivity Reactions in Rats

Miura

Inagaki

Yoshida

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-The inhibitory mechanisms of immediate hypersensitivity reactions by glucocorticoid (GC) were studied in rats. Homologous passive cutaneous anaphylaxis (PCA) mediated by IgE anti bodies and cutaneous reactions caused by histamine, serotonin and leukotriene C4 were elicited at the same time in the same rats. Three kinds of GC, hydrocortisone, prednisolone and dexamethasone, in hibited all these reactions significantly. Although mediator-induced cutaneous reactions were inhibited transiently around 2 hours after GC administration, inhibition of PCA was more potent and lasted long er. A time lag seemed to be essential for both inhibitions. IgE antibody-mediated histamine release in vivo in the rat peritoneal cavity was also inhibited by GC administration significantly, and the inhibition was long lasting when compared to those of the mediator-induced cutaneous reactions. Tyrosine amino transferase (TAT) activity in the rat liver increased significantly by GC administration, and the in creased TAT activity was completely abrogated by simultaneous administration of 5 mg/kg of cyclohex imide (CH). In the same experimental condition, although inhibition of histamine-induced cutaneous reaction by GC was completely abrogated, the inhibition of PCA elicited at the same time in the same rats was only partially attenuated. Furthermore, the same dose of CH little affected the dexamethasone inhibition of histamine release in the rat peritoneal cavity, although the increase of TAT activity in the liver of the same rats was completely abrogated. These results demonstrate that PCA is inhibited by GC through at least 2 mechanisms, inhibition of mediator release from mast cells and non-specific in hibition of vascular permeability increase caused by released mediators. Although the latter action of GC is dependent upon protein synthesis, the former seems to be mediated by a unique mechanism in dependent of protein synthesis.

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Lack of involvement of leukotriene and platelet activating factor in passive cutaneous anaphylaxis in rats

Cited by 17 publications

References 14 publications

Immediate inhibition by oral l -ephedrine of passive cutaneous anaphylaxis of rats: indirect inhibition of anaphylactic chemical mediator release from the mast cell

Immediate inhibition by oral l -ephedrine of passive cutaneous anaphylaxis of rats: indirect inhibition of anaphylactic chemical mediator release from the mast cell

Inhibition of hind-paw edema and cutaneous vascular plasma extravasation by 2-chloro-3-methoxycarbonylpropionamido-1,4-naphthoquinone (PP1D1) in mice

Mechanisms for Glucocorticoid Inhibition of Immediate Hypersensitivity Reactions in Rats

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