Role of endogenous histamine in postanaphylactic phase of allergic inflammation was examined by using a rat model of allergic inflammation of air pouch type. Histamine in the exudate revealed a biphasic increase. The anaphylactic increase was followed by rapid decrease and then by a gradual rising in postanaphylactic phase with the maximum attained around 24 hr after the antigenic challenge. It again decreased gradually. The histamine increase in the postanaphylactic phase was accompanied by the increase of histidine decarboxylase activity in inflammatory tissues. Local administration of pyrilamine, an H1 antagonist, together with either methysergide, a serotonin antagonist, or cimetidine, an H2 antagonist, was unable to inhibit vascular permeability response in the postanaphylactic phase. When histaminase was administered locally in the postanaphylactic phase to reduce histamine in the exudate, neutrophil accumulation in the exudate was enhanced without any change in exudate accumulation. Enhancement of the neutrophil accumulation was also inducible with local administration of cimetidine but not with pyrilamine. Local administration of histamine inhibited the neutrophil accumulation dose-dependently. These results suggest that endogenous histamine released in the postanaphylactic phase contributes to downward regulation of neutrophil accumulation in the inflammatory site without affecting the vascular permeability.
|Number of pages||7|
|Journal||Journal of Pharmacology and Experimental Therapeutics|
|Publication status||Published - 1987 Jun 1|
ASJC Scopus subject areas
- Molecular Medicine